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In order to define the molecular mechanism involved in the enhancement of spontaneously hypertensive rat (SHR) cell proliferation, we compared the actions of fetal calf serum and angiotensin II on both SHR and Wistar-Kyoto rat (WKY) aortic smooth muscle cells. Both compounds were more mitogenic on the SHR cells than on the controls. However, phospholipase C hyper-responsiveness was present only after angiotensin stimulation. This was also true of the expression of c-jun, c-fos and c-myc. Oncogene overexpression therefore appears to be more strongly related to phospholipase C hyperreactivity than to enhanced proliferation of SHR aortic smooth muscle cells.
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