(Circulation. 1995;91:1314-1319.)
© 1995 American Heart Association, Inc.
Articles |
Nitric Oxide Is Responsible for Flow-Dependent Dilatation of Human Peripheral Conduit Arteries In Vivo
From the Department of Pharmacology, VACOMED, IFRMP, Rouen University Medical School and Rouen Hospital (France) (R.J., V.R., E.H.B., C.T.) and the Department of Clinical Pharmacology, Basel University Hospital (Switzerland) (W.E.H., L.L., T.F.L.).
Correspondence to T.F. Lüscher, MD, Cardiology, University Hospital, CH 4031, Bern, Switzerland.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Experimental evidence suggests that flow-dependent dilatation of conduit arteries is mediated by nitric oxide (NO) and/or prostacyclin. The present study was designed to assess whether NO or prostacyclin also contributes to flow-dependent dilatation of conduit arteries in humans.
Methods and Results Radial artery internal diameter (ID) was measured continuously in 16 healthy volunteers (age, 24±1 years) with a transcutaneous A-mode echo-tracking system coupled to a Doppler device for the measurement of radial blood flow. In 8 subjects, a catheter was inserted into the brachial artery for measurement of arterial pressure and infusion of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 8 µmol/min for 7 minutes; infusion rate, 0.8 mL/min). Flow-dependent dilatation was evaluated before and after L-NMMA or aspirin as the response of the radial artery to an acute increase in flow (reactive hyperemia after a 3-minute cuff wrist occlusion). Under control conditions, release of the occlusion induced a marked increase in radial blood flow (from 24±3 to 73±11 mL/min; P<.01) followed by a delayed increase in radial diameter (flow-mediated dilatation; from 2.67±0.10 to 2.77±0.12 mm; P<.01) without any change in heart rate or arterial pressure. L-NMMA decreased basal forearm blood flow (from 24±3 to 13±3 mL/min; P<.05) without affecting basal radial artery diameter, heart rate, or arterial pressure, whereas aspirin (1 g PO) was without any hemodynamic effect. In the presence of L-NMMA, the peak flow response during hyperemia was not affected (76±12 mL/min), but the duration of the hyperemic response was markedly reduced, and the flow-dependent dilatation of the radial artery was abolished and converted to a vasoconstriction (from 2.62±0.11 to 2.55±0.11 mm; P<.01). In contrast, aspirin did not affect the hyperemic response nor the flow-dependent dilatation of the radial artery.
Conclusions The present investigation demonstrates that NO, but not prostacyclin, is essential for flow-mediated dilatation of large human arteries. Hence, this response can be used as a test for the L-arginine/NO pathway in clinical studies.
Key Words: blood flow • endothelium-derived factors • L-NMMA • arteries • dilation
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Large arteries accommodate changes in blood flow by increasing their internal diameter (ID). Such a flow-dependent dilatation represents a fundamental mechanism that opposes neurogenic and myogenic vasoconstriction, increases conductance during exercise, and maintains shear stress within physiological values. In animals, flow-dependent dilatation is endothelium dependent and mediated by nitric oxide (NO) and/or prostacyclin.1 2 3 4 5 However, whether a similar mechanism also occurs in human arteries remains uncertain. This is especially critical because flow-dependent dilatation of large arteries in vivo has been used as an index of endothelial function in humans and is impaired in atherosclerosis.6 7 8 Thus, the present study was designed to assess whether NO or prostacyclin contributes to flow-dependent dilatation of peripheral arteries in humans.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Subjects
The study was performed in 16 healthy volunteers (10 men and 6 women; age, 24±1 years). All subjects were normotensive and nonsmokers and were not taking any medication at the time of the experiment. Blood cholesterol and blood glucose were 6.05±0.36 mmol/L and 4.32±1.07 mmol/L, respectively. The protocol was approved by the Basel Hospital ethical committee, and written informed consent was obtained from all participants.
Measurements of Radial Artery Hemodynamics
Measurements were
performed while subjects were supine in a
quiet, air-conditioned room maintained at a constant temperature
(22°C to 24°C). Radial artery ID was measured continuously with a
high-precision A-mode echo-tracking device (NIUS 02, Asulab) with a
resolution on the diameter evolution of <1
µm.9 10 11
Briefly, a 10-MHz focused transducer was positioned over the radial
artery. The probe was set perpendicular to the artery by a stereotaxic
arm with micrometric screws, while proper positioning was adjusted with
a stereo Doppler mode. After switching to A-mode, the echoes from both
anterior and posterior walls of the artery were visualized on a screen
and tagged by electronic trackers, allowing continuous recording of the
artery ID as shown previously.9 The processed
radiofrequency line was visualized on a computer screen, and the
operator selected the peaks corresponding to the interfaces, after
which the exact position of each selected peak was determined by an
interpolation technique. Finally, radial artery blood velocity was
continuously recorded by an 8-MHz Doppler probe (Doptek 2002, Deltex).
Radial artery flow was calculated from the measurements of velocity and
ID. Positioning of the probes and of the electronic trackers was always
performed by the same investigator, after which calculation of radial
parameters was performed automatically without any further intervention
by the investigator.
Fig 1
shows a representative
tracing of the
measured parameters, ie, radial diameter, radial blood flow, and
arterial blood pressure throughout five consecutive cycles, showing
that the echo tracking technique allows continuous tracking of the
diameter signal throughout the cardiac cycle, even though the
systolic-diastolic differences in diameter are, in the
present case, <20 µm.
