Isoproterenol Inhibition of Potassium Release from Rat Parotid Gland

Abstract

The mechanism of isoproterenol-induced inhibition of potassium release from rat parotid slices has been determined. Spontaneous potassium release from the slices was significantly inhibited by isoproterenol at concentrations above 10^-6 M. This isoproterenol effect was completely abolished in the presence of propranolol (10^-5M) and ouabain (10^-3 M) and was abolished during Na⁺-exclusion from the incubation medium. Isoproterenol caused an enhancement of the microsomal Na⁺, K⁺-ATPase activity at concentrations above 10^-5 M, and this activity was inhibited by propranolol (10^-5 M). The stimulatory effect of isoproterenol on the Na⁺, K⁺-ATPase exhibited a strong correlation with the inhibition of potassium release on each dose of isoproterenol. Moreover, dibutyryl cyclic AMP at concentrations above 10^-4 M inhibited potassium release in a dose-dependent manner and cyclic AMP caused an enhancement of the microsomal Na⁺, K⁺-ATPase activity. These results suggest that the inhibitory effect of isoproterenol on potassium release is clearly derived from the elevated Na⁺, K⁺-ATPase activity and that it may in part be mediated by cyclic AMP.