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The effects of angiotensin II on blood perfusion in the rat renal papilla
Author(s) -
Walker L. L.,
Rajaratne A. A. J.,
BlairWest J. R.,
Harris P. J.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0273o.x
Subject(s) - losartan , angiotensin ii , bradykinin , medicine , endocrinology , vasoconstriction , perfusion , angiotensin ii receptor type 1 , sodium nitroprusside , receptor antagonist , renin–angiotensin system , receptor , antagonist , blood pressure , nitric oxide
1 Systemic infusion of angiotensin II (AII) increased papillary blood perfusion (PBP) measured by laser‐Doppler flowmetry in rats, aged about 5 weeks. 2 The mechanisms involved in this response were determined by infusion of AII in the presence of systemic doses of losartan (a type 1 AII receptor antagonist), HOE‐140 (a bradykinin B 2 receptor antagonist), and an inhibitor of NO production ‐ N ω ‐nitro‐L‐arginine (NOLA). 3 Mean arterial blood pressure (MAP) and PBP increased in a dose‐dependent manner in response to intravenous infusions of AII. Infusion of losartan abolished these responses to AII but HOE‐140 was without effect. Infusion of NOLA abolished the increase in PBP but did not affect the pressor response to AII. Systemic infusion of sodium nitroprusside restored the response to AII in experiments with NOLA infusion. 4 The results indicate that the increase in PBP caused by AII is mediated via angiotensin AT 1 receptors and does not involve bradykinin B 2 receptors. The AII‐induced increase in PBP is dependent upon the presence of NO, thus providing a mechanism for maintenance of papillary perfusion in the face of generalized renal vasoconstriction due to AII.