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

The effects of beta-agonists (epinephrine, isoproterenol, and ITP) and beta-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 beta-adrenergic agonists or antagonists was added to the perfusion medium. Following epinephrine, a combined beta 1- and beta 2-agonist, urinary potassium excretion (UKV; 0.55 +/- 0.55 vs. 0.36 +/- 0.04 mueq/min, P less than 0.001) and fractional excretion of potassium (FEK; 24.6 +/- 2.4 vs. 18.2 +/- 2.0%, P less than 0.001) both decreased. When isoproterenol, a nonspecific beta-agonist, was added to the perfusate, UKV (0.49 +/- 0.10 vs. 0.27 +/- 0.04 mueq/min, P less than 0.02) and FEK (29.0 +/- 5.2 vs. 16.3 +/- 2.9%, P less than 0.01) again decreased. ITP, a specific beta 1-agonist also caused a decrease in UKV (0.60 +/- 0.13 vs. 0.39 +/- 0.04 mueq/min, P less than 0.02) and FEK (30.2 +/- 5.1 vs. 17.8 +/- 2.8%, P less than 0.02). In contrast, when propranolol, a nonspecific beta-antagonist, was added to the perfusate, the opposite effects on renal potassium handling were observed. UKV (0.45 +/- 0.05 vs. 0.70 +/- 0.07 mueq/min, P less than 0.001) and FEK (23.0 +/- 2.1 vs. 42.5 +/- 3.1%, P less than 0.001) both increased. Metoprolol (50 ng/ml), a specific beta 1-antagonist, increased UKV (0.56 +/- 0.10 vs. 0.68 +/- 0.15 mueq/min, P less than 0.02) and FEK (31.0 +/- 3.8 vs. 48.0 +/- 7.1%, P less than 0.02). A similar effect was observed when a higher dose of metoprolol (200 ng/ml) was employed.(ABSTRACT TRUNCATED AT 250 WORDS)