Evidence that estrogen suppresses rho-kinase function in the cerebral circulation in vivo

Sophocles Chrissobolis, Klaudia Budzyn, Philip D Marley, Christopher G Sobey
Stroke; a Journal of Cerebral Circulation 2004, 35 (9): 2200-5

BACKGROUND AND PURPOSE: Premenopausal women are less susceptible to cardiovascular diseases than men or postmenopausal women. Such disease states are often associated with increased vascular RhoA/Rho-kinase activity and decreased activity of nitric oxide (NO). This study tested whether female gender is associated with lower Rho-kinase activity or higher NO activity in cerebral arteries in vivo and whether estrogen contributes to any such gender differences.

METHODS: Changes in basilar artery diameter were measured with the use of a cranial window preparation in anesthetized Sprague-Dawley rats. Some female rats were ovariectomized (OVX) and treated subcutaneously daily for 14 days with vehicle (dimethyl sulfoxide) or 17beta-estradiol. Vascular expression of RhoA or Rho-kinase was assessed by Western blotting.

RESULTS: The Rho-kinase inhibitor Y-27632 was selectively approximately 3-fold more potent as a cerebral vasodilator in males versus females. Expression of total RhoA or Rho-kinase did not differ between males and females. In OVX rats, vasodilator responses to Y-27632 resembled responses in males. Treatment of OVX rats with 17beta-estradiol normalized the vasodilator effects of Y-27632 to be equivalent to responses in intact female controls. The NO synthase inhibitor N-nitro-l-arginine methyl ester caused approximately 50% greater constriction of the basilar artery in females versus males, but responses in OVX rats treated with either vehicle or 17beta-estradiol did not differ from those recorded in intact females.

CONCLUSIONS: These data indicate that vascular Rho-kinase function is suppressed in females because of the effects of estrogen, whereas the higher NO activity in females is estrogen independent.

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