Effects of 17[beta]-estradiol on coronary microvascular responses
to endothelin-1.
Lamping, Kathryn G., and Daniel W. Nuno.
Department of Internal Medicine and the Cardiovascular Center,
College of Medicine, University of Iowa, Iowa City, Iowa 52242
APStracts 3:0173H, 1996.
The objective of this study was to examine the effects of 17[beta]
-estradiol on responses of coronary microvessels to endothelin-1 (ET
-1). Using isolated pressurized coronary microvessels from the left
ventricle of male or female dogs, constrictions to ET-1 were similar
in vessels from male and female dogs. 17[beta]-estradiol (1 [mu]M)
attenuated constriction to ET-1 of small arteries from both male (%
constriction at 10 [mu]M control: 39 +/- 9%; estradiol: 3 +/- 2%;
p<0.05) and female (% constriction at 10 [mu]M control: 39 +/-
8%; estradiol: 6 +/- 3%; p<0.05) dogs similarly. In contrast,
testosterone (1 [mu]M) had no effect on constriction to ET-1.
Constrictions to ET-1 were completely abolished by BQ123 (1 [mu]M), a
selective ETA receptor antagonist and enhanced by BQ788 (1 [mu]M), a
selective ETB receptor antagonist. Constrictions to ET-1 alone were
not altered by indomethacin (10 [mu]M) or nitro-L-arginine (100
[mu]M). 17[beta]-estradiol produced dose-dependent relaxation of
coronary microvessels preconstricted with ET-1 which was similar to
the response to testosterone and progesterone. Indomethacin (indo) or
nitro-L-arginine (LNNA) alone had no effect on relaxation to
17[beta]-estradiol. However, the combination of indo and LNNA
attenuated relaxation to 17[beta]-estradiol (% dilation at 100 [mu]M
control: 64 +/- 13%; indo plus LNNA: 21 +/- 6%; p<0.05), but did
not affect relaxation to testosterone. Thus, estradiol attenuated
constrictions of coronary microvessels to ET-1 more than similar
concentrations of testosterone. The ability of estradiol to modulate
responses to endothelin may involve release of vasodilator
prostaglandins and/or nitric oxide by estradiol.
Received 18 September 1995; accepted in final form 22 March 1996.
APS Manuscript Number H874-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96