PATHOPHYSIOLOGY OF SMOOTH-MUSCLE IN HYPERTENSION

Structural changes of the arteries in hypertension are determined by t he unique genetics of the animals and by various growth promoters and growth inhibitors. Vascular smooth muscle cell growth promoting factor s include fibroblast growth factor, platelet-derived growth factor, an d vasoactive peptides such as norepinephrine, angiotensin II, and endo thelin. Endothelial cells secrete three types of growth inhibiting fac tors. These are heparin - heparan sulfate, transforming growth factor beta, and nitric oxide. The effect of sympathetic innervation on vascu lar growth is probably dependent on its interaction with the renin-ang iotensin system. In the mesenteric vascular bed, the elevated resistan ce in the arterial system is present in both the macroarteries and in the more distal microarteries and veins. Changes in resistance arterie s include hypertrophy and reduction in outer diameter (remodelling). I n the resistance arteries from human essential hypertensives, remodell ing is the predominant finding. Long-term treatment with an angiotensi n I converting enzyme inhibitor but not with a beta-blocker was effect ive in reversing this type of vascular change. Studies have suggested that in addition to angiotensin II, endothelin may play a role in vasc ular remodelling of resistance arteries.