Hepatic clearance of renin after angiotensin blockade.
Several investigators have reported that hepatic metabolism of renin can be altered in pathophysiological states (e.g., high-output heart failure, cirrhosis, acute metal toxicity). The hypothesis that circulating angiotensin II may play a role in regulating renin metabolism by the liver was tested in anesthetized dogs. Captopril (SQ 14255) or an angiotensin II-competitive antagonist [( Sar1-Ile8]angiotensin II) was used for blockade of the renin-angiotensin system in two separate groups of dogs. The administration of captopril resulted in a significant fall in the percent extraction of renin by the liver (P less than 0.01) and in the clearance of renin (P less than 0.05). The group receiving the competitive antagonist and time-control animals showed no significant change in renin extraction or renin clearance by the liver. Our data do not support a role for angiotensin II in the regulation of hepatic metabolism of renin, since experiments utilizing the antagonist failed to produce a change. The mechanism by which captopril alters renin metabolism appears to be independent of its blockade of angiotensin II.
D000804:Angiotensin II / Q000037:antagonists & inhibitors*; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D008099:Liver / Q000378:metabolism*; D008102:Liver Circulation / Q000187:drug effects; D008297:Male; D012079:Renal Circulation / Q000187:drug effects; D012083:Renin / Q000097:blood / Q000378:metabolism*; D013448:Sulfobromophthalein / Q000378:metabolism
D013448:Sulfobromophthalein; D000804:Angiotensin II; D002216:Captopril; D012083:Renin