Biology of Blood Vessels in Hypertension

Abstract

Increased peripheral vascular resistance is the hemodynamic characteristic of essential hypertension and is associated with structural and functional changes in resistance vessels. The major structural alterations constitute reduced vessel lumen diameter with thickening of the vascular wall. Only a 10% narrowing of the vessel lumen and a slight thickening of the vessel wall, which includes the medial and intimal layers, are sufficient to significantly increase peripheral resistance. At the cellular level, there is a significant increase in cell mass and collagen and elastin deposition with vascular smooth muscle hypertrophy and hyperplasia. Direct hemodynamic forces, as well as circulating and local growth regulators, stimulate cell growth in hypertensive vessels. Functional alterations that increase peripheral resistance include enhanced vascular reactivity to vasoconstrictor agents or impaired relaxation and reflect changes in excitation-contraction coupling and/or electrical properties of cells. Excess systemic or local production of vasoconstrictors or growth factors, abnormal agonist-receptor interactions, increased cell membrane permeability, defective transmembrane ion transport, intracellular calcium overload, exaggerated responses of the phosphoinositide signaling system, and altered endothelial function result in increased vascular smooth muscle growth and contractility. Whether these changes are a primary cause or secondary consequence of hypertension remains unclear but is a major focus of investigation. (Cardiol Rev 1993;1:2, 87-96)