Contraction and endothelium-dependent relaxation in mesenteric
microvessels from pregnant rats.
Pascoal, Istenio F., Marshall D. Lindheimer, Carol Nalbantian-Brandt,
and Jason G. Umans.
Departments of Medicine and of Obstetrics and Gynecology, and the
Committee on Clinical Pharmacology, Division of the Biological
Sciences, University of Chicago, Chicago, IL 60637
APStracts 2:0353H, 1995.
We assessed KCl and phenylephrine (PE)-induced vasoconstriction as
well as acetylcholine(ACh)-induced endothelium-dependent vasodilation
in small isometrically-mounted mesenteric arteries from virgin and
gravid rats, studied in the absence and presence of N-nitro-L
-arginine (NNLA). Neither maximal vasoconstriction nor PE potency
differed significantly between vessels from virgin and pregnant rats,
either in the absence or presence of NNLA. NNLA resulted in similar
two-fold leftward shifts in the PE dose-response curves for both
groups. ACh-induced relaxation was potentiated in vessels from gravid
rats (EC50 0.25 [mu]M vs. 0.04 [mu]M, virgin and gravid rats,
respectively). Following NNLA, maximal relaxation was inhibited
significantly more in vessels from gravid rats (62% vs. 31%).
Likewise, maximal slope of ACh dose-response curves and ACh potency
were decreased in this group so that values no longer differed from
those in virgins. We conclude that pregnancy does not alter basal NO
synthesis in these isolated microvessels, but that it does enhance
ACh-induced NO release, while apparently inhibiting the action of an
NO-independent endothelium-derived vasodilator.
Received 3 February 1995; accepted in final form 2 June 1995.
APS Manuscript Number H100-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 August 1995.