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In experiments involving L-NMMA, an 18-gauge catheter was inserted under local anesthesia (lidocaine 1%) into the left brachial artery for continuous measurement of arterial pressure (Statham P23Pb)12 and infusion of L-NMMA.13
Study Protocol
Subjects were allowed to rest 30 minutes after
instrumentation,
then heart rate, arterial pressure, radial artery flow, and diameter
were recorded for 5 minutes. After baseline measurements, an arterial
occlusion cuff placed at the wrist (ie, distal to the site of radial
artery measurements) was inflated for 3 minutes at 180 mm Hg and was
deflated to allow reactive hyperemia. All parameters were recorded
continuously throughout cuff inflation and during hyperemia until
radial artery diameter had returned to baseline (ie, within 7 minutes
after release of the cuff).
Subsequently, subjects received L-NMMA (Clinalfa; 8 µmol/min for 7 minutes; infusion rate, 0.8 mL/min) or aspirin 1 g PO. Five minutes after L-NMMA or 2 hours after aspirin, all parameters were again measured at baseline, and the same occlusion-hyperemia protocol was repeated. All measurements represent means of 15 cardiac cycles. Parameters were measured at baseline, peak increase in radial blood flow during hyperemia, and peak increase in radial artery ID. In addition, since experiments performed in dogs suggested that L-NMMA could reduce the duration of the hyperemic phase,14 15 we also calculated parameters characteristic of the duration of hyperemia, ie, the area under the curve of the flow response and the time elapsing between peak hyperemia and return to 50% of this peak (t1/2). Results are expressed as mean±SEM for 8 subjects in each group. Results were analyzed by repeated-measures ANOVA, followed, when ANOVA was significant, by a Tukey test, and a value of P<.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Stability of Hemodynamic Measurements and Reproducibility of Hyperemic Test Under Control Conditions
The stability of the measured hemodynamic parameters was assessed by two consecutive measurements over 30 minutes (t0 and t30) in 8 subjects who did not receive any treatment and in whom the probes were left in place throughout the observation period. Results are shown in Fig 2
. There were no changes in
arterial pressure, radial artery flow (t0, 31±7 and
t30, 30±8 mL/min), or radial artery diameter
(t0, 3.06±0.15 and t30,
3.05±0.14 mm) throughout the observation period. From these
experiments, intraobserver variability was calculated to be 5.7±2.6%
for radial flow and 1.3±0.4% for radial diameter.
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The
reproducibility of the hyperemic test was also assessed in the same
8 subjects as two consecutive ischemia-hyperemia cycles without any
treatment. Results are shown in Fig 2
. There were no
differences
between the two hyperemic tests, whether in terms of peak radial flow
(t0, 100±17 and t30, 102±13
mL/min), peak radial diameter (t0, 3.18±0.15 and
t30, 3.22±0.15 mm), or duration of the hyperemic
phase (area under the curve: t0, 6.8±1.2 and
t30, 6.4±1.0 arbitrary units [AU];
t1/2: t0, 32±6 and
t30, 31±5 seconds).
Effect of L-NMMA on Baseline Parameters and on Flow-Dependent
Dilatation
In the absence or in the presence of L-NMMA, hyperemia was
not
associated with any changes in heart rate or blood pressure, and
administration of L-NMMA did not induce any changes in heart rate or
arterial blood pressure (Table).
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In control conditions,
deflation of the occluding cuff increased radial
artery flow (from 24±3 to 73±11 mL/min; percent change from
baseline,
214±34%; P<.01; Figs 3 and 4)
and radial artery diameter (from 2.67±0.10 to
2.77±0.12 mm; percent change from baseline, 3.6±0.8%;
P<.01; Figs 3 and 4). However, the
increase in diameter was
delayed compared with the increase in blood flow; indeed, the time to
peak increase in flow was 7.1±2.4 seconds, whereas the time to peak
increase in diameter was 77.1±15.8 seconds (P<.01).
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P<.05 and
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At baseline (ie, before cuff wrist occlusion), L-NMMA decreased radial
flow (from 24±3 to 13±3 mL/min; P<.05; Fig
3) and
increased radial resistance (from 2.98±0.41 to 6.14±0.97
mm Hg · min/mL; P<.01) but did not significantly
affect radial artery diameter (from 2.67±0.10 to 2.62±0.11 mm;
P=NS). After L-NMMA, deflation of the occluding cuff was
associated with an increase in radial artery flow to 76±12 mL/min
(P<.01 versus baseline, Fig 3). These values
obtained at
peak hyperemia were not different from those obtained in the absence of
L-NMMA. However, the percent increase in flow during hyperemia was
higher than that observed in the absence of L-NMMA (Fig 4;
control,
214±34%; L-NMMA, 493±53%; P<.01). In addition,
L-NMMA
reduced the area under the curve (control, 6.8±1.2 and L-NMMA,
4.0±0.7 AU; P<.01; Fig 5) as well as
t1/2 (control, 31.6±6.2 and L-NMMA, 13.3±1.3 seconds;
P<.05; Fig 5). Thus, despite a similar peak
increase in
flow, L-NMMA markedly reduced the duration of hyperemia. After L-NMMA,
hyperemia was associated with a significant decrease in radial artery
diameter, to 2.55±0.11 mm (percent change from baseline,
-2.8±0.4%;
P<.01; Figs 3 and 4). This value was
lower than that
obtained in the absence of L-NMMA (2.77±0.12 mm; P<.01).
