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-Estradiol decreases vascular tone in cerebral arteries by shifting COX-dependent vasoconstriction to vasodilation
Department of Pharmacology, College of Medicine, University of California, Irvine, California 92697-4625
Submitted 8 January 2003 ; accepted in final form 9 March 2003
We have previously shown that estrogen treatment increases cerebrovascular
cyclooxygenase-1, prostacyclin synthase, and production of prostacyclin.
Therefore, vascular tone and prostanoid production were measured to
investigate functional consequences of estrogen exposure. Middle cerebral
arteries were isolated from ovariectomized female Fischer-344 rats with or
without chronic in vivo 17
-estradiol treatment. In vivo
17-estradiol treatment increased cerebral artery diameter; functional
endothelium was required for expression of these differences. The nonspecific
cyclooxygenase inhibitor indomethacin constricted, whereas arachidonic acid
dilated, cerebral arteries from estrogen-treated animals. Estrogen exposure
increased production of prostacyclin by cerebral arteries. Conversely, in
estrogen-deficient animals, indomethacin dilated and arachidonic acid
constricted cerebral blood vessels. This correlated with vasorelaxation
following inhibition of the thromboxane-endoperoxide receptor with SQ-29548
but not after selective blockade of thromboxane synthase with furegrelate,
suggesting prostaglandin endoperoxide (i.e., PGH2) activity.
Removal of the endothelium or selective blockade of cyclooxygenase-1 with
SC-560 abolished estrogen-mediated differences in the effects of arachidonate
on vessel diameter and on prostacyclin production by cerebral arteries. These
data suggest 17-estradiol decreases cerebrovascular tone by shifting the
primary end product of the endothelial cyclooxygenase-1 pathway from the
constrictor prostaglandin PGH2 to the vasodilator prostacyclin.
These effects of estrogen may contribute to the heightened thromboresistance
and enhanced cerebral blood flow documented in preversus postmenopausal
women.
cyclooxygenase; prostacyclin; prostaglandin endoperoxide
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