Endothelial Injury in Hypertension
There are attractive reasons for considering the possibility that platelet mitogen released at sites of endothelial denudation accounts for the smooth muscle cell proliferation found in arteriosclerosis of hypertensive large and small arteries (1–3). The first question in this research is whether endothelial injury occurs. Endothelial injury is well documented in acute renal hypertension (4), and a number of studies have tried to identify a direct toxic effect of angiotensin II (5–8). This is supported by evidence that vasoactive agents are capable of opening cell junctions of postcapillary venular endothelium (9). This effect, however, is specific for these vessels and may relate to the incomplete junctional complexes seen only in the postcapillary venular endothelium (10). There have been reports that angiotensin II has a similar effect on the arterial endothelium. This effect is said to occur under conditions of normal or low blood pressure—thus suggesting a direct effect on endothelial contractility (7).
KeywordsPermeability Angiotensin Renin Thymidine Dura
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