Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1994;24:212-219

This Article
Right arrow Full Text (PDF)
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 Antony, I.
Right arrow Articles by Nitenberg, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Antony, I.
Right arrow Articles by Nitenberg, A.

Hypertension, Vol 24, 212-219, Copyright © 1994 by American Heart Association


ARTICLES

Coronary artery constriction caused by the cold pressor test in human hypertension

I Antony, E Aptecar, G Lerebours and A Nitenberg
Service d'Explorations Fonctionnelles, Centre Hospitalier et Universitaire Xavier Bichat, Paris, France.

Hypertensive patients with angiographically normal coronary arteries may have myocardial ischemia when metabolic demand increases. Abnormal epicardial coronary artery vasomotion in response to sympathetic stimulation may contribute to ischemia in such patients. We studied the vasomotor response of smooth coronary arteries to a cold pressor test in 10 hypertensive patients without other risk factors and in 9 control subjects. Vessel dimensions were measured by quantitative angiography, and blood flow was calculated using an intracoronary Doppler catheter in the left anterior descending coronary artery. In response to cold pressor stimulation, arteries of control subjects dilated 13.0 +/- 5.9% (P < .001), and they constricted 8.2 +/- 8.5% in hypertensive patients (P < .001). Rate-pressure product increased from 9466 +/- 1677 to 12,547 +/- 2367 beats per minute (bpm).mm Hg in control subjects (P < .001) and from 13,720 +/- 1823 to 17,353 +/- 2037 bpm.mm Hg in hypertensive patients (P < .001). Coronary blood flow velocity and blood flow increased 51 +/- 26% (P < .05) and 87 +/- 27% (P < .001), respectively, in control subjects and 68 +/- 52% (P < .05) and 36 +/- 33% (P < .01) in hypertensive patients. At peak cold pressor test, despite a significant higher rate-pressure product in hypertensive patients, blood flow was similar in both groups, suggesting an uncoupling between myocardial metabolic demand and supply. Thus, hypertension impairs the vasodilator response of angiographically normal coronary arteries to a cold pressor test. This abnormal response may be due to enhanced catecholamine reactivity and/or impairment of endothelial flow-mediated vasodilator response.


This article has been cited by other articles:


Home page
Psychosom. Med.Home page
K. F. Harris and K. A. Matthews
Interactions Between Autonomic Nervous System Activity and Endothelial Function: A Model for the Development of Cardiovascular Disease
Psychosom Med, March 1, 2004; 66(2): 153 - 164.
[Abstract] [Full Text] [PDF]


Home page
Diabetes CareHome page
A. Nitenberg, P. Valensi, R. Sachs, E. Cosson, J.-R. Attali, and I. Antony
Prognostic Value of Epicardial Coronary Artery Constriction to the Cold Pressor Test in Type 2 Diabetic Patients With Angiographically Normal Coronary Arteries and No Other Major Coronary Risk Factors
Diabetes Care, January 1, 2004; 27(1): 208 - 215.
[Abstract] [Full Text] [PDF]


Home page
Diabetes CareHome page
S. H. Golden, N.-Y. Wang, M. J. Klag, L. A. Meoni, and F. L. Brancati
Blood Pressure in Young Adulthood and the Risk of Type 2 Diabetes in Middle Age
Diabetes Care, April 1, 2003; 26(4): 1110 - 1115.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
N. H. Buus, M. Bottcher, F. Hermansen, M. Sander, T. T. Nielsen, and M. J. Mulvany
Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia
Circulation, November 6, 2001; 104(19): 2305 - 2310.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
T.-M. Lee, S.-F. Su, W.-Y. Suo, C.-Y. Lee, M.-F. Chen, Y.-T. Lee, and C.-H. Tsai
Distension of urinary bladder induces exaggerated coronary constriction in smokers with early atherosclerosis
Am J Physiol Heart Circ Physiol, December 1, 2000; 279(6): H2838 - H2845.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
T.-M. Lee, S.-F. Su, M.-F. Chen, and C.-H. Tsai
Acute effects of urinary bladder distention on the coronary circulation in patients with early atherosclerosis
J. Am. Coll. Cardiol., August 1, 2000; 36(2): 453 - 460.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
D. Chemla, E. Aptecar, J.-L. Hebert, C. Coirault, D. Loisance, Y. Lecarpentier, and A. Nitenberg
Short-term variability of pulse pressure and systolic and diastolic time in heart transplant recipients
Am J Physiol Heart Circ Physiol, July 1, 2000; 279(1): H122 - H129.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
I. Antony, G. Lerebours, and A. Nitenberg
Angiotensin-Converting Enzyme Inhibition Restores Flow-Dependent and Cold Pressor Test–Induced Dilations in Coronary Arteries of Hypertensive Patients
Circulation, December 15, 1996; 94(12): 3115 - 3122.
[Abstract] [Full Text]


Home page
CirculationHome page
I. Antony, G. Lerebours, and A. Nitenberg
Loss of Flow-Dependent Coronary Artery Dilatation in Patients With Hypertension
Circulation, March 15, 1995; 91(6): 1624 - 1628.
[Abstract] [Full Text]