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Non‐contribution of renin‐angiotensin system to pressor response to N G ‐nitro‐L‐arginine in dogs
Author(s) -
Ishikawa Tomohisa,
Nejishima Hiromasa,
Imamura Takuya,
Nakayama Koichi
Publication year - 2002
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1046/j.1472-8206.2002.00065.x
Subject(s) - captopril , bradykinin , renin–angiotensin system , medicine , angiotensin ii , endocrinology , plasma renin activity , blood pressure , candesartan , angiotensin converting enzyme , nitric oxide synthase , nitric oxide , chemistry , receptor
Acute systemic blockade of nitric oxide (NO) production by nonselective inhibitors of NO synthase (NOS) isoforms, including N G ‐nitro‐L‐arginine methyl ester (L‐NAME) and N G ‐nitro‐L‐arginine (L‐NNA), has been shown to produce a long‐lasting pressor response in conscious and anaesthetised animals. The present study was undertaken to clarify whether the renin‐angiotensin system contributes to the development of this pressor response to L‐NNA. Systemic blood pressure and heart rate were continuously monitored in dogs anaesthetised with pentobarbital. Plasma renin activity in the blood obtained from a femoral artery and a renal vein was measured by use of radioimmunoassay. The acute pressor response produced by the intravenous administration of L‐NNA was accompanied by reduced renin activity in both systemic and renal vascular beds. Captopril, an angiotensin converting enzyme inhibitor, counteracted the pressor response to L‐NNA, whereas candesartan, an angiotensin AT 1 ‐receptor antagonist, had no apparent effect on it. The counteraction by captopril of the L‐NNA‐induced pressor response was likely to be attributable to enhancement by captopril of depressor responses to bradykinin, as HOE‐140, a bradykinin B 2 receptor antagonist, neutralised the effect of captopril. These results suggest that the pressor response acutely produced by the intravenous injection of a NOS inhibitor is not mediated by the renin‐angiotensin system in anaesthetised dogs.