AJP - Heart AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 266: H220-H227, 1994;
0363-6135/94 $5.00
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
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ligier, B.
Right arrow Articles by Traystman, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ligier, B.
Right arrow Articles by Traystman, R. J.

AJP - Heart and Circulatory Physiology, Vol 266, Issue 1 220-H227, Copyright © 1994 by American Physiological Society


ARTICLES

Adrenal blood flow and secretory effects of adrenergic receptor stimulation

B. Ligier, M. J. Breslow, K. Clarkson, H. Raff and R. J. Traystman
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287.

To evaluate effects of adrenergic receptor stimulation on regional adrenal blood flow and secretion, pentobarbital-anesthetized dogs (n = 5-6/group) received the beta-agonist isoproterenol (group I), the alpha 1-agonist phenylephrine (group II), or the alpha 2-agonist dexmedetomidine (group III). Measurements of adrenal cortical (CQ) and medullary (MQ) blood flow (radiolabeled microspheres) and catecholamine secretion were made before and during agonist infusion. Isoproterenol increased catecholamine secretion but had no direct effect on MQ or CQ. In contrast, phenylephrine increased MQ and CQ four- and twofold, respectively. Dexmedetomidine had no effect on MQ or catecholamine secretion. To evaluate whether blood flow effects of phenylephrine were due to increases in mean arterial blood pressure (MAP) or related to activation of alpha 1-adrenergic receptors, two additional groups of animals received phenylephrine; group IV had MAP maintained at baseline by controlled hemorrhage into a pressurized bottle; group V received prazosin before phenylephrine. Prevention of MAP increase did not prevent the vasodilation response to phenylephrine, but it was completely blocked by prazosin. Canine adrenal homogenates incubated with the alpha 1-adrenoceptor ligand, 125I-labeled 2-[beta-(4-hydroxyphenyl)ethlaminomethyl]tetralone, demonstrated specific and saturable binding, supporting the presence of alpha 1-adrenergic receptors. We conclude that increases in MQ and CQ elicited by phenylephrine appear to be due to alpha 1-receptor stimulation. The mechanism responsible for this vasodilation is not known.


This article has been cited by other articles:


Home page
J. Neurosci.Home page
T. Cesetti, J. M. Hernandez-Guijo, P. Baldelli, V. Carabelli, and E. Carbone
Opposite Action of beta 1- and beta 2-Adrenergic Receptors on CaV1 L-Channel Current in Rat Adrenal Chromaffin Cells
J. Neurosci., January 1, 2003; 23(1): 73 - 83.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online