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.
