title: Regional renal haemodynamics of angiotensin II infusion under prostaglandin, kinin or converting enzyme inhibition in the Wistar rat.
abstract: OBJECTIVE
  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 papillary circulation is modulated by bradykinins, prostaglandins or NO (NO). In anaesthetised Wistar rats, total renal blood flow (RBF) was measured, as was cortical (CBF) and papillary (PBF) blood flow, using the laser-Doppler technique, in responses to Ang II (30 ng kg(-1) min(-1)) alone and after ACE inhibition (enalapril) or bradykinin/prostaglandin synthesis inhibition (ketoprofen, aprotinin). PBF was also measured after blockade of NO formation with or without pretreatment with an Ang II receptor antagonist (losartan).
  
  
  RESULTS
  (i) PBF did not change in response to Ang II infusion but MAP increased (+ 10%) and RBF and CBF decreased. (ii) Treatment with aprotinin 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.
  
  
  CONCLUSIONS
  Bradykinin and prostaglandins do not appear to cause the lack of renal papillary 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 affect the sensitivity of renal papillary autoregulation. This may be an important aspect of the blood pressure lowering effect of ACE inhibitors.
authors.affiliation: Institute of Physiology and Pharmacology, Department of Physiology, University of Göteborg, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Rudenstam
authors.forename: J
authors.initials: J
authors.lastname: Creutz
authors.forename: G
authors.initials: G
authors.lastname: Göthberg
authors.forename: G
authors.initials: G
authors.lastname: Karlström
authors.forename: G
authors.initials: G
authors.lastname: Bergström
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D001920:Bradykinin / Q000037:antagonists & inhibitors*; D004656:Enalapril / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D007660:Ketoprofen / Q000494:pharmacology; D007679:Kidney Medulla / Q000098:blood supply; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D011448:Prostaglandin Antagonists; D000804:Angiotensin II; D009569:Nitric Oxide; D004656:Enalapril; D007611:Aprotinin; D007660:Ketoprofen; D019808:Losartan; D001920:Bradykinin