To determine if pancreatic sympathetic nerves can contribute to increased glucagon secretion during hypoglycemia, plasma glucagon and pancreatic glucagon secretion in situ were measured before and during insulin-induced hypoglycemia in three groups of halothane-anesthetized dogs. All dogs were bilaterally vagotomized to eliminate the input from pancreatic parasympathetic nerves. One group of dogs received only vagotomy (VAGX). A second group was vagotomized and adrenalectomized (VAGX + ADX). A third group received vagotomy, adrenalectomy, plus surgical denervation of the pancreas (VAGX + ADX + NERVX) to prevent activation of pancreatic sympathetic nerves. In dogs with VAGX only, hypoglycemia increased plasma epinephrine (Epi), pancreatic norepinephrine (NE) output (+320 ± 140 pg/min, P < 0.05), arterial plasma glucagon (+28 ± 12 pg/ml, P < 0.01), and pancreatic glucagon output (+ 1,470 ± 370 pg/min, P < 0.01). The addition of ADX eliminated the increase of Epi but did not increase pancreatic NE output (+370 ± 190 pg/min P < 0.025), arterial plasma glucagon (+20 ± 5 pg/ml, P < 0.01), or pancreatic glucagon output (+ 810 ± 200 pg/min, P < 0.01). In contrast, the addition of pancreatic denervation eliminated the increase of pancreatic NE output (-20 ± 40 pg/min, P < 0.05 vs. VAGX), the arterial glucagon (+ 1 ± 2 pg/ml, P < 0.01 vs. VAGX), and pancreatic glucagon output responses (+210 ± 280 pg/min, P < 0.025 vs. VAGX) to hypoglycemia. Thus activation of pancreatic sympathetic nerves can contribute to the increased glucagon secretion during severe insulin-induced hypoglycemia in dogs.
|Original language||English (US)|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|Issue number||1 33-1|
|State||Published - 1996|
- pancreatic denervation
ASJC Scopus subject areas
- Physiology (medical)