Immunohistochemical evidence that angiotensins I and II are formed by intracellular mechanism in juxtaglomerular cells.
The existence of angiotensin II (AII) immunoreactivity in juxtaglomerular (JG) cells of rat kidney, which has been demonstrated previously by immunohistochemical studies, can be explained either as the product of intracellular synthesis or by the internalization of receptor-bound AII originating in plasma. To resolve these two alternative mechanisms, attempts were made to identify AI in JG cells of rat kidney by immunohistochemical staining using specific antibodies to AI. Although AI-like immunoreactivity was not detected in normal rat kidney, rats treated with the angiotensin-converting enzyme inhibitors, MK-421 or captopril, showed AI-like immunoreactivity in JG cells. The presence of renin and AII-like immunoreactivity was demonstrated in the same cells by specific antibodies to respective antigens used on adjacent serial sections. These findings support an intracellular mechanism of the formation of AII and suggest an intracellular renin angiotensin system, presumably separate from the extracellular system.
D000803:Angiotensin I / Q000096:biosynthesis*; D000804:Angiotensin II / Q000096:biosynthesis*; D000809:Angiotensins / Q000096:biosynthesis*; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D004151:Dipeptides / Q000494:pharmacology; D004656:Enalapril; D007124:Immunoenzyme Techniques; D007606:Juxtaglomerular Apparatus / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000096:biosynthesis; D012084:Renin-Angiotensin System / Q000187:drug effects
D000809:Angiotensins; D004151:Dipeptides; D000804:Angiotensin II; D004656:Enalapril; D000803:Angiotensin I; D002216:Captopril; D012083:Renin