Abstract
Chronic infusion of norepinephrine (NE) or epinephrine in rats by an Alzet osmotic minipump (0.1 mg/kg/hr s.c.) caused a 40 mm Hg increase in systolic blood pressure with no change in heart rate. The administration of chlorisondamine or bretylium, drugs which inhibit sympathetic neuronal function by blocking ganglia and by inhibiting release of neuronal NE, respectively, decreased systolic blood pressure to the same level in NE-infused and vehicle-infused rats whereas heart rate increased only in NE-infused animals. Infusion of NE or epinephrine resulted in a marked elevation in the plasma level of the infused amine and a smaller elevation of its counterpart. Chlorisondamine caused a 30 to 70% reduction in plasma levels of NE and epinephrine during the infusion of these catecholamines. Acute infusion of NE at a rate which caused a slow pressor response was accompanied by an elevation of impulse frequency in the preganglionic cervical sympathetic nerve. In contrast, a faster rate of NE infusion which produced a more rapid pressor response was accompanied by the classical decrease in impulse frequency. These studies demonstrate that the maintenance of elevated blood pressure during catecholamine infusion in rats is dependent upon a paradoxical increase in the activity of the sympathetic nervous system.
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