HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: 294/1/H156    most recent 01137.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Girouard, H. Articles by Iadecola, C. Search for Related Content PubMed PubMed Citation Articles by Girouard, H. Articles by Iadecola, C.

The neurovascular dysfunction induced by angiotensin II in the mouse neocortex is sexually dimorphic

¹Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College; and ²Harold and Margaret Milliken Hatch Laboratory of Neuroendociniology, The Rockefeller University, New York, New York

Submitted 2 October 2007 ; accepted in final form 1 November 2007

Women are less susceptible to the cerebrovascular complications of hypertension, such as a stroke and vascular dementia. The mechanism of such protection may be related to a reduced vulnerability of women to the cerebrovascular actions of hypertension. To test this hypothesis, we used a model of hypertension based on infusion of angiotensin II (ANG II), an octapeptide that plays a key role in hypertension and produces cerebrovascular dysregulation. Cerebral blood flow (CBF) was monitored by laser-Doppler flowmetry in anesthetized (urethane-chloralose) C57BL/6J male and female mice equipped with a cranial window. ANG II administration (0.25 µg·kg^–1·min^–1 iv x 30–45 min) elevated arterial pressure equally in both sexes but attenuated the CBF increase induced by whisker stimulation or by the endothelium-dependent vasodilator acetylcholine (ACh) in male but not in female mice. The administration of ANG II for 7 days (2.74 mg·kg^–1·day^–1), using osmotic minipumps, also attenuated these cerebrovascular responses in male, but not female, mice. The reduced susceptibility to the effect of ANG II in female mice was abolished by ovariectomy and reinstated by estrogen administration to ovariectomized mice. Administration of estrogen to male mice abolished the ANG II-induced attenuation of CBF responses. We conclude that female mice are less susceptible to the cerebrovascular dysregulation induced by ANG II, an effect related to estrogen. Such protection from the deleterious cerebrovascular effects of hypertension may play a role in the reduced vulnerability to the cerebrovascular complications of hypertension observed in women.

hypertension; functional hyperemia; endothelium-dependent relaxation; estrogen

This article has been cited by other articles:

				G. Wang, T. A. Milner, R. C. Speth, A. C. Gore, D. Wu, C. Iadecola, and J. P. Pierce Sex differences in angiotensin signaling in bulbospinal neurons in the rat rostral ventrolateral medulla Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2008; 295(4): R1149 - R1157. [Abstract] [Full Text] [PDF]