Effect of epinephrine on 86Rb efflux, 45Ca outflow and insulin release from pancreatic islets perifused in the presence of propranolol.

Abstract

Pancreatic islets prelabelled with either 86Rb or 45Ca were perifused in the presence of propranolol (0.1 microM) and, when required, exposed to epinephrine (0.1 microM). In the absence of D-glucose, epinephrine failed to cause any obvious change in either 86Rb or 45Ca outflow. In the presence of 16.7 mM D-glucose, however, epinephrine lowered both 86Rb and 45Ca outflow, this coinciding with suppression of insulin release. Epinephrine also suppressed the increment in 86Rb outflow evoked by a rise in glucose-concentration from 8.3 to 16.7 mM. Epinephrine did not abolish the early fall in 45Ca efflux evoked by the administration of D-glucose (16.7 mM) to islets previously deprived of the hexose but, within the same experiments, impaired the secondary rise in effluent radioactivity. Likewise, epinephrine prevented the increase in 45Ca outflow provoked by a rise in hexose concentration from 8.3 to 16.7 mM. These findings are compatible with the recent proposal that epinephrine interferes with the entry of Ca2+ into the B-cell, as mediated by voltage-sensitive Ca2+ channels, but do not rule out a multifactorial coupling between the occupancy of alpha 2-adrenergic receptors and the eventual inhibition of insulin release.