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Potassium Stimulation of Insulin Release by the Perfused Rat Pancreas

Department of Physiological Sciences, University of California Davis, California 95616

Abstract

The insulin release pattern in response to different concentrations of potassium (8, 12, 16 and 30 mEq/1) was determined using the perfused rat pancreas. A rapid burst of insulin secretion was observed during the first 2 min of potassium infusion, particularly in response to the higher potassium levels (16 and 30 mEq/1). This was followed by a rapid decline to almost basal levels which continued until the potassium infusion was terminated. This pattern of release indicates an actual secretory phenomenon and not an insulin leakage by damaged β cells. No burst of secretion was seen when the potassium concentration was slowly increased. This suggests that a rapid increase in the stimulant level is needed in order to produce rapid depolarization of the cell, which in turn may lead to the burst of insulin.

The role, of the adrenergic system in potassiuminduced insulin secretion was investigated. Isoproterenol, a predominantly β adrenergic agent, caused a marked decrease in potassium—induced insulin release. This attenuation was completely reversed by the presence of an —adrenergic blocking agent (phentolamine), thus suggesting that the isoproterenol inhibition probably occurred primarily via —adrenergic receptors. The action of the (β—adrenergic receptors was studied by infusing the (β—adrenergic blocking agent, propranolol, and observing its effect on potassium—induced insulin release. A marked decrease of insulin secretion was seen, but a substantial release of hormone still occurred. This indicates that even though the (β—adrenergic receptors may play a role in potassium— induced insulin secretion, they are not the sole mechanism by which potassium stimulates insulin release. (Endocrinology 92: 1126, 1973

Footnotes

¹ Present address: Universidad Central de Venezuela Facultad de Ciencias Veterinarias, Maracay (Edo. Aragua), Venezuela

² Dr. Donald L. Curry, Department of Physiological Sciences, University of California, Davis, California 95616.

Received August 9, 1972.

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