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Am J Physiol Regul Integr Comp Physiol 292: R2179-R2187, 2007. First published March 22, 2007; doi:10.1152/ajpregu.00026.2007
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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Roles of nitric oxide and angiotensin II in the impaired baroreflex gain of pregnancy

Daisy L. Daubert,1 Dongmei Liu,2 Irving H. Zucker,2 and Virginia L. Brooks1

1Oregon Health & Science University, Department of Physiology and Pharmacology, Portland, Oregon; and 2University of Nebraska Medical Center, Department of Cellular and Integrative Physiology, Omaha, Nebraska

Submitted 16 January 2007 ; accepted in final form 16 March 2007

The present study tested the hypothesis that nitric oxide (NO) contributes to impaired baroreflex gain of pregnancy and that this action is enhanced by angiotensin II. To test these hypotheses, we quantified baroreflex control of heart rate in nonpregnant and pregnant conscious rabbits before and after: 1) blockade of NO synthase (NOS) with N{omega}-nitro-L-arginine (20 mg/kg iv); 2) blockade of the angiotensin II AT1 receptor with L-158,809 (5 µg·kg–1·min–1 iv); 3) infusion of angiotensin II (1 ng·kg–1·min–1 nonpregnant, 1.6–4 ng·kg–1·min–1 pregnant iv); 4) combined blockade of angiotensin II AT1 receptors and NOS; and 5) combined infusion of angiotensin II and blockade of NOS. To determine the potential role of brain neuronal NOS (nNOS), mRNA and protein levels were measured in the paraventricular nucleus, nucleus of the solitary tract, caudal ventrolateral medulla, and rostral ventrolateral medulla in pregnant and nonpregnant rabbits. The decrease in baroreflex gain observed in pregnant rabbits (from 23.3 ± 3.6 to 7.1 ± 0.9 beats·min–1·mmHg–1, P < 0.05) was not reversed by NOS blockade (to 8.3 ± 2.5 beats·min–1·mmHg–1), angiotensin II blockade (to 5.0 ± 1.1 beats·min–1·mmHg–1), or combined blockade (to 12.3 ± 4.8 beats·min–1·mmHg–1). Angiotensin II infusion with (to 5.7 ± 1.0 beats·min–1·mmHg–1) or without (to 8.4 ± 2.4 beats·min–1·mmHg–1) NOS blockade also failed to improve baroreflex gain in pregnant or nonpregnant rabbits. In addition, nNOS mRNA and protein levels in cardiovascular brain regions were not different between nonpregnant and pregnant rabbits. Therefore, we conclude that NO, either alone or via an interaction with angiotensin II, is not responsible for decrease in baroreflex gain during pregnancy.

conscious rabbits; L-158,809; neuronal nitric oxide synthase; N{omega}-nitro-L-arginine; AT1-receptor blockade



Address for reprint requests and other correspondence: V. L. Brooks, Dept. of Physiology and Pharmacology, L-334, Oregon Health & Science Univ., 3181 SW Sam Jackson Park Rd., Portland, OR 97239 (e-mail: brooksv{at}ohsu.edu)




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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
D. L. Daubert, M.-Y. Chung, and V. L. Brooks
Insulin resistance and impaired baroreflex gain during pregnancy
Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2007; 292(6): R2188 - R2195.
[Abstract] [Full Text] [PDF]




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