Thus, L-NMMA abolished flow-dependent dilatation of the radial artery
and converted it to a vasoconstriction.
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Effect of Aspirin on Baseline Parameters and Flow-Dependent
Dilatation
Administration of aspirin did not induce any changes in
heart rate
(control, 65±3 and aspirin, 62±2 beats per minute) or mean
arterial
pressure (control, 75±3 and aspirin, 76±3 mm Hg). The effect of
aspirin on reactive hyperemia and flow-dependent dilatation is shown in
Fig 6. Aspirin did not affect radial blood flow or
radial diameter at baseline (radial flow: control, 31±7 and aspirin,
28±7 mL/min; radial diameter: control, 3.06±0.15 and aspirin,
3.06±0.15 mm) or during hyperemia (radial flow: control, 100±17
and
aspirin, 89±13 mL/min; radial diameter: control, 3.18±0.15 and
aspirin, 3.18±0.15 mm). Furthermore, aspirin did not affect the
duration of the hyperemia (area under the curve: control, 6.8±1.2 and
aspirin, 5.9±1.2 AU; t1/2: control, 34±6 and aspirin,
31±8 seconds).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The main results of the present study performed in the human radial artery are that (1) local administration of the NO synthase inhibitor L-NMMA did not affect the peak increase in flow during hyperemia but reduced the duration of the hyperemia; (2) in the presence of L-NMMA, flow-dependent dilatation of the radial artery was abolished and converted to a vasoconstriction; and (3) in contrast to L-NMMA, cyclooxygenase inhibition with aspirin did not affect the reactive hyperemic response or the flow-dependent dilatation of the radial artery. These results demonstrate that NO is essential for the flow-mediated dilatation of the human radial artery in vivo.
Administration of L-NMMA decreased radial blood flow but did not affect radial diameter. The decrease in radial flow after L-NMMA is consistent with the existence of a basal release of NO in this vascular bed, in agreement with previous results obtained with plethysmographic techniques.13 16 In contrast, the modest effect of L-NMMA on radial diameter would suggest that basal release of NO is minimal at the level of these large peripheral arteries. In recent experiments in which L-NMMA was injected into the human left anterior descending (LAD) coronary artery, the L-arginine analogue also did not induce any change in proximal LAD diameter, although it induced a small decrease in distal LAD diameter, again suggesting that basal release of NO does not contribute significantly to the tone of large conduit arteries in humans.17 Hence, as shown previously in isolated arteries, the basal release of NO is not uniform in the circulation and may differ in arteries of different sizes18 19 as well as of different anatomic origin.20 Most likely, the basal release of NO is larger in the forearm microcirculation than in conduit vessels like the the radial artery.
One possibility to explain the apparent lack of effect of L-NMMA on radial diameter would be that the number of subjects on whom experiments were performed was insufficient to detect a significant reduction in radial diameter after L-NMMA. However, it should be noted that inclusion of three additional subjects who received L-NMMA according to the same protocol but were not subjected to hyperemia did not affect the outcome of the results on radial diameter (baseline, 2.93±0.11 and L-NMMA, 2.90±0.14 mm; percent change from baseline, -1.5±1.7%; P=.49; data not shown). Another possibility is that the dose of L-NMMA used was not sufficient to block the endothelial synthesis of NO. Although we have not assessed the effect of an NO-dependent vasodilator (such as acetylcholine) in the present experiments, it must be noted that the dose of L-NMMA used (8 µmol/min for 7 minutes) is higher than that previously shown by different investigators to blunt the forearm response to acetylcholine.13
In the present experiments, aspirin administered at a dose known to be effective in blocking vascular cyclooxygenase21 did not affect reactive hyperemia or flow-dependent dilatation of the radial artery. The lack of effect of aspirin on postischemic flow is not in agreement with the study of Carlsson and Wennmalm,22 in which reactive hyperemia of the forearm was inhibited by aspirin as well as other inhibitors of cyclooxygenase. There are, however, several possible explanations for these different results. First, it must be noted that, in our experiments, blood flow was measured with a Doppler system, whereas in the study of Carlsson and Wennmalm, flow was measured by plethysmography. Indeed, the hyperemia-induced increase in flow, as assessed by plethysmography, is caused by dilatation of both small arteries and veins.23 Since the venous ischemic vasodilatation is mediated primarily by cyclooxygenase products and reduced after aspirin blockade,24 the aspirin-induced decrease in postischemic hyperemia observed with the plethysmographic method may be explained at least in part by the decrease in venodilatation in this model. The effect of aspirin in our experiments may be minimal because of the small contribution of veins in our model, and this could explain the discrepancy observed. Second, it is possible that the contribution of the venous vasodilatation and/or of cyclooxygenase products may have increased with the duration of ischemia.23 In this context, the lack of effect of aspirin in our experiments may be explained by the relatively short period of ischemia used in the present experiments. Third, it must also be noted that, in our study, occlusion was performed at the level of the wrist, whereas in that of Carlsson and Wennmalm, ischemia involved the whole forearm. Thus, it is possible that the differences in the effect of cyclooxygenase inhibitors may simply be due to differences in the regulation of hand and forearm circulation.
