Mechanism of Increased Sodium Reabsorption during Propranolol Administration

The mechanism of diminished sodium excretion induced by propranolol was investigated in the dog. Propranolol (0.3 to 5 mg/kg) was given intravenously in a bolus to 16 dogs, eight of which had the renal perfusion pressure controlled by a suprarenal aortic clamp. In another group of six dogs propranolol (0.1 to 5 , µg/kg/min) was infused into one renal artery for 45 min. Cardiac output (dye dilution), mean arterial and right atrial pressures, heart rate, renal clearances of inulin, creatinine, and para-aminohippurate, and sodium excretion were measured. Total peripheral resistance, central blood volume, stroke volume, renal plasma flow, renal blood flow, renal vascular resistance, glomerular filtration rate, and filtration fraction were calculated. Intravenous propranolol resulted in significant decreases in cardiac output (–25%) and heart rate (–14%) and increases in total peripheral resistance (28%) and renal vascular resistance (37%). Renal blood flow decreased by 25% and filtration fraction increased 21% as urinary sodium excretion diminished 36%. Glomerular filtration did not change significantly. Infusions of propranolol into one renal artery resulted in either no change in sodium excretion or bilateral changes; thus an intrarenal effect of the drug was not demonstrable. The data suggest that the changes in renal hemodynamics associated with propranolol administration are secondary to alterations in systemic hemodynamics, particularly a decrease in cardiac output. These alterations in renal hemodynamics, including an increase in renal vascular resistance and filtration fraction, most likely account for the decrease in sodium excretion rather than a direct effect of propranolol on sodium reabsorption.