Sympathetic hyperactivity in early stages of hypertension: the Ann Arbor data set

Patients with borderline hypertension frequently have a hyperkinetic circulation that is neurogenic and can be normalized with autonomic blockade of the heart. The abnormality is of central nervous system origin and due to increased sympathetic stimulation and decreased vagal inhibition of the heart. A subset of patients characterized by high plasma renin and norepinephrine values clearly has a neurogenic hypertension since their blood pressure becomes normal after cardiac blockade and vascular alpha-adrenergic blockade. Since many patients with borderline hypertension have a high cardiac output, and the majority of patients with more advanced hypertension have increased vascular resistance, two questions arise. Is the "hyperkinetic state" a special condition unrelated to established hypertension or is there, in the course of hypertension, a transition from "high output" to "high resistance" state? The literature strongly suggests that patients with hyperkinetic borderline hypertension later proceed to develop the established high resistance form of hypertension. The most likely mechanism for this transition is a change in cardiac and vascular responsiveness due to prolonged excess sympathetic stimulation combined with structural pressure-induced changes in these organs. This analysis of the events in the course of hypertension is of necessity based on an arbitrary definition of the hyperkinetic state usually set at a cardiac index at least two standard deviations above the normal mean. A bivariate analysis of our data (268 normotensive and 186 patients with borderline hypertension) suggests that there indeed are two different populations in this data set. Based on this commingling analysis, the occurrence of a hyperkinetic state was five-fold as frequent in patients with borderline hypertension than in the normotensive population.(ABSTRACT TRUNCATED AT 250 WORDS)