Our results show that local infusion of L-NMMA did not affect the peak but markedly reduced the duration of the hyperemic response, as evidenced by the decrease in both the area under the curve and the time to return to 50% of peak hyperemia. To the best of our knowledge, this is the first study in which the effect of local administration of L-NMMA on hyperemic response was investigated in humans. In dogs, intracoronary administration of NO synthase inhibitors also reduces excess flow and repayment of flow debt after brief ischemia, suggestive of a reduction in the duration of the hyperemic phase.14 15 Although we cannot exclude the possibility that this shortening of the hyperemic phase is the consequence of a nonspecific action of L-NMMA secondary to its effect on baseline blood flow, these results in human peripheral arteries confirm results obtained in dogs and would suggest that the synthesis of NO from L-arginine plays a role primarily in the maintenance of reactive hyperemia. On the other hand, the absence of effect of L-NMMA on peak hyperemic response suggests that the initial phase of hyperemia is independent of NO and is probably the consequence of ischemia-induced reduction in oxygen tension in vascular smooth muscle cells, which in turn causes relaxation; alternatively, the decreased myogenic forces secondary to the reduction in perfusion pressure during ischemia may be responsible for the initial increase in flow immediately after release of the cuff.25
The mechanism by which NO could modulate the delayed phase of reactive hyperemia is not clear. One possibility is that NO is released in response to adenosine, which is believed to be a major contributor of reactive hyperemia.26 Indeed, the coronary flow response to adenosine is inhibited by L-NMMA in dogs.15 Another possibility is that the delayed phase of hyperemia is at least in part the consequence of a flow-mediated vasodilatation at the level of small resistance arteries. In isolated resistance arteries, increases in flow velocity indeed induce endothelium-dependent vasodilatation.27 28 29 However, the existence of a similar flow-dependent dilatation of human resistance vessels has not been investigated.
In our experiments, the abrupt increase in flow during hyperemia was
followed by a delayed increase in radial artery diameter, in agreement
with results previously obtained in the same arterial bed in
humans.30 31 In the present experiments, the duration
of the ischemic period was limited to 3 minutes. As a result, the
hyperemia-induced changes in radial flow and diameter were less marked
than those observed in hyperemia after longer periods of
ischemia.30 31 We chose to limit the duration of
ischemia
to 3 minutes to obtain modest changes in flow and thus in diameter to
avoid losing the tracked echo signal during hyperemia, as might have
been the case in the event of larger changes in diameter. The
relatively modest increase in hyperemic flow in the present study
may also be a consequence of the lower metabolic demand of the hand (in
the case of a wrist occlusion like the one used here) compared with the
traditionally studied forearm. However, despite this short duration of
ischemia and moderate increase in flow during hyperemia, the increase
in radial diameter measured in the present experiments was
3.6±0.8%, which corresponds to an average increase of 98±25
µm, a
value well above the dynamic resolution of the technique. Indeed, Fig
1
shows that the echo-tracking technique allows continuous tracking of
the diameter signal throughout the cardiac cycle, even though the
systolic-diastolic differences in diameter are <20 µm,
suggesting that the dynamic resolution of the system, in our
conditions, is well under this 20-µm value. Furthermore, the
stability of the observed diameter response was assessed in experiments
in which subjects underwent two consecutive hyperemic tests without
treatment. In these experiments, we found no significant changes in
baseline radial diameter or radial flow or in the response of the
radial artery during hyperemia (Fig 2). Thus, we believe that
the
echo-tracking technique used allows precise evaluation of the
hyperemia-induced changes in radial artery diameter as well as an
accurate determination of the effects of acute treatments (such as
L-NMMA or aspirin) on radial hemodynamics and on flow-dependent
dilatation of the radial artery.
Under these conditions, we observed that the flow-dependent vasodilatation of the radial artery was not affected by aspirin but was abolished by L-NMMA, demonstrating that it was independent of the release of vasoactive prostanoids and entirely mediated by NO. This finding confirms, in humans, results previously obtained in vitro5 32 or in conscious, chronically instrumented dogs.33 One intriguing aspect of our results is that administration of L-NMMA unmasked a flow-mediated vasoconstriction of the radial artery. Such a paradoxical vasoconstriction also occurs during exercise in patients with coronary artery disease.34 Hence, inhibition of NO mimics the response of atherosclerotic arteries to increased shear.6 7 8 One possible explanation is that flow stimulates the endothelium to release a vasoconstrictor substance (for example endothelin35 ) whose effects are normally masked by the NO-dependent dilatation. The fast time course of the response, however, argues against a role for endothelin. Indeed, in isolated vascular tissue, endothelin is synthetized on a de novo basis, a process that requires 2 to 4 hours.35 Another possibility is that the vasoconstriction could reflect an unmasking of a hyperemia-induced sympathetic vasoconstriction in the presence of L-NMMA. Indeed, NO inhibits sympathetic nerve activity36 as well as norepinephrine-induced vasoconstriction.20 Hence, flow-mediated vasodilatation continuously opposes adrenergic vasoconstriction, as shown in vitro.32 37
In conclusion, the present investigation demonstrates that NO is essential for flow-mediated dilatation of human radial arteries in vivo. Thus, this test can be used as a reliable noninvasive estimate of the capacity of human endothelial cells to release NO in response to a physiological stimulus as well as an estimate of endothelial dysfunction in diseased states.
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Acknowledgments |
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These studies were supported by the Swiss National Science Foundation (grant 32-36575.92), the Schweizerische Rentenanstalt, the Freiwillige Akademische Gesellschaft Basel, Switzerland, and the Association Charles Nicolle, Rouen, France.
