Autoregulation of glomerular blood flow during converting-enzyme inhibition by captopril.
We investigated the effects of local angiotensin-converting enzyme (ACE) inhibition by captopril on the autoregulatory efficiency of glomerular blood flow (GBF). The microvasculature of the nonfiltering rat kidney was observed via in vivo television microscopy. Clamping of the aorta above the renal arteries allowed controlled reductions in renal perfusion pressure. Perfusion pressure reductions (PPR) dilated preglomerular vessels and, within the autoregulatory range, GBF was well maintained. Local captopril application markedly attenuated pressure dependent vasodilation and abolished autoregulation of GBF. Autoregulatory response could be restored in the presence of captopril by adding angiotensin II (A II) to the tissue bath. These results indicate that autoregulation of GBF in the rat kidney is, at least partially, dependent on intrarenal renin-angiotensin activity.
Steinhausen
M
M
I. Physiologisches Institut, Universität Heidelberg, Federal Republic of Germany.
Holz
F G
FG
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D007678:Kidney Glomerulus / Q000098:blood supply* / Q000187:drug effects; D051381:Rats; D011920:Rats, Inbred WF; D012039:Regional Blood Flow / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D000804:Angiotensin II; D002216:Captopril