Isoproterenol inhibition of potassium release from rat parotid gland.

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(-5) M) 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.