TY - JOUR
T1 - Autonomic nervous system mediation of the pancreatic polypeptide response to insulin-induced hypoglycemia in conscious rats
AU - Havel, Peter J
AU - Parry, Susan J.
AU - Curry, Donald L.
AU - Stern, Judith S.
AU - Akpan, Jones O.
AU - Gingerich, Ronald L.
PY - 1992/4
Y1 - 1992/4
N2 - To investigate the neural regulation of pancreatic polypeptide (PP) secretion during hypoglycemia in the rat, insulin was administered to chronically cannulated rats, and plasma PP responses were compared between saline-treated animals and animals pretreated with a ganglionic blocking agent (hexamethonium), a muscarinic antagonist (atropine), combined α- and β-adrenergic receptor blockade (propranolol + tolazoline), or combined adrenergic blockade + atropine. PP was measured using a new RIA which selectively detects PP in rat plasma. In control rats (n = 10), plasma PP increased from a baseline level of 30 ± 3 pg/ml to 271 ± 41 pg/ml during hypoglycemia (plasma glucose = 29 ± 2 mg/dl) (ΔPP = +241 ± 42 pg/ml, P < 0.0005), demonstrating that in rats, as in other species, insulin-induced hypoglycemic is a potent stimulus for PP release. PP only increased by 31 ± 10 pg/ml during similar hypoglycemia in 7 hexamethonium-treated rats (P < 0.01 vs. control animals). Thus, at least 90% of the PP response to hypoglycemic is neurally mediated. The plasma PP response to hypoglycemic was +85 ± 24 pg/ml in atropine-treated rats (P 0.01 vs. control rats), suggesting that approximately 65% of the PP response is mediated via muscarinic acetylcholine receptors on the islet F cell. The PP response to hypoglycemia in rats with combined adrenergic blockade (Δ = +168 ± 32 pg/ml) was slightly, but not significantly smaller than that in control rats. The combination of combined blockade + atropine resulted in a PP response (Δ = +26 ± 7 pg/ml) to hypoglycemia that was similar to that in hexamethonium-treated rats (P < 0.01 vs. control rats). These results suggest: 1) The PP response to hypoglycemia is predominetely the result of muscarinic, cholinergic activation. 2) There is a minor adrenergic contribution to the response. 3) The plasma PP response mey be useful as an index of autonomic neural input to the islet during hypoglycemia.
AB - To investigate the neural regulation of pancreatic polypeptide (PP) secretion during hypoglycemia in the rat, insulin was administered to chronically cannulated rats, and plasma PP responses were compared between saline-treated animals and animals pretreated with a ganglionic blocking agent (hexamethonium), a muscarinic antagonist (atropine), combined α- and β-adrenergic receptor blockade (propranolol + tolazoline), or combined adrenergic blockade + atropine. PP was measured using a new RIA which selectively detects PP in rat plasma. In control rats (n = 10), plasma PP increased from a baseline level of 30 ± 3 pg/ml to 271 ± 41 pg/ml during hypoglycemia (plasma glucose = 29 ± 2 mg/dl) (ΔPP = +241 ± 42 pg/ml, P < 0.0005), demonstrating that in rats, as in other species, insulin-induced hypoglycemic is a potent stimulus for PP release. PP only increased by 31 ± 10 pg/ml during similar hypoglycemia in 7 hexamethonium-treated rats (P < 0.01 vs. control animals). Thus, at least 90% of the PP response to hypoglycemic is neurally mediated. The plasma PP response to hypoglycemic was +85 ± 24 pg/ml in atropine-treated rats (P 0.01 vs. control rats), suggesting that approximately 65% of the PP response is mediated via muscarinic acetylcholine receptors on the islet F cell. The PP response to hypoglycemia in rats with combined adrenergic blockade (Δ = +168 ± 32 pg/ml) was slightly, but not significantly smaller than that in control rats. The combination of combined blockade + atropine resulted in a PP response (Δ = +26 ± 7 pg/ml) to hypoglycemia that was similar to that in hexamethonium-treated rats (P < 0.01 vs. control rats). These results suggest: 1) The PP response to hypoglycemia is predominetely the result of muscarinic, cholinergic activation. 2) There is a minor adrenergic contribution to the response. 3) The plasma PP response mey be useful as an index of autonomic neural input to the islet during hypoglycemia.
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M3 - Article
C2 - 1347741
AN - SCOPUS:0026603541
VL - 130
SP - 2225
EP - 2229
JO - Endocrinology
JF - Endocrinology
SN - 0013-7227
IS - 4
ER -