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ASSESSMENT OF NEURONAL UPTAKE OF NORADRENALINE IN HUMANS: DEFECTIVE UPTAKE IN SOME PATIENTS WITH ESSENTIAL HYPERTENSION
Author(s) -
Esler Murray,
Leonard Paul,
Kelleher Dianne,
Jackman Graham,
Bobik Alex,
Skews Helen,
Jennings Garry,
Korner Paul
Publication year - 1980
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1980.tb00106.x
Subject(s) - desipramine , medicine , adrenergic , endocrinology , endogeny , norepinephrine , pathogenesis , essential hypertension , adrenergic receptor , receptor , chemistry , dopamine , blood pressure , hippocampus , antidepressant
SUMMARY 1. Disappearance of tritiated noradrenaline from plasma, after infusion to steady‐state, was studied to assess neuronal uptake of noradrenaline in essential hypertension. 2. Plasma tritiated noradrenaline disappearance was biexponential. Rapid removal was dependent on neuronal uptake, being slowed both in normal subjects after desipramine, and in patients with sympathetic nerve dysfunction (autonomic insufficiency). 3. In nine of thirty‐eight hypertensive patients the t1½ similarly was prolonged. Endogenous noradrenaline escaping uptake after release, and spilling over into plasma, was increased in these patients. 4. Defective neuronal uptake of noradrenaline, by exposing adrenergic receptors to high local transmitter concentration, may be important in the pathogenesis of essential hypertension in some patients.