Regional renal haemodynamics of angiotensin II infusion under prostaglandin, kinin or converting enzyme inhibition in the Wistar rat

Aims: Renal medullary blood flow is important in blood pressure regulation and is surprisingly unaffected by the vasoconstrictor action of angiotensin II (Ang II). This study tested if the effect of Ang II on the renal papill ary circulation is modulated by bradykinins, prostaglandins or NO (NO). In anaesthetised Wistar rats. total renal blood flow (RBF) was measured, as wa s cortical (CBF) and papillary (PBF) blood flow, using the laser-Doppler te chnique, in responses to Ang II (30 ng kg(-1) min(-1)) alone and after ACE inhibition (enalapril) or bradykinin/prostaglandin synthesis inhibition (ke toprofen, aprotinin). PBF was also measured after blockade of NO formation with or without pretreatment with an Ang II receptor antagonist (losartan). Major findings: (i) PBF did not change in response to Ang II infusion but MAP increased (+10%) and RBF and CBF decreased. (ii) Treatment with aprotin in and ketoprofen left MAP, RBF and CBF unchanged but decreased PBF. Ang II did not decrease PBF further but a significant increase in MAP was seen. ( iii) Enalapril treatment left PBF unchanged but decreased MAP and increased RBF and CBF. When Ang II was infused PBF and MAP increased markedly. (iv) L-NAME reduced PBF independently of losartan treatment. Principal conclusio n: Bradykinin and prostaglandins do not appear to cause the lack of renal p apillary vasoconstriction to Ang II. However, the increase in PBF to Ang II seen after enalapril treatment suggests that enalapril treatment, possibly via its effects on kinin breakdown and subsequent NO formation, might affe ct the sensitivity of renal papillary autoregulation. This may be an import ant aspect of the blood pressure lowering effect of ACE inhibitors.