Effect of Epinephrine on ⁸⁶Rb Efflux, ⁴⁵Ca Outflow and Insulin Release from Pancreatic Islets Perifused in the Presence of Propranolol

Summary

Pancreatic islets prelabelled with either ⁸⁶Rb or ⁴⁵Ca were perifused in the presence of propranolol (0.1 μM) and, when required, exposed to epinephrine (0.1 μM). 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 α₂ adrenergic receptors and the eventual inhibition of insulin release.

Key words

Epinephrine - Insulin - ⁴⁵Ca²⁺ and ⁸⁶Rb⁺ Fluxes - Pancreatic Islets