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Am J Physiol Regul Integr Comp Physiol 292: R955-R961, 2007. First published October 12, 2006; doi:10.1152/ajpregu.00192.2006
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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Nitric oxide impairs baroreflex gain during acute psychological stress

Daisy L. Daubert and Virginia L. Brooks

Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon

Submitted 16 March 2006 ; accepted in final form 5 October 2006

Psychological stress can suppress baroreflex function, but the mechanism has not been fully elucidated. Nitric oxide in the brain and in the adrenal cortex, as well as plasma glucocorticoids, increases during stress and has been shown to suppress reflex gain in unstressed animals. Therefore, the purpose of this study was to test the hypothesis that stress, caused by exposure to a novel environment, decreases baroreflex gain in rabbits through the actions of nitric oxide to increase corticosterone release. Baroreflex control of heart rate and plasma corticosterone levels was quantified before and after blockade of nitric oxide synthase (NOS) with N{omega}-nitro-L-arginine (L-NNA; 20 mg/kg iv) in conscious rabbits exposed to a novel environment and in the same rabbits once they had been conditioned to the environment. Stress significantly reduced baroreflex gain from –23.4 ± 2 to –12.2 ± 1.6 beats·min–1·mmHg–1 (P < 0.05) and increased plasma corticosterone levels from 5.4 ± 0.7 to 15.5 ± 5.0 ng/ml (P < 0.05). NOS blockade increased gain in stressed animals (to –27.2 ± 5.4 beats·min–1·mmHg–1, P < 0.05) but did not alter gain in unstressed rabbits (–26.8 ± 4.9 beats·min–1·mmHg–1) such that gain was equalized between the two states. NOS blockade increased plasma corticosterone levels in unstressed animals (to 14.3 ± 2.1 ng/ml, P < 0.05) but failed to significantly alter levels in stressed rabbits (14.0 ± 3.9 ng/ml). In conclusion, psychological stress may act via nitric oxide, independently of increases in corticosterone, to decrease baroreflex gain.

conscious rabbits; corticosterone; novel environment; N{omega}-nitro-L-arginine



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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