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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/H1638    most recent 00502.2009v1 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 Google Scholar Articles by Xue, B. Articles by Johnson, A. K. PubMed PubMed Citation Articles by Xue, B. Articles by Johnson, A. K.

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

Departments of ¹Psychology, ²Integrative Physiology, and ³Pharmacology and ⁴Cardiovascular Center, University of Iowa, Iowa City, Iowa; and ⁵Department of Physiology, University of Arizona, Tucson, Arizona

Submitted June 3, 2009 ; accepted in final form September 2, 2009

The present study tested the hypotheses that 1) nitric oxide (NO) is involved in attenuated responses to ANG II in female mice, and 2) there is differential expression of neuronal NO synthase (nNOS) in the subfornical organ (SFO) and paraventricular nucleus (PVN) in response to systemic infusions of ANG II in males vs. females. Aortic blood pressure (BP) was measured in conscious mice with telemetry implants. N^G-nitro-L-arginine methyl ester (L-NAME; 100 µg·kg^·–1day^–1), an inhibitor of NOS, was administrated into the lateral cerebral ventricle for 14 days before and during ANG II pump implantation. Central infusion of L-NAME augmented the pressor effects of systemic ANG II in females (21.5 ± 2.2 vs. 9.2 ± 1.5 mmHg) but not in males (29.4 ± 2.5 vs. 30.1 ± 2.5 mmHg). Central administration of N⁵-(1-imino-3-butenyl)-L-ornithine (L-VNIO), a selective nNOS inhibitor, also significantly potentiated the increase in BP induced by ANG II in females (17.5 ± 3.2 vs. 9.2 ± 1.5 mmHg). In gonadectomized mice, central L-NAME infusion did not affect the pressor response to ANG II in either males or females. Ganglionic blockade after ANG II infusion resulted in a greater reduction in BP in central L-NAME- or L-VNIO-treated females compared with control females. Western blot analysis of nNOS protein expression indicated that levels were 12-fold higher in both the SFO and PVN of intact females compared with those in intact males. Seven days of ANG II treatment resulted in a further increase in nNOS protein expression only in intact females (PVN, to 51-fold). Immunohistochemical studies revealed colocalization of nNOS and estrogen receptors in the SFO and PVN. These results suggest that NO attenuates the increase in BP induced by ANG II through reduced sympathetic outflow in females and that increased nNOS protein expression associated with the presence of female sex hormones plays a protective role against ANG II-induced hypertension in female mice.

sex hormone; nitric oxide/nitric oxide synthase; blood pressure

This article has been cited by other articles:

				L. L. Yanes and J. F. Reckelhoff A new piece in the hypertension puzzle: central blood pressure regulation by sex steroids Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1583 - H1584. [Full Text] [PDF]