Effect of electrical field stimulation on insulin and glucagon secretion from the pancreas of normal and diabetic rats

The effect of electrical field stimulation (EFS) on insulin (INS) and gluca gon (GLU) secretion from normal and diabetic rat pancreas is poorly underst ood. In our study, EFS (5 - 20 Hz, 50 V amplitude and 1.0 ms pulse width), when applied alone, resulted in a significant (p < 0.05) increase in INS se cretion from the pancreas of both normal and diabetic rats. Atropine (10(-5 ) M) did not inhibit the EFS (5 Hz)-evoked INS secretion in normal pancreas and failed to alter the effect of EFS (10-20 Hz) on INS secretion from the pancreas of both normal and diabetic rats. Propranolol (Prop) inhibited IN S secretion to below basal level in the presence of EFS (5 Hz) but not at E FS (10-20 Hz). Tetrodotoxin (TTX) also significantly (p = 0.002) inhibited INS secretion from normal pancreas in the presence of EFS (5-20 Hz). The de crease in insulin secretion observed when pancreatic tissue fragments were incubated in Prop and TTX in the presence of EFS was reversed by yohimbine (10-5 M). In contrast, TTX did not significantly modify INS secretion from diabetic pancreas in the presence of EFS. EFS (5-20 Hz) significantly (p < 0.05) increased GLU release from normal and diabetic rat pancreas when appl ied alone. Neither atropine, Prop nor TTX significantly modified GLU releas e from the pancreas of either normal or diabetic rats. This suggests that G LU secretion may be controlled through a different pathway. The EFS-evoked INS and GLU secretion is probably executed via different mechanisms. These mechanisms include 1) activation of cholinergic nerves by EFS; 2) EFS of al pha- and beta -adrenergic nerves; 3) activation of non-adrenergic non-choli nergic pathway by EFS; 4) EFS-induced depolarization and subsequent action potential in pancreatic endocrine cells and 5) electroporosity caused by EF S-induced membrane permeability. All of these effects may be summative. In conclusion, EFS (5-20 Hz), when applied alone, can evoke significant increa ses in INS and GLU secretion from the pancreas of both normal and diabetic rats. insulin secretion is controlled via alpha-2 adrenergic (inhibition) a nd beta-adrenergic (stimulation) receptors. Glucagon secretion is enhanced by alpha2 adrenergic stimulation.