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This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/H1025    most recent 00021.2008v1 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 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 Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Xue, B. Articles by Hay, M. Search for Related Content PubMed PubMed Citation Articles by Xue, B. Articles by Hay, M.

Central estrogen inhibition of angiotensin II-induced hypertension in male mice and the role of reactive oxygen species

Departments of ¹Molecular Physiology and Biophysics, ²Psychology, ³Pharmacology, and ⁴Integrative Physiology and ⁵Cardiovascular Center, University of Iowa, Iowa City, Iowa

Submitted 9 January 2008 ; accepted in final form 9 June 2008

It has been shown that reactive oxygen species (ROS) contribute to the central effect of ANG II on blood pressure (BP). Recent studies have implicated an antihypertensive action of estrogen in ANG II-infused female mice. The present study used in vivo telemetry recording and in vitro living mouse brain slices to test the hypothesis that the central activation of estrogen receptors in male mice inhibits ANG II-induced hypertension via the modulation of the central ROS production. In male wild-type mice, the systemic infusion of ANG II induced a significant increase in BP (30.1 ± 2.5 mmHg). Either central infusion of Tempol or 17β-estradiol (E₂) attenuated the pressor effect of ANG II (10.9 ± 2.3 and 4.5 ± 1.4 mmHg), and the protective effect of E₂ was prevented by the coadministration of an estrogen receptor, antagonist ICI-182780 (23.6 ± 3.1 mmHg). Moreover, the ganglionic blockade on day 7 after the start of ANG II infusions resulted in a smaller reduction of BP in central Tempol- and in central E₂-treated males, suggesting that estrogen inhibits the central ANG II-induced increases in sympathetic outflow. In subfornical organ slices, the application of ANG II resulted in a 21.5 ± 2.5% increase in ROS production. The coadministration of irbesartan, an ANG II type 1 receptor antagonist, or the preincubation of brain slices with Tempol blocked ANG II-induced increases in ROS production (–1.8 ± 1.6% and –1.0 ± 1.8%). The ROS response to ANG II was also blocked by E₂ (–3.2 ± 2.4%). The results suggest that the central actions of E₂ are involved in the protection from ANG II-induced hypertension and that estrogen modulation of the ANG II-induced effects may involve interactions with ROS production.

sex hormone; blood pressure; oxidative stress; subfornical organ

This article has been cited by other articles:

				B. Xue, M. Singh, F. Guo, M. Hay, and A. K. Johnson Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1638 - H1646. [Abstract] [Full Text] [PDF]