In vivo inhibition of nitric oxide synthesis does not depend on renin-angiotensin system activation

dc.creatorZappellini, A
dc.creatorTeixeira, SA
dc.creatorMuscara, MN
dc.creatorZatz, R
dc.creatorAntunes, E
dc.creatorDeNucci, G
dc.date1996
dc.dateDEC 19
dc.date2014-12-02T16:27:19Z
dc.date2015-11-26T17:28:59Z
dc.date2014-12-02T16:27:19Z
dc.date2015-11-26T17:28:59Z
dc.date.accessioned2018-03-29T00:16:03Z
dc.date.available2018-03-29T00:16:03Z
dc.identifierEuropean Journal Of Pharmacology. Elsevier Science Bv, v. 317, n. 41700, n. 285, n. 291, 1996.
dc.identifier0014-2999
dc.identifierWOS:A1996WB93500015
dc.identifier10.1016/S0014-2999(96)00734-0
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/69440
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/69440
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/69440
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1285179
dc.descriptionThe 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.
dc.description317
dc.description41700
dc.description285
dc.description291
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationEuropean Journal Of Pharmacology
dc.relationEur. J. Pharmacol.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectnitric oxide (NO)
dc.subjectrenin-angiotensin system
dc.subjectN-omega-Nitro-L-arginine methyl ester (L-NAME)
dc.subjecthoe 140
dc.subjectenalapril
dc.subjectblood
dc.subjectArginine Methyl-ester
dc.subjectHypertension
dc.subjectBlockade
dc.subjectPathway
dc.subjectRats
dc.subjectNo
dc.subjectSynthase
dc.subjectPressure
dc.subjectAssay
dc.titleIn vivo inhibition of nitric oxide synthesis does not depend on renin-angiotensin system activation
dc.typeArtículos de revistas


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