AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 1 98-105, Copyright © 1989 by American Physiological Society

ARTICLES

Systemic vascular autoregulation amplifies pressor responses to vasoconstrictor agents

P. J. Metting, P. M. Stein, B. A. Stoos, K. A. Kostrzewski and S. L. Britton
Department of Physiology, Medical College of Ohio, Toledo 43699.

Experiments were performed in seven conscious dogs to evaluate the contribution of total systemic autoregulation to the increase in mean arterial pressure (MAP) produced by the intravenous administration of pressor agents. Each dog was instrumented for the measurement of aortic pressure, central venous pressure, and cardiac output, and all dogs received hexamethonium to block autonomic ganglionic transmission. Angiotensin II (ANG II), arginine vasopressin (AVP), or norepinephrine (NE) were titrated over a 15- to 20-min period until MAP was increased to a new steady-state value approximately 50-55% above the normotensive control. Then while a constant infusion of the pressor agents was maintained, MAP was controlled via a gravity reservoir for 15-min periods at either the hypertensive value or at the animal's normotensive value. With all three pressor agents, total peripheral resistance (TPR) was greater when MAP was controlled at the hypertensive value than when the vasculature was protected from the elevated pressure by controlling MAP at the normotensive value. Thus a portion of the increase in TPR during the infusion of ANG II, AVP, or NE was due to autoregulatory-mediated vasoconstriction elicited by the increase in MAP. The fractions of the increases in TPR and MAP contributed by primary vasoconstriction vs. autoregulation were determined from the pressure-flow relationships. The pressure-induced increases in TPR accounted for 74% of the total increase in MAP produced by AVP, 62% of the pressor response to NE, and 34% of the response to ANG II. These results demonstrate that the direct vasoconstrictor effects of pressor agents can be significantly amplified by secondary autoregulatory responses.

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