DURING hypoglycemic stress, glucagon secretion increases and insulin secretion decreases. The traditional view is that these changes are due to the effect of low circulating glucose levels acting directly on the pancreatic islet. In contrast, a number of studies suggest that these responses are due to activation of autonomic nervous system that accompanies hypoglycemia in vivo, a view that we favor. Although central nervous system and autonomic neural control of the endocrine pancreashas been reviewed before (1–4), this review will focus specifically on the autonomic activation produced by glucopenic stress and its potential contribution to the accompanying changes of glucagon and insulin secretion. The goal of this review is not to negate the traditional view that hypoglycemia has direct actions on the islet, but rather to suggest that the autonomic contribution may have been underestimated in a whole class of experiments because of unrecognized redundancy in the autonomic input to the islet.

The first section will review the supporting evidence that each of three autonomic inputs to the pancreas is activated during this stress. The three inputs are: 1) pancreatic parasympathetic nerves, 2) adrenal medullary epinephrine, and 3) pancreatic sympathetic nerves. The various techniques for measuring these autonomic inputs to the pancreas will be discussed, and the factors which influence the magnitude of the autonomic activation will be outlined.