Corelease of galanin and NE from pancreatic sympathetic nerves during severe hypoglycemia in dogs

Peter J Havel, T. O. Mundinger, R. C. Veith, B. E. Dunning, G. J. Taborsky

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

To determine whether norepinephrine (NE) and galanin are coreleased during reflex activation of the sympathetic nervous system by hypoglycemia, we administered insulin to halothane-anesthetized (0.8%) dogs and measured the spillover of NE and galanin-like immunoreactivity (GLIR) into pancreatic venous plasma. Insulin injection produced hypoglycemia [plasma glucose (PG) = 34 ± 3 mg/dl] but did not activate pancreatic noradrenergic (Δpancreatic NE output = +20 ± 130 pg/min) or galaninergic nerves (ΔGLIR output = +40 ± 50 fmol/min). To determine whether more severe hypoglycemia would activate these nerves, insulin was administered to dogs infused with somatostatin (SS; 2.5 μg/min) to block the counterregulatory increase of glucagon secretion. SS reduced the glucagon response to hypoglycemia by >90%, which allowed PG to decrease to 14 ± 1 mg/dl. Pancreatic NE output increased by 470 ± 140 pg/min (P < 0.005); however, pancreatic GLIR output did not increase significantly (Δ = +70 ± 50 fmol/min). When SS was discontinued, pancreatic NE output increased by 490 ± 200 pg/min (P < 0.025), and GLIR output increased by an additional +160 ± 70 fmol/min (P < 0.025; total Δ from baseline = +230 ± 90 fmol/min, P < 0.025), suggesting that SS may restrain pancreatic NE and galanin release. Pancreatic NE and GLIR spillover were also increased during severe hypoglycemia when ganglionic neurotransmission was partially impaired with hexamethonium but not when the neural pathway was interrupted by spinal cord transection. We conclude that NE and galanin are coreleased from pancreatic sympathetic nerves when these nerves are centrally activated during severe hypoglycemia in halothane-anesthetized dogs.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume263
Issue number1 26-1
StatePublished - 1992

Fingerprint

Galanin
Hypoglycemia
Norepinephrine
Dogs
Halothane
Insulin
Glucagon
Plasmas
Glucose
Neural Pathways
Hexamethonium
Sympathetic Nervous System
Neurology
Somatostatin
Spinal Cord Injuries
Synaptic Transmission
Reflex
Chemical activation
Injections

Keywords

  • catecholamines
  • glucagon
  • halothane anesthesia
  • hexamethonium
  • neuroglucopenia
  • neuropeptide
  • norepinephrine
  • somatostatin
  • spinal cord transection
  • stress

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology

Cite this

Corelease of galanin and NE from pancreatic sympathetic nerves during severe hypoglycemia in dogs. / Havel, Peter J; Mundinger, T. O.; Veith, R. C.; Dunning, B. E.; Taborsky, G. J.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 263, No. 1 26-1, 1992.

Research output: Contribution to journalArticle

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abstract = "To determine whether norepinephrine (NE) and galanin are coreleased during reflex activation of the sympathetic nervous system by hypoglycemia, we administered insulin to halothane-anesthetized (0.8{\%}) dogs and measured the spillover of NE and galanin-like immunoreactivity (GLIR) into pancreatic venous plasma. Insulin injection produced hypoglycemia [plasma glucose (PG) = 34 ± 3 mg/dl] but did not activate pancreatic noradrenergic (Δpancreatic NE output = +20 ± 130 pg/min) or galaninergic nerves (ΔGLIR output = +40 ± 50 fmol/min). To determine whether more severe hypoglycemia would activate these nerves, insulin was administered to dogs infused with somatostatin (SS; 2.5 μg/min) to block the counterregulatory increase of glucagon secretion. SS reduced the glucagon response to hypoglycemia by >90{\%}, which allowed PG to decrease to 14 ± 1 mg/dl. Pancreatic NE output increased by 470 ± 140 pg/min (P < 0.005); however, pancreatic GLIR output did not increase significantly (Δ = +70 ± 50 fmol/min). When SS was discontinued, pancreatic NE output increased by 490 ± 200 pg/min (P < 0.025), and GLIR output increased by an additional +160 ± 70 fmol/min (P < 0.025; total Δ from baseline = +230 ± 90 fmol/min, P < 0.025), suggesting that SS may restrain pancreatic NE and galanin release. Pancreatic NE and GLIR spillover were also increased during severe hypoglycemia when ganglionic neurotransmission was partially impaired with hexamethonium but not when the neural pathway was interrupted by spinal cord transection. We conclude that NE and galanin are coreleased from pancreatic sympathetic nerves when these nerves are centrally activated during severe hypoglycemia in halothane-anesthetized dogs.",
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T1 - Corelease of galanin and NE from pancreatic sympathetic nerves during severe hypoglycemia in dogs

