Responses to angiotensin peptides are mediated by at1 receptors in
the rat.
Champion, Hunter C., Marc A. Czapla, and Philip J. Kadowitz.
Department of Pharmacology, Tulane University School of Medicine,
New Orleans, LA 70112
APStracts 4:0220E, 1997.
The effects of the angiotensin AT1 and AT2 receptor antagonists
candesartan and PD 123,319 on hemodynamic responses to angiotensin
peptides were investigated in the anesthetized rat. Injections of
angiotensin II and III caused dose-related increases in systemic
arterial and in hindquarters perfusion pressure that were reduced in
a nonsurmountable manner by candesartan. Pressor responses to
angiotensin IV were also attenuated, and a vasodepressor or
vasodilator response to the angiotensin peptides was not unmasked by
the AT1 receptor antagonists candesartan or losartan. The AT2
receptor antagonist PD 123,319 had no significant effect on increases
in systemic arterial and hindquarters perfusion pressure in response
to the angiotensin peptides. Pressor responses to angiotensin
peptides were not altered by adrenergic nerve terminal and alpha
-receptor blocking agents or by the cyclooxygenase inhibitor sodium
meclofenamate but were increased by an inhibitor of nitric oxide
synthase. The present results suggest that pressor responses to the
angiotensin peptides are mediated by the activation of AT1 receptors,
and that AT2 receptors, the adrenergic system, or cyclooxygenase
products do not appear to modulate hemodynamic responses to the
angiotensin peptides in the anesthetized rat.
Received 17 July 1997; accepted in final form 29 September 1997.
APS Manuscript Number E338-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997