Total cholesterol levels in SMC cultured with hyperlipidemic serum, increased more under hypoxic conditions than under normal conditions. No difference was noted in cholesterol synthesis from acetic acid. TG levels in SMC were inhibited markedly under hypoxic conditions. TG synthesis induced by serum in the hypoxic cells was decreased when compared with control cells. Thus hypoxic conditions accelerate cellular uptake of cholesterol, an initial step in atherogenesis. Proliferation rate of SMC prepared by the explant method was greater for SHRsp than WKY. SHRsp-SMC prepared by the enzyme method proliferated at the same rate as those prepared by the explant method. However, proliferation rate of WKY-SMC by enzyme method was extremely low. Nitroprusside inhibited strongly the proliferation of SHRsp-SMC. DBcGMP and ANP did not inhibit the proliferation of SMC. Methylene blue did not interrupt the inhibitory effect of Nitroprusside. It is suggested that Nitroprusside has an unknown biological action. TPA inhibited fetal calf serum induced DNA synthesis in quiescent SMC. The TPA effect was additive to the inhibitory effect of Nitroprusside. SMC cultured on cover slips showed increased intracellular (Ca2+)i to norepinephrine but not Phenylephrine and PDGF. Suspended SMC did not respond against NE, Phenylephrine and PDGF. In suspended SMC and SMC cultured on cover slip, angiotensin II caused increases in (Ca2+)i. A specific inhibitor of AGII, (Sarl, Ile8) AGII, blocked increases in Fura fluorescence elicited by AGII.
