Effects of KCl on 45Ca uptake and efflux in the rat vas deferens

Abstract

The effects of KCl 160 mM on 45Ca uptake and efflux in the rat isolated vas deferens were investigated using a modification of the lanthanum method and a superfusion system respectively. In the prostatic half, basal cellular 45Ca uptake was 679 +/- 21 nmol g-1 tissue wet weight and KCl 160 mM increased this by 155%. In the epididymal half, basal cellular 45Ca uptake was 730 +/- 28 nmol 45Ca g-1 and KCl 160 mM increased this by 46%. Verapamil 2.04 microM or nifedipine 0.29 microM had no or little effect on basal 45Ca efflux or on basal 45Ca uptake. The KCl-induced increase in 45Ca uptake in both halves was inhibited by verapamil 2.04 microM or nifedipine 0.29 microM, concentrations which markedly reduce the contractile response. It is concluded that high K+ contracts the rat vas deferens by stimulation of the entry of extracellular Ca2+ to the intracellular compartment. KCl 160 mM produced a large, rapid and reversible increase in the rate of 45Ca efflux into Ca2+-containing and Ca2+-free Krebs-Henseleit solutions, which was not inhibited by verapamil 2.04 microM, nifedipine 0.29 microM or nitroprusside 1,678 microM. The relative size of the slow component of 45Ca efflux was larger in the prostatic half compared to the epididymal half of bisected tissues, suggesting that the postulated high affinity binding sites are predominant in this region. However, the rates of the fast and slow components of 45Ca efflux from prostatic and epididymal halves were identical. KCl 160 mM produced a similar increase in 45Ca efflux in prostatic and epididymal halves.