Study of noradrenaline uptake and spillover to plasma in normal subjects and patients with essential hypertension.
Noradrenaline uptake was studied in normal subjects, and in patients with essential hypertension. Uptake of noradrenaline by blood platelets was low-affinity in type. Platelets do not provide a satisfactory in vitro model of neuronal noradrenaline uptake. Study of disappearance of tritiated noradrenaline from the circulation was more helpful. Plasma disappearance was biexponential. The rapid removal component was slowed if neuronal noradrenaline uptake was reduced, either by desipramine in normal subjects, or in patients with idiopathic peripheral autonomic insufficiency, who have sympathetic nerve dysfunction. The t1 1/2 similarly was prolonged in a proportion of patients with essential hypertension, providing presumptive evidence of a defect in neuronal noradrenaline uptake. Spillover of endogenous noradrenaline to plasma, of transmitter escaping uptake after release, and plasma noradrenaline concentration, were increased in these patients. 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.
D001693:Biological Transport, Active; D001792:Blood Platelets / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D006207:Half-Life; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007700:Kinetics; D009474:Neurons / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D012016:Reference Values
D009638:Norepinephrine