Effects of pressure overload on vascular smooth muscle cells

Summary

Hypertension, or high blood pressure, is an abnormal increase in the systemic arterial circulation usually caused by narrowing of the arterioles, the small-resistance vessels. The lumen may be reduced by structural changes of the vessel such as hypertrophy (cell enlargement) or hyperplasia (increased cell number), or by vasoconstriction caused by hormones and sympathetic nerve activity (Folkow, 1978; Lever, 1986). In this disorder the heart pumps a normal output of blood into a high-resistance circuit and blood pressure rises. Hypertension is associated with an increased risk of ischaemic heart disease and cerebrovascular disease. Hypertension is therefore an important disorder.

Mammalian arteries consist of an inner continuous monolayer of endothelium that is non-thrombogenic and serves as a structural semipermeable barrier and intermediary between the blood and the underlying cells of the vessel wall. Smooth muscle cells (smc) lie within the media of the vessel and are responsible for the structural integrity of the vessel as well as vasomotor tone. Endothelial cells and smc exist in a quiescent state; however, in response to various stimuli they are capable of exuberant proliferation. As an example, when an artery is denuded of its endothelium, platelets adhere, thrombus formation is initiated, and both endothelial cells and smc are stimulated to proliferate (Ross, 1986). Endothelial proliferation is an effort to promote healing of the endothelium while smc proliferation occurs in response to mitogens in the vascular lumen.