Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1995;92:1576-1581

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gwirtz, P. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gwirtz, P. A.

(Circulation. 1995;92:1576-1581.)
© 1995 American Heart Association, Inc.


Articles

Coronary {alpha}1-Constrictor Tone During Renovascular Hypertension

Patricia A. Gwirtz, PhD

From the Department of Physiology, University of North Texas Health Science Center at Fort Worth.

Correspondence to Patricia A. Gwirtz, Professor, Department of Physiology, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd, Fort Worth, TX 79107-2690.

Background A coronary {alpha}1-adrenergic constrictor tone exists under conditions associated with increased sympathetic stimulation but not during resting conditions in the normal heart. During renovascular hypertension, elevated circulating angiotensin II may enhance sympathetic stimulation of the heart, even at rest. This study tested the hypothesis that an {alpha}1-adrenergic constrictor tone imposes limitations on coronary blood flow in resting dogs after development of renovascular hypertension, exacerbates coronary {alpha}-constrictor tone during exercise, and increases coronary vascular adrenergic responsiveness.

Methods and Results Left circumflex blood flow velocity (CFV), aortic pressure (AoP), and heart rate (HR) were examined in five quietly resting dogs during control conditions and after selective {alpha}1-adrenergic blockade using an intracoronary injection of 0.5 mg prazosin. In the normotensive state, AoP was 87±7 mm Hg (mean±SD), HR was 105±25 beats per minute, and CFV was 28±6 cm/s. These parameters were not affected by {alpha}1-adrenergic blockade. During submaximal exercise, removal of an {alpha}1-adrenergic constrictor resulted in a 14±4% increase in CFV (P<.05). Two weeks after development of renovascular hypertension induced by stenosis of the left renal artery, mean AoP was 114±7 mm Hg (P<.05 versus normotensive state), HR was 111±28 beats per minute, and CFV was 21±8 cm/s. In contrast to the normotensive state, {alpha}1-adrenergic blockade caused a 28±6% increase in CFV at rest (P<.05) and a 27±13% increase in CFV during exercise in the hypertensive state (P<.05 versus exercise before blockade and versus normotensive state). This resting coronary constrictor tone was associated with enhanced vasoconstrictor responsiveness to norepinephrine and phenylephrine.

Conclusions It appears that renovascular hypertension results in a significant coronary {alpha}1-adrenergic constrictor tone in the resting dog and an enhanced constrictor tone during exercise.


Key Words: hypertension, renal • autonomic agents • coronary disease • exercise • receptors, adrenergic, alpha




This article has been cited by other articles:


Home page
Exp Biol MedHome page
J. D. Tune, K. N. Richmond, M. W. Gorman, and E. O. Feigl
Control of Coronary Blood Flow during Exercise
Exp Biol Med, April 1, 2002; 227(4): 238 - 250.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
D. W. Stepp, D. Merkus, Y. Nishikawa, and W. M. Chilian
Nitric oxide limits coronary vasoconstriction by a shear stress-dependent mechanism
Am J Physiol Heart Circ Physiol, August 1, 2001; 281(2): H796 - H803.
[Abstract] [Full Text] [PDF]