Neurogenic mechanisms initiating essential hypertension.
Evidence for increased sympathetic drive, as assessed both by measurements of plasma norepinephrine and by studies of tritiated norepinephrine kinetics, is most frequently obtained in young hypertensive patients. During the initial phases of hypertension, the increased sympathetic drive may persistently elevate arterial pressure through effects on the heart, the blood vessels, and the kidneys. In some patients, signs of a hyperkinetic circulation--including elevated heart rate and, less often, high cardiac output--predominate. In others, elevated vascular resistance, reflecting increased alpha-adrenergic tone, is the principal hemodynamic aberration. Even in patients with high cardiac output, a relative increase of vascular alpha-adrenergic tone accounts for their higher blood pressure. Increased sympathetic drive to the kidneys diminishes the efficiency of pressure diuresis, which is designed to restore normal arterial pressure. Although increased plasma norepinephrine levels are not consistently observed among older hypertensive patients compared with age-matched controls, neurogenic hypertension is not only a temporary event. In fact, tachycardia, which is neutrogenically mediated, doubles the risk of sustained hypertension later in life. The precise sequence of events in the transition from a principally neurogenic hypertension early in life to a predominantly nonneurogenic hypertension later in life is not known, although it likely includes decreased beta-receptor sensitivity with consequently reduced tachycardia and beta-mediated vasodilation. Functional diminution in endothelium-dependent vasodilation may augment sensitivity to vasoconstrictors such as norepinephrine and serotonin. Moreover, structural vascular changes nonspecifically enhance vascular reactivity to all vasoactive compounds and may provide a more permanent basis for altered pressure diuresis. Thus, hypertension initiated predominantly by neurogenic mechanisms could be sustained later without excessive sympathetic drive.
Egan
B M
BM
Department of Internal Medicine, Medical College of Wisconsin, Milwaukee.
D000818:Animals; D001696:Biomechanical Phenomena; D002319:Cardiovascular System / Q000473:pathology; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008955:Models, Cardiovascular; D008959:Models, Neurological; D009424:Nervous System Physiological Phenomena; D009638:Norepinephrine / Q000097:blood; D011941:Receptors, Adrenergic / Q000502:physiology
D011941:Receptors, Adrenergic; D009638:Norepinephrine