Involvement of uptake1 and uptake2 in terminating the cardiovascular activity of noradrenaline in normotensive and genetically hypertensive rats.

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Abstract
In pithed, pancuronium-treated rats, inhibition of Uptake1 with desmethylimipramine (2.5 mg/kg i.v.) increased the time course of the pressor response to vasomotor nerve stimulation (1 and 5 Hz for 5 s) but not the time course of the pressor response to injected noradrenaline (norepinephrine) (10 and 50 ng i.v.). Subsequent inhibition of Uptake2 with metanephrine (3 mg/kg, i.v.) did not affect the time course of responses to either vasomotor nerve stimulation or injected noradrenaline. Uptake1 but not Uptake2 is important in terminating the activity of noradrenaline released from rat vasomotor nerves and neither process inactivates intraluminal catecholamine. Chronotropic responses of rat atria to adrenergic nerve stimulation were prolonged by blockade of both Uptake1 and Uptake2, in agreement with previous evidence for involvement of both processes in terminating sino-atrial adrenergic responses. Animals from the Otago strain of genetically hypertensive animals were identical to normotensives in their vascular handling of catecholamine but lacked an atrial Uptake2 process. This defect may be related to the high resting heart rate and abnormal cardiac catecholamine turnover observed to exist in the Otago hypertensive rats.