Calcium channel blockers enhance extrarenal potassium disposal in the rat

A. Sugarman, T. Kahn

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

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·kg-1·h-1 for 60 min) alone or in combination with either verapamil or nifedipine. The increment in plasma potassium concentration during the potassium infusion (ΔP(K)) with either verapamil or nifedipine was less than control (P < 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. ΔP(K) with ADX was higher than control (P < 0.01). Verapamil or nifedipine with ADX resulted in a lower ΔP(K) than ADX alone (P < 0.05). Further studies were then conducted with the selective β2-adrenergic blocker butoxamine hydrochloride to rule out enhanced peripheral sympathetic activity of the β2-adrenergic system in facilitating the potassium disposal. ΔP(K) with butoxamine was greater than control (P < 0.01) but not significantly different from ADX. Verapamil or nifedipine in conjuction with butoxamine resulted in a lower ΔP(K) than butoxamine alone (P < 0.01). Changes in arterial pH and plasma bicarbonate were similar in all groups. In conclusion, during potassium infusion the ΔP(K) 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.

Original languageEnglish
Pages (from-to)F695-F701
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume250
Issue number4 (19/4)
DOIs
StatePublished - 1986
Externally publishedYes

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