Received November 17, 1994; accepted January 3, 1995.
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  M. Seddon, N. Melikian, R. Dworakowski, H. Shabeeh, B. Jiang, J. Byrne, B. Casadei, P. Chowienczyk, and A. M. Shah Effects of Neuronal Nitric Oxide Synthase on Human Coronary Artery Diameter and Blood Flow In Vivo Circulation, May 26, 2009; 119(20): 2656 - 2662. [Abstract] [Full Text] [PDF]
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R. Corti, A. J. Flammer, N. K. Hollenberg, and T. F. Luscher Cocoa and Cardiovascular Health Circulation, March 17, 2009; 119(10): 1433 - 1441. [Abstract] [Full Text] [PDF]
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J. Steffel and T. F. Luscher Predicting the Development of Atherosclerosis Circulation, February 24, 2009; 119(7): 919 - 921. [Full Text] [PDF]
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M. E. Widlansky Shear stress and flow-mediated dilation: all shear responses are not created equally Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H31 - H32. [Full Text] [PDF]
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M. E. J. Lott, C. Hogeman, M. Herr, M. Bhagat, and L. I. Sinoway Sex differences in limb vasoconstriction responses to increases in transmural pressures Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H186 - H194. [Abstract] [Full Text] [PDF]
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K. Pahkala, O. J. Heinonen, H. Lagstrom, P. Hakala, O. Simell, J. S.A. Viikari, T. Ronnemaa, M. Hernelahti, L. Sillanmaki, and O. T. Raitakari Vascular Endothelial Function and Leisure-Time Physical Activity in Adolescents Circulation, December 2, 2008; 118(23): 2353 - 2359. [Abstract] [Full Text] [PDF]
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L. M Title, E. Lonn, F. Charbonneau, M. Fung, K. J Mather, S. Verma, and T. J Anderson Relationship between brachial artery flow-mediated dilatation, hyperemic shear stress, and the metabolic syndrome Vascular Medicine, November 1, 2008; 13(4): 263 - 270. [Abstract] [PDF]
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S. K. Nishiyama, D. W. Wray, and R. S. Richardson Aging affects vascular structure and function in a limb-specific manner J Appl Physiol, November 1, 2008; 105(5): 1661 - 1670. [Abstract] [Full Text] [PDF]
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D. H. J. Thijssen, M. M. van Bemmel, L. M. Bullens, E. A. Dawson, N. D. Hopkins, T. M. Tinken, M. A. Black, M. T. E. Hopman, N. T. Cable, and D. J. Green The impact of baseline diameter on flow-mediated dilation differs in young and older humans Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1594 - H1598. [Abstract] [Full Text] [PDF]
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M. Dhindsa, S. M. Sommerlad, A. E. DeVan, J. N. Barnes, J. Sugawara, O. Ley, and H. Tanaka Interrelationships among noninvasive measures of postischemic macro- and microvascular reactivity J Appl Physiol, August 1, 2008; 105(2): 427 - 432. [Abstract] [Full Text] [PDF]
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T. J. Barstow and B. J. Wong Commentary on Viewpoint: The human cutaneous circulation as a model of generalized microvascular function J Appl Physiol, July 1, 2008; 105(1): 376 - 376. [Full Text] [PDF]
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K. E. Pyke, V. Poitras, and M. E. Tschakovsky Brachial artery flow-mediated dilation during handgrip exercise: evidence for endothelial transduction of the mean shear stimulus Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2669 - H2679. [Abstract] [Full Text] [PDF]
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D. S. Celermajer Reliable Endothelial Function Testing: At Our Fingertips? Circulation, May 13, 2008; 117(19): 2428 - 2430. [Full Text] [PDF]
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J. Padilla, R. A Harris, L. D Rink, and J. P Wallace Characterization of the brachial artery shear stress following walking exercise Vascular Medicine, May 1, 2008; 13(2): 105 - 111. [Abstract] [PDF]
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P. Minuz, H. Jiang, C. Fava, L. Turolo, S. Tacconelli, M. Ricci, P. Patrignani, A. Morganti, A. Lechi, and J. C. McGiff Altered Release of Cytochrome P450 Metabolites of Arachidonic Acid in Renovascular Disease Hypertension, May 1, 2008; 51(5): 1379 - 1385. [Abstract] [Full Text] [PDF]
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J. R. Meendering, B. N. Torgrimson, N. P. Miller, P. F. Kaplan, and C. T. Minson Estrogen, medroxyprogesterone acetate, endothelial function, and biomarkers of cardiovascular risk in young women Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1630 - H1637. [Abstract] [Full Text] [PDF]
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M. Kooijman, D. H. J. Thijssen, P. C. E. de Groot, M. W. P. Bleeker, H. J. M. van Kuppevelt, D. J. Green, G. A. Rongen, P. Smits, and M. T. E. Hopman Flow-mediated dilatation in the superficial femoral artery is nitric oxide mediated in humans J. Physiol., February 15, 2008; 586(4): 1137 - 1145. [Abstract] [Full Text] [PDF]
