Calcium channel blockers enhance extrarenal potassium disposal in the rat.

The effect of calcium channel blockers on the extrarenal disposition of an acute potassium load was examined in acutely nephrectomized rats infused with KCl (0.75 meq X kg-1 X h-1 for 60 min) alone or in combination with either verapamil or nifedipine. The increment in plasma potassium concentration during the potassium infusion (delta PK) with either verapamil or nifedipine was less than control (P less than 0.05 and 0.01, respectively). Studies were repeated in acutely adrenalectomized rats (ADX) to evaluate whether the changes in plasma potassium were consequent to the enhanced activity of epinephrine and other adrenal hormones. delta PK with ADX was higher than control (P less than 0.01). Verapamil or nifedipine with ADX resulted in a lower delta PK than ADX alone (P less than 0.05). Further studies were then conducted with the selective beta 2-adrenergic blocker butoxamine hydrochloride to rule out enhanced peripheral sympathetic activity of the beta 2-adrenergic system in facilitating the potassium disposal. delta PK with butoxamine was greater than control (P less than 0.01) but not significantly different from ADX. Verapamil or nifedipine in conjunction with butoxamine resulted in a lower delta PK than butoxamine alone (P less than 0.01). Changes in arterial pH and plasma bicarbonate were similar in all groups. In conclusion, during potassium infusion the delta PK is lower in the presence of calcium channel blockers. The alteration in potassium transport produced by calcium channel blockers does not appear to be dependent on adrenal function or peripheral sympathetic activity. Impaired calcium entry into cells may alter potassium transport in the intact animal.