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J Physiol Volume 519, Number 1, 273-278, August 15, 1999
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The Journal of Physiology (1999), 519.1, pp. 273-278
© Copyright 1999 The Physiological Society

The effects of angiotensin II on blood perfusion in the rat renal papilla

L. L. Walker, A. A. J. Rajaratne, J. R. Blair-West and P. J. Harris

Department of Physiology, The University of Melbourne, Parkville, Victoria 3052, Australia


Systemic infusion of angiotensin II (AII) increased papillary blood perfusion (PBP) measured by laser-Doppler flowmetry in rats, aged about 5 weeks.


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 B2 receptor antagonist), and an inhibitor of NO production - Nomega-nitro-L-arginine (NOLA).


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.


The results indicate that the increase in PBP caused by AII is mediated via angiotensin AT1 receptors and does not involve bradykinin B2 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.


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