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M. Gomaraschi, D. Baldassarre, M. Amato, S. Eligini, P. Conca, C. R. Sirtori, G. Franceschini, and L. Calabresi Normal Vascular Function Despite Low Levels of High-Density Lipoprotein Cholesterol in Carriers of the Apolipoprotein A-IMilano Mutant Circulation, November 6, 2007; 116(19): 2165 - 2172. [Abstract] [Full Text] [PDF]
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M. E. Tschakovsky, K. E. Pyke, and S. Fergus Reply to Drs. Harris and Padilla J Appl Physiol, September 1, 2007; 103(3): 1109 - 1109. [Full Text] [PDF]
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S. K. Nishiyama, D. Walter Wray, K. Berkstresser, M. Ramaswamy, and R. S. Richardson Limb-specific differences in flow-mediated dilation: the role of shear rate J Appl Physiol, September 1, 2007; 103(3): 843 - 851. [Abstract] [Full Text] [PDF]
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G. I. Boger, T. K. Rudolph, R. Maas, E. Schwedhelm, E. Dumbadze, A. Bierend, R. A. Benndorf, and R. H. Boger Asymmetric Dimethylarginine Determines the Improvement of Endothelium-Dependent Vasodilation by Simvastatin: Effect of Combination With Oral L-Arginine J. Am. Coll. Cardiol., June 12, 2007; 49(23): 2274 - 2282. [Abstract] [Full Text] [PDF]
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H. Viswambharan, J. M. Carvas, V. Antic, A. Marecic, C. Jud, C. E. Zaugg, X.-F. Ming, J.-P. Montani, U. Albrecht, and Z. Yang Mutation of the Circadian Clock Gene Per2 Alters Vascular Endothelial Function Circulation, April 24, 2007; 115(16): 2188 - 2195. [Abstract] [Full Text] [PDF]
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I. J. Kullo and A. R. Malik Arterial Ultrasonography and Tonometry as Adjuncts to Cardiovascular Risk Stratification J. Am. Coll. Cardiol., April 3, 2007; 49(13): 1413 - 1426. [Abstract] [Full Text] [PDF]
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D. Giannini, A. Leone, D. Di Bisceglie, M. Nuti, G. Strata, F. Buttitta, L. Masserini, and A. Balbarini The Effects of Acute Passive Smoke Exposure on Endothelium-Dependent Brachial Artery Dilation in Healthy Individuals Angiology, April 1, 2007; 58(2): 211 - 217. [Abstract] [PDF]
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K. E. Pyke and M. E. Tschakovsky Peak vs. total reactive hyperemia: which determines the magnitude of flow-mediated dilation? J Appl Physiol, April 1, 2007; 102(4): 1510 - 1519. [Abstract] [Full Text] [PDF]
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J. E. Deanfield, J. P. Halcox, and T. J. Rabelink Endothelial Function and Dysfunction: Testing and Clinical Relevance Circulation, March 13, 2007; 115(10): 1285 - 1295. [Full Text] [PDF]
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K. F. Hoth, D. F. Tate, A. Poppas, D. E. Forman, J. Gunstad, D. J. Moser, R. H. Paul, A. L. Jefferson, A. P. Haley, and R. A. Cohen Endothelial Function and White Matter Hyperintensities in Older Adults With Cardiovascular Disease Stroke, February 1, 2007; 38(2): 308 - 312. [Abstract] [Full Text] [PDF]
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J. Bellien, M. Iacob, L. Gutierrez, M. Isabelle, A. Lahary, C. Thuillez, and R. Joannides Crucial Role of NO and Endothelium-Derived Hyperpolarizing Factor in Human Sustained Conduit Artery Flow-Mediated Dilatation Hypertension, December 1, 2006; 48(6): 1088 - 1094. [Abstract] [Full Text] [PDF]
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A. A. Quyyumi and M. Ozkor Vasodilation by Hyperpolarization: Beyond NO Hypertension, December 1, 2006; 48(6): 1023 - 1025. [Full Text] [PDF]
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A. E. Donald, M. Charakida, T. J. Cole, P. Friberg, P. J. Chowienczyk, S. C. Millasseau, J. E. Deanfield, and J. P. Halcox Non-Invasive Assessment of Endothelial Function: Which Technique? J. Am. Coll. Cardiol., November 7, 2006; 48(9): 1846 - 1850. [Abstract] [Full Text] [PDF]
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J. J. Oliver, V. P. Melville, and D. J. Webb Effect of Regular Phosphodiesterase Type 5 Inhibition in Hypertension Hypertension, October 1, 2006; 48(4): 622 - 627. [Abstract] [Full Text] [PDF]
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D. J. Green, A. J. Maiorana, M. E. Tschakovsky, K. E. Pyke, C. J. Weisbrod, and G. O'Driscoll Relationship between changes in brachial artery flow-mediated dilation and basal release of nitric oxide in subjects with Type 2 diabetes Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1193 - H1199. [Abstract] [Full Text] [PDF]
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A. Nohria, M. Gerhard-Herman, M. A. Creager, S. Hurley, D. Mitra, and P. Ganz Role of nitric oxide in the regulation of digital pulse volume amplitude in humans J Appl Physiol, August 1, 2006; 101(2): 545 - 548. [Abstract] [Full Text] [PDF]
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R. Kohler, W.-T. Heyken, P. Heinau, R. Schubert, H. Si, M. Kacik, C. Busch, I. Grgic, T. Maier, and J. Hoyer Evidence for a Functional Role of Endothelial Transient Receptor Potential V4 in Shear Stress-Induced Vasodilatation Arterioscler. Thromb. Vasc. Biol., July 1, 2006; 26(7): 1495 - 1502. [Abstract] [Full Text] [PDF]
