Abstract

The role of vascular smooth muscle cells (VSMC) in the intraparietal conversion of angiotensin I (AngI) to angiotensin II (AngII) was investigated in rat aortic tissue. The responses of rat aortic vascular smooth muscle cells to AngI and AngII were assessed by studying contraction of endothelium-denuded aortic rings and by measuring intracellular Ca++ ion concentration in primary cultures of VSMC free of endothelial cells. In both preparations, AngI and AngII induced identical responses which were inhibited by saralasin, a blocker of AngII receptors. In the presence of captopril, an inhibitor of the angiotensin converting enzyme, the increase in calcium caused by AngI was abolished in VSMC cultures and the contractile effect of this peptide in aortic rings was strongly decreased, whereas the responses to AngII remained unaffected. These results demonstrate that VSMC are able to convert AngI to AngII.

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