Altered adrenergic control in hypercholesterolemia.
Vascular reactivity is altered by hypercholesterolemia and atherosclerosis. Animal studies have shown that serotonergic mechanisms of vasoconstriction are enhanced, while the changes with adrenergic mechanisms are still equivocal. Serum lipids are increased with beta-blocker and diuretic therapy for hypertension. Thus, the increase in serum lipids may be responsible for both structural and functional abnormalities of the vascular system in hypertensive patients. In contrast, recent reports have suggested that alpha 1-adrenergic receptor inhibition, useful in hypertension therapy, may exert a beneficial effect on plasma lipids. We have also collected preliminary data in our laboratory examining the effects of alpha 1-adrenergic receptor inhibition with prazosin on plasma cholesterol levels and vascular reactivity in monkeys with hypercholesterolemia. We observed large reductions in both total cholesterol and the very-low-density lipoprotein (VLDL) + low-density lipoprotein (LDL) fraction of cholesterol in these animals during treatment with prazosin. Thus, in addition to its sympatholytic action on the vasculature, alpha 1-adrenergic receptor inhibition appears to exert a beneficial effect in reducing total cholesterol levels.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001161:Arteriosclerosis / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000503:physiopathology*; D008055:Lipids / Q000097:blood
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D008055:Lipids