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R. Kelly, T. Ruane-O'Hora, M. I. M. Noble, A. J. Drake-Holland, and H. M. Snow Differential inhibition by hyperglycaemia of shear stress- but not acetylcholine-mediated dilatation in the iliac artery of the anaesthetized pig J. Physiol., May 15, 2006; 573(1): 133 - 145. [Abstract] [Full Text] [PDF]
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J. Bellien, R. Joannides, M. Iacob, P. Arnaud, and C. Thuillez Evidence for a basal release of a cytochrome-related endothelium-derived hyperpolarizing factor in the radial artery in humans Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1347 - H1352. [Abstract] [Full Text] [PDF]
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K. S. Dyson, J. K. Shoemaker, and R. L. Hughson Effect of acute sympathetic nervous system activation on flow-mediated dilation of brachial artery Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1446 - H1453. [Abstract] [Full Text] [PDF]
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I. Eskurza, Z. D. Kahn, and D. R. Seals Xanthine oxidase does not contribute to impaired peripheral conduit artery endothelium-dependent dilatation with ageing J. Physiol., March 15, 2006; 571(3): 661 - 668. [Abstract] [Full Text] [PDF]
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R. P. Bochmann, W. Seibel, E. Haase, V. Hietschold, H. Rodel, and A. Deussen External compression increases forearm perfusion J Appl Physiol, December 1, 2005; 99(6): 2337 - 2344. [Abstract] [Full Text] [PDF]
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N. Nair, R. K Oka, L. D Waring, E. M Umoh, C B. Taylor, and J. P Cooke Vascular compliance versus flow-mediated vasodilation: correlation with cardiovascular risk factors Vascular Medicine, November 1, 2005; 10(4): 275 - 283. [Abstract] [PDF]
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K. E Pyke and M. E Tschakovsky The relationship between shear stress and flow-mediated dilatation: implications for the assessment of endothelial function J. Physiol., October 15, 2005; 568(2): 357 - 369. [Abstract] [Full Text] [PDF]
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C. Heiss, P. Kleinbongard, A. Dejam, S. Perre, H. Schroeter, H. Sies, and M. Kelm Acute Consumption of Flavanol-Rich Cocoa and the Reversal of Endothelial Dysfunction in Smokers J. Am. Coll. Cardiol., October 4, 2005; 46(7): 1276 - 1283. [Abstract] [Full Text] [PDF]
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R. Joannides and J. Bellien Flow-mediated dilatation revisited J Appl Physiol, October 1, 2005; 99(4): 1623 - 1623. [Abstract] [Full Text] [PDF]
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D. Green Point: Flow-mediated dilation does reflect nitric oxide-mediated endothelial function J Appl Physiol, September 1, 2005; 99(3): 1233 - 1234. [Full Text] [PDF]
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M. E. Tschakovsky and K. E. Pyke Counterpoint: Flow-mediated dilation does not reflect nitric oxide-mediated endothelial function J Appl Physiol, September 1, 2005; 99(3): 1235 - 1237. [Full Text] [PDF]
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REBUTTAL FROM DR. GREEN J Appl Physiol, September 1, 2005; 99(3): 1237 - 1237. [Full Text] [PDF]
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REBUTTAL FROM DRS. TSCHAKOVSKY AND PYKE J Appl Physiol, September 1, 2005; 99(3): 1237 - 1238. [Full Text] [PDF]
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J. Hetzel, B. Balletshofer, K. Rittig, D. Walcher, W. Kratzer, V. Hombach, H.-U. Haring, W. Koenig, and N. Marx Rapid Effects of Rosiglitazone Treatment on Endothelial Function and Inflammatory Biomarkers Arterioscler. Thromb. Vasc. Biol., September 1, 2005; 25(9): 1804 - 1809. [Abstract] [Full Text] [PDF]
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E. D. Beishuizen, J. T. Tamsma, J. W. Jukema, M. A. van de Ree, J. C. M. van der Vijver, A. E. Meinders, and M. V. Huisman The Effect of Statin Therapy on Endothelial Function in Type 2 Diabetes Without Manifest Cardiovascular Disease Diabetes Care, July 1, 2005; 28(7): 1668 - 1674. [Abstract] [Full Text] [PDF]
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K. Sydow, C. E Mondon, and J. P Cooke Insulin resistance: potential role of the endogenous nitric oxide synthase inhibitor ADMA Vascular Medicine, July 1, 2005; 10(1_suppl): S35 - S43. [Abstract] [PDF]
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J. Bellien, R. Joannides, M. Iacob, P. Arnaud, and C. Thuillez Calcium-Activated Potassium Channels and NO Regulate Human Peripheral Conduit Artery Mechanics Hypertension, July 1, 2005; 46(1): 210 - 216. [Abstract] [Full Text] [PDF]
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D. R. Witte, J. Westerink, E. J. de Koning, Y. van der Graaf, D. E. Grobbee, and M. L. Bots Is the Association Between Flow-Mediated Dilation and Cardiovascular Risk Limited to Low-Risk Populations? J. Am. Coll. Cardiol., June 21, 2005; 45(12): 1987 - 1993. [Abstract] [Full Text] [PDF]
