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J. Biol. Chem., Vol. 280, Issue 20, 19704-19710, May 20, 2005

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Estrogen Induces Vascular Wall Dilation

MEDIATION THROUGH KINASE SIGNALING TO NITRIC OXIDE AND ESTROGEN RECEPTORS AND ^*

Xiaomei Guo, Mahnaz Razandi||, Ali Pedram||, Ghassan Kassab, and Ellis R. Levin¶||

From the ^||Division of Endocrinology, Veterans Affairs Medical Center, Long Beach, California 90822 and the Departments of Medicine and Biomedical Engineering, University of California, Irvine, California 92717

Estrogen has been shown to affect vascular cell and arterial function in vitro and in vivo. Here we examined the ability of estradiol (E₂) to cause rapid arterial dilation of elastic and muscular arteries in vivo and the mechanisms involved. E₂ administration caused a rapid increase in the outer wall diameter of both types of arteries in ovariectomized female mice. This resulted from estrogen receptor (ER)-mediated stimulation of nitric oxide production, demonstrated by preinjecting the mice arteries with a soluble inhibitor of nitric oxide (monomethyl L-arginine) and by showing the absence of E₂ action in eNOS-/- mice. Rapid activation of both ERK/MAP kinase and phosphatidylinositol 3-kinase activity was found in the E₂-exposed arteries, and inhibiting either kinase prevented the vasodilatory action of E₂. Kinase activation and vasodilator responses to E₂ were absent in either ER or ER knock-out mice, implicating both receptor subtypes as mediating this E₂ action. These results indicate that E₂ modulation of arterial tonus through plasma membrane ER and rapid signaling could underlie many previously observed actions of estrogen reported to occur in women.

Received for publication, February 2, 2005 , and in revised form, March 7, 2005.

^* This work was supported by grants from the Research Service of the Department of Veterans Affairs and National Institutes of Health Grants HL59890 (to E. R. L.) and HL055554-06 (to G. K.), and American Heart Association Grant 0140036N (GSK). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed: Medical Service (111-I), Long Beach Veterans Affairs Medical Center/University of California, 5901 E. 7th St., Long Beach, CA 90822. Tel.: 562-826-5748; Fax: 562-826-5515; E-mail: ellis.levin{at}med.va.gov.

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