Effect of epinephrine on renal potassium excretion in the isolated perfused rat kidney

The effects of β-agonists (epinephrine, isoproterenol, and ITP) and β-antagonists (propranolol, metoprolol, and butoxamine) on renal potassium excretion were examined using the isolated perfused rat kidney preparation. Following 30 min of control perfusion, one of the above β-adrenergic agonists or antagonists was added to the perfusion medium. Following epinephrine, a combined β₁- and β₂-agonist, urinary potassium excretion (U(K)V; 0.55 ± 0.05 vs. 0.36 ± 0.04 μeq/min, P < 0.001) and fractional excretion of potassium (FE(K); 24.6 ± 2.4 vs. 18.2 ± 2.0%, P < 0.001) both decreased. When isoproterenol, a nonspecific β-agonist, was added to the perfusate, U(K)V (0.49 ± 0.10 vs. 0.27 ± 0.04 μeq/min, P < 0.02) and FE(K) (29.0 ± 5.2 vs. 16.3 ± 2.9%, P < 0.01) again decreased. ITP, a specific β₁-agonist also caused a decrease in U(K)V (0.60 ± 0.13 vs. 0.39 ± 0.04 μeq/min, P < 0.02) and FE(K) (30.2 ± 5.1 vs. 17.8 ± 2.8%, P < 0.02). In contrast, when propranolol, a nonspecific β-antagonist, was added to the perfusate, the opposite effect on renal potassium handling were observed. U(K)V (0.45 ± 0.05 vs. 0.70 ± 0.07 μeq/min, P < 0.001) and FE(K) (23.0 ± 2.1 vs. 42.5 ± 3.1%, P < 0.001) both increased. Metoprolol (50 ng/ml), a specific β₁-antagonist, increased U(K)V (0.56 ± 0.10 vs. 0.68 ± 0.15 μeq/min, P < 0.02) and FE(K) (31.0 ± 3.8 vs. 48.0 ± 7.1%, P < 0.02). A similar effect was observed when a higher dose of metoprolol (200 ng/ml) was employed. Butoxamine, a specific β₂-antagonist, when added at concentrations of 1 and 10 μg/ml, did not affect potassium excretion. These results indicate that, in the isolated perfused rat kidney preparation, epinephrine has a direct inhibitory effect on renal potassium excretion. The ability of isoproterenol to decrease U(K)V suggests that the effect of epinephrine is mediated via the β-adrenergic receptor. In contrast, propranolol, a nonspecific β-adrenergic blocker, enhances potassium excretion. The effect of propranolol can be mimicked by metoprolol, a β₁-antagonist, but not butoxamine, a β₂-antagonist. These data suggest that the effects of β-adrenergic blockade are mediated via the β₁-receptor.