(Hypertension. 2000;35:1119.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From the Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, PROSIVAD-CONICET, Buenos Aires, Argentina.
Correspondence to María de los Angeles Costa, Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junin 956, 7 mo (1113), Buenos Aires, Argentina. E-mail mcosta{at}huemul.ffyb.uba.ar
AbstractThe aim of the present study was to determine the relationship between the hypotensive effect of the atrial natriuretic peptide (ANP) and the nitric oxide (NO) pathway. NG-nitro-L-arginine methyl ester bolus (L-NAME, 1 mg/kg) reverted the decrease in mean arterial pressure induced by ANP administration (5 µg/kg bolus and 0.2 µg · kg-1 · min-1 infusion), and the injection of L-NAME before peptide administration suppressed the ANP hypotensive response. To confirm these findings, a histochemical reaction was used to determine NADPH-diaphorase activity (a NO synthase marker) in the endothelium and smooth muscle of aorta and arterioles of the small and large intestine. ANP increased aorta and arteriole endothelium staining after both in vivo administration and in vitro tissue incubation. In both cases, L-NAME prevented the ANP effect on NADPH-diaphorase activity. Tissues incubated with 8-bromoguanosine 3', 5'-cyclic monophosphate mimicked ANP action. In addition, ANP administration increased urinary excretion of NOx end products. These findings indicate that ANP increases NO synthesis capability and NO production and suggest that the cGMP pathway may be involved. In conclusion, the NO pathway could be an intercellular messenger in the ANP endothelium-dependent vasorelaxation mechanism.
Key Words: natriuretic peptides nitric oxide arterial pressure NADPH diaphorase cyclic GMP vasodilation
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