Abstract
Summary and conclusions
Dogs were given d,1-propranolol before and after thoracic inferior vena cava constriction (TIVCC) or renal artery constriction (RAC) to determine if the increase in plasma renin activity (PRA) and associated biological activity could be suppressed. Oral propranolol administration (240 mg twice daily) was begun at least 2 days prior to TIVCC in six dogs; heart rate was reduced from 133 to 95 beats/min but PRA did not change with propranolol administration. After TIVCC and during continued propranolol administration, daily renal sodium excretion fell from an average value of 50 to less than 3 mEq sodium/day and PRA was elevated two- to fourfold. With prolonged propranolol adminstration during TIVCC, PRA returned toward normal levels but renal sodium excretion remained low. At this time, hourly measurements of sodium excretion showed no change after a 240-mg oral dose of propranolol although very high plasma levels of propranolol were achieved; also, PRA was unchanged and low. The effects of RAC were studied before and during an intravenous propranolol infusion (0.2 mg/kg/hour) in conscious animals. Before propranolol administration, arterial pressure increased during RAC from 120 to 136 mm Hg and PRA doubled. Propranolol infusion lowered heart rate from 110 to 84 beats/min, but arterial pressure and PRA were not attenuated by propranolol during RAC. The data indicate that non-beta-adrenergic mechanisms are involved in renin release during TIVCC and RAC.
The authors wish to thank Mr. Henry L. LeMien, Jr., of Ayerst Laboratories for the supply of propranolol and for help in the analysis of plasma propranolol.
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