Artículos de revistas
In vivo inhibition of nitric oxide synthesis does not depend on renin-angiotensin system activation
Registro en:
European Journal Of Pharmacology. Elsevier Science Bv, v. 317, n. 41700, n. 285, n. 291, 1996.
0014-2999
WOS:A1996WB93500015
10.1016/S0014-2999(96)00734-0
Autor
Zappellini, A
Teixeira, SA
Muscara, MN
Zatz, R
Antunes, E
DeNucci, G
Institución
Resumen
The role of the renin-angiotensin system in the haemodynamic changes induced by acute administration of N-omega-nitro-L-arginine methyl ester in anaesthetised dogs was investigated. The left femoral artery and vein were cannulated for blood pressure measurement and drug administration, respectively. A Swan-Ganz catheter was introduced through the right femoral vein and advanced to the pulmonary artery. Pulmonary arterial pressure, right atrial pressure and cardiac output were also determined. N-omega-Nitro-L-arginine methyl ester (0.01-10.0 mg/kg) was administered alone (control animals, n = 18) or in the presence of the angiotensin-converting enzyme inhibitors, captopril (2 mg/kg, n = 9) or enalapril (2 mg/kg, n = 7) or of the bradykinin B-2 receptor antagonist D-[Arg-Hyp(3),Thi(5),D-Tic(7),Oic(8)]bradykinin (Hoe 140, 0.1 mg/kg, n = 6). Cerebellum nitric oxide synthase and serum angiotensin-converting enzyme activities were also measured. N-omega-Nitro-L-arginine methyl ester induced dose-dependent increases in blood pressure and systemic vascular resistance and decreases in heart rate and cardiac output. Nitric oxide synthase activity was inhibited 58% by N-omega-nitro-L-arginine methyl ester (from 3.37 +/- 0.30 to 1.40 +/- 0.24 pmol/min per mg protein, P < 0.05, n = 5). Both enalapril and captopriI potentiated the cardiovascular changes induced by bradykinin (300 ng/kg, bolus). Moreover, enalapril inhibited angiotensin-converting enzyme activity from 12.8 +/- 1.2 to 1.1 +/- 0.2 nmol/ml per min (P < 0.05, it = 6). Under these conditions, N-omega-nitro-L-arginine methyl ester administration elicited the same haemodynamic changes as those observed in non-treated animals, except for preventing the decrease in systolic index. Hoe 140 had no effect on the cardiovascular responses to N-omega-nitro-L-arginine methyl ester. These results indicate that the renin-angiotensin system does not modulate these haemodynamic changes. 317 41700 285 291