The Effects of Epinephrine on Norepinephrine Release in Essential Hypertension

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 7; no. 2; pp. 187 - 195
• Main Authors: NEZU, MITSUHIRO, MIURA, YUKIO, ADACHI, MAKI, ADACHI, MICHIKO, KIMURA, SHINOBU, TORIYABE, SHUNICHI, ISHIZUKA, YUKI, OHASHI, HIROFUMI, SUGAWARA, TAKASHI, TAKAHASHI, MASAKI, NOSHIRO, TAKAO, YOSHINAGA, KAORU
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01-03-1985; Hagerstown, MD Lippincott
• Subjects: Adolescent; Adult; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - drug effects; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Epinephrine - blood; Epinephrine - pharmacology; Epinephrine - physiology; Female; Glucagon - pharmacology; Humans; Hypertension - blood; Hypertension - drug therapy; Male; Medical sciences; Middle Aged; Norepinephrine - blood; Norepinephrine - metabolism; Propranolol - pharmacology; Pulse - drug effects; Random Allocation; Epinephrine; Hypertension; Norepinephrine; Catecholamine; Essential; Aminoacid derivative hormone
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.7.2.187

The effects of endogenous epinephrine (E), released by glucagon injection, and exogenously infused E on plasma norepinephrine (NE) and cardiovascular responses before and after [3-blockade were studied in patients with essential hypertension and in age-matched normotensive controls. The resting plasma NE and E levels were significantly higher in the borderline hypertensive subjects (NE251 ± 21 pg/ml [SEM], p < 0.005; E57 ± 5, p < 0.05, n = 18) than in controls (NE129 ± 12; E39 ± 5, n = 18). An intravenous injection of glucagon (1.0 nig) induced a transient rise of both plasma catecholamine levels and blood pressure in every subject studied. Plasma E levels rose transiently and returned to the basal levels by 20 minutes after the injection, whereas plasma NE levels showed a more prolonged rise over 20 minutes. β-Blockade with propranolol did not affect the plasma E response to glucagon, but inhibited the prolonged rise of plasma NE levels. An intravenous infusion of exogenous E (1.25–1.50 μg/min) for 30 minutes caused an apparent rise of both plasma NE levels and blood pressure, which lasted more than 60 minutes after stopping the E infusion. Propranolol did not affect the time course of plasma E but again inhibited the prolonged rise of both plasma NE levels and blood pressure. No significant differences could be observed in the cardiovascular or plasma NE responses to glucagon or to E infusion between normal and hypertensive subjects. These findings lend support to the view that plasma E can act physiologically as a sustained stimulator of presynaptic β-adrenergic receptors, which leads to an enhanced NE release from peripheral sympathetic nerve terminals and a rise of blood pressure in humans.