Cerasola G, Cottone S, D'Ignoto G, Grasso L, Contorno A, Carone M B, Fulantelli M A
Institute of Internal Medicine, University of Palermo, Italy.
J Clin Hypertens. 1987 Dec;3(4):670-80.
Recently, it has been showed that Epinephrine (E) plays an important role in the pathogenesis of essential hypertension in rats. Furthermore, some literature data demonstrated the existence of high E plasma levels at rest and after stress in essential hypertension. To evaluate the sympatho-adrenal activity, both in basal condition and after stress, and its relationship with the renin-angiotensin-aldosterone (RAA) system, 31 borderline hypertensives (BH), 30 essential hypertensives (EH), and 15 healthy subjects were studied. After a wash-out period and electrolyte evaluation, all subjects were studied at rest, during dynamic exercise, and after 30 minutes of recovery; at the same time blood pressure and heart rate were automatically recorded and blood samples were collected for plasma renin activity (PRA), E, Norepinephrine (NE) and aldosterone plasma concentrations assay. BH showed a percentage increase of mean blood pressure greater than EH (p less than 0.01) during dynamic exercise. PRA showed no significant differences between the 3 groups examined at rest; on the contrary, PRA levels and the percentage increases were significantly higher in BH than in EH (p less than 0.05 respectively). E plasma levels and its percentage increases were significantly greater in BH than both in EH (p less than 0.05) and in controls after exercise. Furthermore, raised E plasma levels lasted significantly throughout the recovery period (p less than 0.05) only in BH. A significant correlation between both E plasma levels and percentage increases with NE percentage increases was observed after exercise in BH. Our results demonstrate a sympatho-adrenal overactivity in borderline hypertension, which is characterized by a prolonged E hyper-responsiveness, a renin hyper-secretion and a high hemodynamic response to stress. In borderline hypertension, E, excessively released from the adrenal gland, may act as a sympathetic cotransmitter inducing functional adrenoceptors hyperactivity.
