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Stress-Induced Down-Regulation of Nitric Oxide Synthase in the Rat Heart

Objectives: beta 3 -adrenoceptor (beta 3 -AR) is expressed in a smaller proportion than beta 1 -AR and beta 2 -AR in the hearts of rats and humans and is activated in the presence of high concentrations of catecholamines. In the myocardium, beta 3 ARs couple to G inhibitory protein that activates nitric oxide synthases (NOS), thus increasing nitric oxide production that reduces inotropism. Beta 2 -ARs and beta 1 -ARs remodeling was described in failing and senescent human and rodent hearts as well as in the heart of foot shock stressed rats. This report aims to evaluate the function and expression of beta 3 -AR as well as the expression of NOS isoforms in the heart of foot shock stressed rats. Methods : Male Wistarrats ( Rattusnorvegicus ; 250-350 g; 12 weeks-old) were submitted to a 30 min session of foot shock stress (1 mA, 1s, 15-25 s interval between pulses) during 3 days and were euthanized immediately after the third stress session. The heart was isolated and dose-response curves to the beta 3 -AR selective agonist, BRL37, 344, was determined in the right atria, in the absence and in the presence of L-NAME. mRNA and protein expressions of beta 3 -AR and nitric oxide synthase (NOS) isoforms were analyzed in the four heart chambers of control and stressed rats. Results: Atria sensitivity to BRL 37, 344 in the presence or absence of L-NAME was not altered. Beta 3 -AR mRNA and protein expressions were similar in the four heart chambers of control and stressed rats; mRNA and protein expressions of endothelial NOS (eNOS) and inducible NOS (iNOS), as well as eNOS phosphorylation were reduced by stress. the expression of proteins involved in the beta-3-AR signaling pathway. If the stress-induced reduction on eNOS and iNOS expressions would impair the cardio protective mechanisms and the systolic and diastolic functions remains to be investigated.