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Vol. 292, Issue 1, 375-380, January 2000
Department of Pharmacology and Neuroscience, Vascular Biology
Interdisciplinary Research Group, Albany Medical College, Albany, New
York
The purpose of this study was to examine the mechanism of enhanced
endothelium-dependent dilation in arteries from female rats compared
with arteries from males. Isolated mesenteric resistance arteries
(~250 µm) from sexually mature male and female Sprague-Dawley rats
were pressurized and outer diameter was measured. Arteries from females
were more sensitive to the endothelium-dependent vasodilator
acetylcholine (Ach) compared with those from males (
log
EC50: male = 6.74 ± 0.06; female = 6.96 ± 0.06; P = .037). After incubation with
N
-nitro-L-arginine (100 µM)
or apamin (30 nM), there was no longer a gender difference in midrange
sensitivity to ACh. In contrast, at higher concentrations of ACh,
N-nitro-L-arginine had a
greater inhibitory effect in the males than in the females.
Indomethacin (10 µM) decreased sensitivity to ACh in arteries from
both males and females, but did not alter the maximal response or
eliminate the gender difference. Finally, there was no gender
difference in vasodilation to the nitric oxide (NO) donor spermine-NO
complex, nor did apamin alter the spermine-NO complex response. In
conclusion, mesenteric arteries from female rats are more sensitive to
ACh than those from males. An enhanced contribution of an
apamin-sensitive KCa channel on the endothelium of female
arteries appears to be responsible for the augmented ACh-stimulated NO
production compared with that of males. In addition, ACh stimulates the
production of a non-NO, noncyclooxygenase, endothelium-derived
hyperpolarizing factor to a greater extent in females compared with males.
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