Hypertension, Vol 7, 187-195, Copyright © 1985 by American Heart Association
M Nezu, Y Miura, M Adachi, M Adachi, S Kimura, S Toriyabe, Y Ishizuka, H Ohashi, T Sugawara and M Takahashi
The effects of endogenous epinephrine (E), released by glucagon injection,
and exogenously infused E on plasma norepinephrine (NE) and cardiovascular
responses before and after beta-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 (NE: 251 +/- 21 pg/ml [SEM], p less than 0.005; E: 57
+/- 5, p less than 0.05, n = 18) than in controls (NE: 129 +/- 12; E: 39
+/- 5, n = 18). An intravenous injection of glucagon (1.0 mg) 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. beta-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 micrograms/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 beta-adrenergic receptors, which leads to an enhanced NE
release from peripheral sympathetic nerve terminals and a rise of blood
pressure in humans.
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The effects of epinephrine on norepinephrine release in essential hypertension
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