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M. S. O'Neill, A. Veves, A. Zanobetti, J. A. Sarnat, D. R. Gold, P. A. Economides, E. S. Horton, and J. Schwartz Diabetes Enhances Vulnerability to Particulate Air Pollution-Associated Impairment in Vascular Reactivity and Endothelial Function Circulation, June 7, 2005; 111(22): 2913 - 2920. [Abstract] [Full Text] [PDF]
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 L. R. Sajja, G. Mannam, N. R. Pantula, and S. Sompalli Role of Radial Artery Graft in Coronary Artery Bypass Grafting Ann. Thorac. Surg., June 1, 2005; 79(6): 2180 - 2188. [Abstract] [Full Text] [PDF]
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A. L. Moens, I. Goovaerts, M. J. Claeys, and C. J. Vrints Flow-Mediated Vasodilation: A Diagnostic Instrument, or an Experimental Tool? Chest, June 1, 2005; 127(6): 2254 - 2263. [Abstract] [Full Text] [PDF]
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K. Sydow, C. E Mondon, and J. P Cooke Insulin resistance: potential role of the endogenous nitric oxide synthase inhibitor ADMA Vascular Medicine, May 1, 2005; 10(2_suppl): S35 - S43. [Abstract] [PDF]
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B. R. Clapp, G. M. Hirschfield, C. Storry, J. R. Gallimore, R. P. Stidwill, M. Singer, J. E. Deanfield, R. J. MacAllister, M. B. Pepys, P. Vallance, et al. Inflammation and Endothelial Function: Direct Vascular Effects of Human C-Reactive Protein on Nitric Oxide Bioavailability Circulation, March 29, 2005; 111(12): 1530 - 1536. [Abstract] [Full Text] [PDF]
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M. R. Skilton, N. T. Lai, K. A. Griffiths, L. M. Molyneaux, D. K. Yue, D. R. Sullivan, and D. S. Celermajer Meal-related increases in vascular reactivity are impaired in older and diabetic adults: insights into roles of aging and insulin in vascular flow Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1404 - H1410. [Abstract] [Full Text] [PDF]
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C. Giannattasio, A. Zoppo, G. Gentile, M. Failla, A. Capra, F.M. Maggi, A. Catapano, and G. Mancia Acute Effect of High-Fat Meal on Endothelial Function in Moderately Dyslipidemic Subjects Arterioscler. Thromb. Vasc. Biol., February 1, 2005; 25(2): 406 - 410. [Abstract] [Full Text] [PDF]
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S. D. Katz, K. Hryniewicz, I. Hriljac, K. Balidemaj, C. Dimayuga, A. Hudaihed, and A. Yasskiy Vascular Endothelial Dysfunction and Mortality Risk in Patients With Chronic Heart Failure Circulation, January 25, 2005; 111(3): 310 - 314. [Abstract] [Full Text] [PDF]
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D. J Green, A. Maiorana, G. O'Driscoll, and R. Taylor Effect of exercise training on endothelium-derived nitric oxide function in humans J. Physiol., November 15, 2004; 561(1): 1 - 25. [Abstract] [Full Text] [PDF]
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T. F. Luscher and R. Corti Flow: The Signal of Life Circ. Res., October 15, 2004; 95(8): 749 - 751. [Full Text] [PDF]
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S. Fazel, R. D. Weisel, and S. Verma A novel technique to assess flow-mediated vasodilation J. Am. Coll. Cardiol., October 6, 2004; 44(7): 1478 - 1480. [Full Text] [PDF]
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S. Y. Honisett, L. Stojanovska, K. Sudhir, B. A. Kingwell, T. Dawood, and P. A. Komesaroff Hormone Therapy Impairs Endothelial Function in Postmenopausal Women with Type 2 Diabetes Mellitus Treated with Rosiglitazone J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4615 - 4619. [Abstract] [Full Text] [PDF]
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K. E. Pyke, E. M. Dwyer, and M. E. Tschakovsky Impact of controlling shear rate on flow-mediated dilation responses in the brachial artery of humans J Appl Physiol, August 1, 2004; 97(2): 499 - 508. [Abstract] [Full Text] [PDF]
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D. J. Green, J. H. Walsh, A. Maiorana, V. Burke, R. R. Taylor, and J. G. O'Driscoll Comparison of resistance and conduit vessel nitric oxide-mediated vascular function in vivo: effects of exercise training J Appl Physiol, August 1, 2004; 97(2): 749 - 755. [Abstract] [Full Text] [PDF]
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S. Bergaya, R. H.P. Hilgers, P. Meneton, Y. Dong, M. Bloch-Faure, T. Inagami, F. Alhenc-Gelas, B. I. Levy, and C. M. Boulanger Flow-Dependent Dilation Mediated by Endogenous Kinins Requires Angiotensin AT2 Receptors Circ. Res., June 25, 2004; 94(12): 1623 - 1629. [Abstract] [Full Text] [PDF]
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F. M. Maggi, S. Raselli, L. Grigore, L. Redaelli, S. Fantappie, and A. L. Catapano Lipoprotein Remnants and Endothelial Dysfunction in the Postprandial Phase J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 2946 - 2950. [Abstract] [Full Text] [PDF]
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U. Paradossi, E. Ciofini, A. Clerico, N. Botto, A. Biagini, and M. G. Colombo Endothelial Function and Carotid Intima-Media Thickness in Young Healthy Subjects Among Endothelial Nitric Oxide Synthase Glu298->Asp and T-786->C Polymorphisms Stroke, June 1, 2004; 35(6): 1305 - 1309. [Abstract] [Full Text] [PDF]
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