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Vol. 291, Issue 2, 524-530, November 1999
Department of Pharmacology and Neuroscience, Albany Medical
College, Albany, New York
The purpose of this study was to determine the effects of in vivo
estrogen manipulations on mechanisms of endothelium-dependent vasodilation. Ovary-intact, ovariectomized (OVX), or OVX with estrogen
replacement (OVX + E2) female Sprague-Dawley rats were studied (n = 8). Mesenteric arteries (~300 µm)
were isolated, cannulated, and pressurized to 60 mm Hg in an
arteriograph containing bicarbonate buffer and vessel diameter was
monitored. Concentration-response curves to the endothelium-dependent
histamine H1 agonist 2-thiazolylethylamine (2-TEA; 1 nM-100 µM) and to acetylcholine (1 nM-10 µM) were performed in
preconstricted arteries. The effect of
N
-nitro-L-arginine (LNA; 100 µM) or LNA + indomethacin (INDO) (10 µM) on agonist-induced vasodilation was
determined. There was no difference between treatment groups in the
sensitivity of mesenteric arteries to 2-TEA or acetylcholine. LNA
produced a significant decrease in sensitivity to 2-TEA in arteries
from ovary-intact and OVX + E2 rats but not in those from
OVX rats. The addition of INDO produced a small additional decrease in
sensitivity to 2-TEA in arteries from ovary-intact rats, a significant
decrease in OVX, and no shift in OVX + E2. LNA + INDO
produced a similar degree of inhibition of the 2-TEA response in the
three treatment groups. In contrast, when acetylcholine was used, the
decrease in sensitivity produced by LNA or LNA + INDO was similar in
the three rat groups. We conclude that estrogen increases the nitric
oxide component of endothelium-dependent dilation and decreases the
cyclooxygenase component. These effects of estrogen appear to be
agonist-specific. Our findings suggest that estrogen modulates cross
talk between the nitric oxide synthase and cyclooxygenase pathways of vasodilation.
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