[Hypertension and vascular diseases: molecular and cellular mechanisms]

Increased blood pressure can be observed in about 15-20% of the Swiss population. Hypertension causes few or no symptoms, but is an important risk factor for myocardial infarction, stroke, renal failure and peripheral vascular disease. All these clinical complications of hypertension are preceded by functional changes of blood vessels and the myocardium (left ventricular hypertrophy). In conduit arteries, hypertension is associated with atherosclerotic changes, while in resistance arteries only increased medial thickness can be observed. In atherosclerosis, functional changes of the endothelium, vascular smooth muscle, platelets and monocytes occur. These changes lead to hypercontractility, increased interaction of circulating blood cells with the blood vessel wall, and to proliferation and migration of vascular smooth muscle cells. These events impair local blood flow and eventually may cause vascular occlusion. The endothelium plays a particularly important role as a regulator of these mechanisms. Accordingly, it is likely that an endothelial dysfunction occurs at the very beginning of the atherosclerotic process. In resistance arteries, remodeling of vascular smooth muscle cells leads to thickening of the media with encroachment on the lumen due to an increased media lumen ratio. These hypertension-induced vascular changes are in part reversible by antihypertensive drugs. Hypertension-induced vascular disease is preceded by numerous alterations in the expression, secretion and action of mediators and receptors of endothelial cells, vascular smooth muscle, platelets and monocytes. It is hoped that increased understanding of the cellular/molecular mechanisms of hypertensive vascular disease will allow more effective therapy (and in the future also gene therapy) as well as better prevention of coronary artery disease in hypertensive patients.