(Circulation. 2001;103:e21.)
© 2001 American Heart Association, Inc.
Correspondence |
Blood Pressure Oscillations: Is There an Independent Antihypertensive Effect?
Mount Sinai Medical Center, New York, NY
To the Editor:
In a recent issue of
Circulation, Nafz and
colleagues1 described the
antihypertensive effects of oscillations of renal perfusion pressure
(RPP) in conscious dogs. One of the key findings in that article was
that plasma renin activity increased in response to a decrease in the
mean RPP to 85 mm Hg; this increase was significantly reduced by
0.1-Hz oscillations in RPP around a similar mean level. In their
discussion, the authors write that the attenuated plasma renin activity
during the RPP oscillations is a "surprise" and attribute this
result to the oscillatory pattern of RPP. We propose an alternative
explanation to the authors’ findings. Oscillations in RPP with a mean
of 85 mm Hg and an amplitude of 10 mm Hg, as performed in the study,
cause RPP to be >90 mm Hg (the threshold level for stimulating renin
release2 ) 
33% of the
time. Thus, the stimulus for renin secretion is only present for 66%
of the time in the oscillation experiment compared with the decrease in
the mean RPP to 85 mm Hg; therefore, the oscillations result in a
diminished renin release.
The authors’ assumption that a low RPP during the trough of
oscillations (RPP of 75 mm Hg) strongly stimulates renin release, but
RPP during peak oscillations (RPP of 95 mm Hg) does not reduce it to
the same extent, would be an argument against our simplistic
explanation. Although this assumption is correct in the steady-state,
one should also consider the time course of the response of renin
secretion to hemodynamic changes. Simchon and
Chien3 demonstrated that the
time constant of the response of renin secretion to changes in renal
blood flow in dogs is 80 s, which is >10 times as long as the
duration of RPP<90 mm Hg in the oscillation experiment (7 s).
Thus, the trough of oscillations would cause a much smaller increase in
renin release compared with the constant low level of RPP.
Keeping that in mind, one would expect the plasma renin activity levels
in the oscillation experiment to be between the control levels and the
levels found at a mean RPP of 85 mm Hg, as was observed in the
study.
References
1.
Nafz B,
Stegemann J, Bestle MH, et al. Antihypertensive effect of 0.1-Hz blood
pressure oscillations to the kidney.
Circulation. 2000;101:553–557.
2. Finke R, Gross R, Hackenthal E, et al. Threshold pressure for the pressure-dependent renin release in the autoregulating kidney of conscious dogs. Pflugers Arch. 1983;399:102–110.[Medline] [Order article via Infotrieve]
3. Simchon S, Chien S. Effects of variations in renal hemodynamics on the time course of renin secretion rate. Am J Physiol. 1983;245:F784–F791.
Response
Johannes Müller Institut für Physiologie, Humboldt Universität, Berlin, Germany
Department of Anesthesia, Glostrup Hospital, Denmark
Klinik für Innere Medizin I, Humboldt Universität, Berlin, Germany
We thank Dr Phillips and his colleagues, who propose 2
hypotheses to explain the influence of 0.1-Hz blood pressure
oscillations (BPO) on plasma renin activity (PRA). The first hypothesis
is based on the assumption that the PRA stimulus-response curve (as
reported by Kirchheim et alR1 )
is valid to the same extent for (1) static conditions versus BPO, (2)
resting versus freely moving dogs, (3) one kidney versus the concerted
action of both, and (4) PRA differences versus systemic PRA. If one
follows these assumptions, the data of Kirchheim et
alR1 can be used to estimate
the influence of BPO on PRA via a linear model. According to this
model, one would calculate PRA to be 17% higher during oscillations
(sinusoidal, 0.1-Hz BPO ranging from 75 to 95 mm Hg) than during a
blood pressure (BP) reduction to 85 mm Hg. Dr Phillips et al’s
hypothesis reduces the system to a pressure-dependent on/off response.
This assumes PRA is zero above a certain threshold-pressure and is
greater than zero and constant if BP is below that threshold-pressure.
However, the relationship between BP and PRA, as reported by Kirchheim
et al,R1 shows a well-defined
slope at BP<90 mm Hg, and PRA is not zero at BP>90 mm Hg. In
conclusion, the reduced PRA during oscillation in our study cannot be
explained by the PRA stimulus-response curve obtained during
steady-state conditions.
The second hypothesis is based on the assumption that a
stimulus can evoke a response only when its duration exceeds the time
delay between the stimulus and response. This assumption is difficult
to defend. For instance, eating increases plasma glucose levels,
although this may not be detectable during the food intake itself.
Notwithstanding that fact, the minimal duration that a reduction in BP
must last to increase renin secretion has not yet been determined.
Simchon and ChienR2 showed
that a decrease in renal blood flow (which was followed by similar
changes in BP) can elevate the renin secretion rate to 125% within
18 s. Although this probably does not reflect the minimum duration
of an effective stimulus, it shows that the duration necessary to evoke
a detectable increase in the renin secretion rate is much smaller than
that proposed by Dr Phillips and colleagues. Thus, the way by which BPO
attenuates PRA during the onset of renovascular hypertension remains to
be clarified.
References
1. Kirchheim HR, Finke R, Hackenthal E, et al. Baroreflex sympathetic activation increases threshold pressure for the pressure-dependent renin release in conscious dogs. Pflügers Arch. 1985;405:127–135.[Medline] [Order article via Infotrieve]
2. Simchon S, Chien S. Effects of variations in renal hemodynamics on the time course of renin secretion rate. Am J Physiol. 1983;245:F784–F791.
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