Venous function in hypertension

Abstract

The results described in this review clearly demonstrate that venous extensibility, contractility and prostaglandin synthesis are altered in veins from hypertensive animals and man. Similarly, venous smooth muscle compliance seems to be impaired in human essential and experimental animal hypertension. Decreased venous compliance and enhanced venous contractility may account for the transient increase in cardiac output observed during the labile phase of hypertension. Alterations in venous contractility may reflect intrinsic changes in the vascular smooth muscle later in the hypertensive process. Alternatively, the veins may respond sooner to a circulating humoral stimulus which will subsequently modify arterial smooth muscle function, or to which the arteries are unresponsive. Therefore, the study of venous and arterial smooth muscle function during the development of the hypertensive process could well identify the site, and perhaps, stimulus for the initial changes that occur in hypertension. Similarly, a study of venous and arterial smooth muscle function in hypertension can adequately define those changes intrinsic to the high blood pressure and those secondary to the increased vascular pressure of the hypertension. Therefore, analysis of the type, mechanism and sequence of venous changes which occur in hypertension can provide insight into rational drug therapy to treat the cause, and not the symptoms, of hypertensive vascular disease.