1. Systemic infusion of angiotensin II (ATI) increased papillary blood perf
usion (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 antag
onist), HOE-140 (a bradykinin B-2 receptor antagonist), and an inhibitor of
NO production - N-omega-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 a
bolished these responses to AII but HOE-140 was without effect. Infusion of
NOLA abolished the increase in PBP but did not affect the presser 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, receptors and does not involve bradykinin B-2 receptors
. The AII-induced increase in PBP is dependent upon the presence of NO, thu
s providing a mechanism for maintenance of papillary perfusion in the face
of generalized renal vasoconstriction due to AII.