Analysis of responses to angiotensin i (3-10) in the hindlimb
vascular bed of the cat.
Garrison, Etoi A., and Philip J. Kadowitz.
Department of Pharmacology, Tulane University School of Medicine,
New Orleans, Louisiana 70112
APStracts 2:0321H, 1995.
Responses to angiotensin I (3-10), the precursor for angiotensin IV,
were investigated in the anesthetized cat. Intravenous injections of
the precursor caused dose-related increases in systemic arterial
pressure that were similar to responses elicited by angiotensin IV
and that were inhibited by captopril. In the hindlimb vascular bed of
the cat under constant-flow conditions, injections of the substrate
into the perfusion circuit in doses of 3-100 [mu]g caused dose
-related increases in hindlimb perfusion pressure that were rapid in
onset and were not altered by the presence of a time-delay coil in
the perfusion circuit. Dose-response curves for the precursor and
angiotensin IV were parallel, and the precursor was approximately 2
-fold less potent than angiotensin IV in its ability to increase
hindlimb perfusion pressure. Responses to the precursor were
inhibited by captopril in a dose that attenuated hindlimb
vasoconstrictor responses to angiotensin I. Increases in hindlimb
perfusion pressure in response to angiotensin I (3-10) were inhibited
by DuP 532 in a dose that attenuated the response to angiotensin IV.
PD 123,319, an AT2 receptor antagonist, had no significant effect on
responses to angiotensin I (3-10). The present results suggest that
angiotensin I (3-10) is rapidly and efficiently converted by an ACE
-dependent pathway into an active peptide, which induces
vasoconstriction by activating AT1 receptors in the peripheral
vascular bed of the cat.
Received 24 March 1995; accepted in final form 20 July 1995.
APS Manuscript Number H286-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 August 1995.