Insulin-Induced Hypoglycemia in Conscious Dogs: Effect of Maintaining Carotid Arterial Glucose Levels on the Adrenocorticotropin, Epinephrine, and Vasopressin Responses*

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Abstract
The purpose of this study was to determine the role of central hypoglycemia in the regulation of the ACTH, vasopressin, and epinephrine responses to insulin administration. In each of six conscious dogs with carotid loops, saline or glucose was infused into both carotid arteries following the injection of 0.025,0.10, or 0.50 U insulin/kg. Intracarotid glucose infusion prevented a fall in superior vena caval glucose concentrations, despite peripheral hypoglycemia as measured by inferior vena caval (IVC) glucose concentrations. Intracarotid glucose infusions attenuated the ACTH and epinephrine responses to hypoglycemia. The logarithm of the peak plasma ACTH concentrations was related to the logarithm of the nadir in the IVC glucose concentrations during both intracarotid saline and glucose infusions, but intracarotid glucose infusions reduced the magnitude of the peak ACTH response for a given nadir in glucose by an average of 65%. The ACTH responses over the 40- to 60-min experimental periods for moderate or large IVC glucose responses were reduced by intracarotid glucose infusion. The intracarotid infusion of glucose also reduced the magnitude of the epinephrine response for a given IVC plasma glucose response; the effect was greatest at lowest glucose concentrations. The total ACTH and epinephrine responses were significantly related to both IVC and superior vena caval plasma glucose responses during glucose and saline infusions. The increases in plasma vasopressin and plasma Na+ were reduced by infusion of glucose into the carotids, but the relation between plasma Na+ and plasma vasopressin responses was not altered. We conclude that: 1) some of the glucose receptors that mediate the ACTH responses to hypoglycemia are within the region perfused by the carotid arterial circulation; 2) most of the glucose receptors that mediate the epinephrine response to severe hypoglycemia are also within this region; however, glucose receptors in this region are relatively unimportant in mediating the response to mild hypoglycemia; and 3) the rise in vasopressin during hypoglycemia is probably mediated primarily by osmoreceptors that sense the rise in plasma Na+ after the injection of insulin.