Common cellular disposition to hypertension and atherosclerosis.
The genetically hypertensive rat models, spontaneously hypertensive rats (SHR) and especially stroke-prone SHR (SHRSP), both develop arterial fat deposits quickly when fed high cholesterol diets. Therefore the morphological and functional characteristics of cultured vascular smooth muscle cells (SMC) from the aorta of SHR, SHRSP and normotensive Wistar-Kyoto (WKY) rats have been compared in order to demonstrate the common cellular mechanisms which induce hypertension and atherosclerosis. Cultured SMC became differentiated after short-term foetal calf serum exclusion from the medium, and despite the general concept of their noncontractility there was opticometric evidence that subcultured SMC contract spontaneously. Smooth muscle cells from SHR, but especially from SHRSP, showed enhanced proliferation which was inhibited by a Ca-antagonist, and accelerated lipid incorporation. It is concluded that these SMC are primarily predisposed to hypertension as well as to atherosclerosis.
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D002478:Cells, Cultured; D004110:Diltiazem / Q000494:pharmacology; D004198:Disease Susceptibility; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D050356:Lipid Metabolism; D008854:Microscopy, Electron; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
D004110:Diltiazem