title: Direct formation of angiotensin II without renin or converting enzyme in the ischemic dog heart.
abstract: An in vivo study was done to determine whether angiotensin II is directly formed by kallikrein or kallikrein-like proteases. Dogs were bilaterally nephrectomized 24 hours before ligation of the coronary artery. This acute coronary artery occlusion led to a regionally increased acidic state in the ischemic tissue and resulted in an elevation of immunoreactive angiotensin II (IR-Angiotensin II) levels in the coronary sinus blood, but not in systemic aortic blood. Elevation of the IR-Angiotensin II level was specifically inhibited by aprotinin, a kallikrein inhibitor. It was not affected by either captopril, a potent angiotensin converting enzyme inhibitor, or by pepstatin, a renin inhibitor. The concentrations of immunoreactive angiotensin I (IR-Angiotensin I), plasma renin activity and angiotensin converting enzyme activity remained unaltered in the presence of coronary artery occlusion. These results suggest that IR-Angiotensin II in the ischemic heart may be generated directly by kallikrein or kallikrein-like proteases, independently of the systemic renin angiotensin system.
authors: Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.
authors: M
authors: M
authors: Gondo
authors: H
authors: H
authors: Maruta
authors: K
authors: K
authors: Arakawa
mesh_terms: D000804:Angiotensin II / Q000096:biosynthesis* / Q000097:blood; D000818:Animals; D001011:Aorta; D007611:Aprotinin / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology; D003327:Coronary Disease / Q000097:blood / Q000378:metabolism*; D004285:Dogs; D009206:Myocardium / Q000378:metabolism*; D009392:Nephrectomy; D011863:Radioimmunoassay
chemical_list: D000804:Angiotensin II; D007611:Aprotinin; D002216:Captopril