Hypertension, Vol 11, 352-359, Copyright © 1988 by American Heart Association
EW Supple, RM Graham and WJ Powell Jr
The role of alpha 2-adrenergic receptor stimulation in the regulation of
systemic vascular capacity and venous return, a major determinant of
cardiac output, is not well understood. With the influence of the central
nervous system isolated from the systemic circulation, the direct
peripheral vascular effects of two specific, chemically distinct alpha
2-adrenergic receptor agonists, UK 14,304 and B-HT 920, were investigated
in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion
and central venous pressure. Five-minute intra- arterial infusions of UK
14,304 (200 micrograms/min) resulted in increased arterial resistance (mean
arterial pressure increased 18 +/- 4 [SEM] mm Hg; p less than 0.01) and a
decrease in systemic vascular capacity (81 +/- 20 ml; p less than 0.01).
This decrease in systemic vascular capacity appears to result from
vasoconstriction, since there was no decrease in transhepatic resistance to
portal flow and no significant change in hepatic vein flow to suggest
redistribution of arterial blood flow. Yohimbine abolished both the
arterial and systemic capacity effects, whereas prazosin did not.
Intra-arterial administration of B-HT 920 (200 theta grams/min) in five
dogs produced similar changes in arterial resistance and systemic capacity.
These findings provide direct evidence for beta 2-adrenergic control, not
only of arterial resistance but also of systemic vascular capacity, which
in the intact animal would increase venous return to the heart.
ARTICLES
Direct effects of alpha 2-adrenergic receptor stimulation on intravascular systemic capacity in the dog
Cardiac Unit, Massachusetts General Hospital, Boston.
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1988 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |