Migration of vascular smooth muscle cells is enhanced in cultures derived from spontaneously hypertensive rat.

Migration of vascular smooth muscle cells (SMC) constitutes a common step in neointimal formation which occurs in several vascular diseases. Whether the migratory response of SMC derived from hypertensive animals is different to that of controls may provide a clue to the link between hypertension and atherosclerosis. We examined the migratory responses of SMC from cell cultures and ring explants (thin aortic ring segment) and compared these responses between normotensive and hypertensive rats at two different ages. Both scrape-wound assay and transwell chambers from cultured aortic SMC as well as aortic ring explant cell outgrowth models were employed. The aortae were obtained from male spontaneously hypertensive rats (SHR) and their normotensive counterpart the Wistar-Kyoto rat (WKY) at 5 and 20 weeks of age. Migration was induced by fetal bovine serum or platelet-derived growth factor (PDGF) and migrated cells were counted at different times following stimulation. We found that SMC migration exhibited a high sensitivity to serum (range of ED50: 2.2-3.6%), migration of SMC from 20-week-old SHR exceeded (by 46%, P<0.025) that of SMC from age-matched WKY and the difference became significant as early as 8 h after stimulation by serum. Chemotaxis induced by PDGF (2 h) exhibited similar differences. An elevated migratory response in SHR-SMC was also found in cells derived from 5-week-old rats in whom the blood pressure was normal. In younger animals, cell outgrowth from SHR aortic ring explants also accumulated more cells compared with WKY without a higher growth rate, thus suggesting that SHR-SMC have a higher migratory response ex vivo. In conclusion, aortic SMC migration appeared to be enhanced in various preparations from SHR. This difference also existed in young animals before the elevation of blood pressure occurred and might contribute partly to the role of hypertension as a risk factor for atherosclerosis.