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Department of Surgery, Mayo Clinic and Foundation, Rochester, Minnesota 55905
Experiments were
designed to determine whether normal fluctuations in endogenous sex
steroid hormones and/or gender affect endothelium-dependent
relaxations in coronary arteries, and, if so, to identify
endothelium-derived factors contributing to these differences. Coronary
arteries from sexually mature, gonadally intact male and female pigs or
ovariectomized pigs were prepared either for study of isometric force
in organ chambers or for measurement of prostanoids and activity of
nitric oxide (NO) synthase. In organ chamber studies,
neither the magnitude nor the sensitivity of endothelium-dependent
relaxations correlated with endogenous estrogen or progesterone in
female pigs. However, relaxations to bradykinin and UK-14304 were
significantly greater and/or shifted leftward in arterial rings
from female compared with male pigs. Indomethacin
(10
5 mol/l) increased
endothelium-dependent relaxations only in arteries from male pigs.
NG-monomethyl-L-arginine reduced
endothelium-dependent relaxations to a similar extent in coronary
arteries from either sex. Neither production nor response to
thromboxane A2 or prostacyclin
differed in coronary arteries from male compared with female pigs.
Activity for calcium-dependent or -independent NO synthase was similar in both sexes. These results suggest that normal fluctuations in
endogenous sex steroid hormones do not affect endothelium-dependent relaxations in coronary arteries from female pigs. There are, however,
gender differences in endothelium-dependent relaxations that are
indomethacin sensitive and may be due to cyclooxygenase products other
than thromboxane A2 or
prostacyclin.
arachidonic acid; eicosanoids; nitric oxide synthase; prostacyclin; estrogen; thromboxane
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