In rats, chronic ganglionic blockade induced by repeated doses of chlorisodamine rapidly and profoundly lowered plasma norepinephrine, but plasma dopamine-beta-hydroxylase (DBH) activity, even after 5 days treatment, was not significantly reduced. Long-term chlorisondamine treatment did not alter cardiac DBH or rapid axonal transport of DBH in sciatic nerve. Blockade of alpha adrenergic receptors by administration of repeated doses of phenoxybenzamine resulted in elevated levels of plasma catecholamines, but produced no change in plasma DBH. Chronic reserpine treatment (2.5 mg/kg on alternate days) increased plasma DBH after 2 and 5 days, whereas vinblastine (3 mg/kg) caused a progressive fall in enzyme activity in plasma over the same time period. It is concluded that plasma DBH activity does not closely parallel adrenergic function and neurotransmitter release in the rat. The level of DBH in plasma appears to reflect the rate of enzyme synthesis and axonal transport, It is likely that mechanisms other than stimulation-coupled exocytotic release determine levels of DBH activity in plasma.
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