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AU - Mundinger, T. O.

AU - Veith, R. C.

AU - Dunning, B. E.

AU - Taborsky, G. J.

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N2 - To determine whether norepinephrine (NE) and galanin are coreleased during reflex activation of the sympathetic nervous system by hypoglycemia, we administered insulin to halothane-anesthetized (0.8%) dogs and measured the spillover of NE and galanin-like immunoreactivity (GLIR) into pancreatic venous plasma. Insulin injection produced hypoglycemia [plasma glucose (PG) = 34 ± 3 mg/dl] but did not activate pancreatic noradrenergic (Δpancreatic NE output = +20 ± 130 pg/min) or galaninergic nerves (ΔGLIR output = +40 ± 50 fmol/min). To determine whether more severe hypoglycemia would activate these nerves, insulin was administered to dogs infused with somatostatin (SS; 2.5 μg/min) to block the counterregulatory increase of glucagon secretion. SS reduced the glucagon response to hypoglycemia by >90%, which allowed PG to decrease to 14 ± 1 mg/dl. Pancreatic NE output increased by 470 ± 140 pg/min (P < 0.005); however, pancreatic GLIR output did not increase significantly (Δ = +70 ± 50 fmol/min). When SS was discontinued, pancreatic NE output increased by 490 ± 200 pg/min (P < 0.025), and GLIR output increased by an additional +160 ± 70 fmol/min (P < 0.025; total Δ from baseline = +230 ± 90 fmol/min, P < 0.025), suggesting that SS may restrain pancreatic NE and galanin release. Pancreatic NE and GLIR spillover were also increased during severe hypoglycemia when ganglionic neurotransmission was partially impaired with hexamethonium but not when the neural pathway was interrupted by spinal cord transection. We conclude that NE and galanin are coreleased from pancreatic sympathetic nerves when these nerves are centrally activated during severe hypoglycemia in halothane-anesthetized dogs.

AB - To determine whether norepinephrine (NE) and galanin are coreleased during reflex activation of the sympathetic nervous system by hypoglycemia, we administered insulin to halothane-anesthetized (0.8%) dogs and measured the spillover of NE and galanin-like immunoreactivity (GLIR) into pancreatic venous plasma. Insulin injection produced hypoglycemia [plasma glucose (PG) = 34 ± 3 mg/dl] but did not activate pancreatic noradrenergic (Δpancreatic NE output = +20 ± 130 pg/min) or galaninergic nerves (ΔGLIR output = +40 ± 50 fmol/min). To determine whether more severe hypoglycemia would activate these nerves, insulin was administered to dogs infused with somatostatin (SS; 2.5 μg/min) to block the counterregulatory increase of glucagon secretion. SS reduced the glucagon response to hypoglycemia by >90%, which allowed PG to decrease to 14 ± 1 mg/dl. Pancreatic NE output increased by 470 ± 140 pg/min (P < 0.005); however, pancreatic GLIR output did not increase significantly (Δ = +70 ± 50 fmol/min). When SS was discontinued, pancreatic NE output increased by 490 ± 200 pg/min (P < 0.025), and GLIR output increased by an additional +160 ± 70 fmol/min (P < 0.025; total Δ from baseline = +230 ± 90 fmol/min, P < 0.025), suggesting that SS may restrain pancreatic NE and galanin release. Pancreatic NE and GLIR spillover were also increased during severe hypoglycemia when ganglionic neurotransmission was partially impaired with hexamethonium but not when the neural pathway was interrupted by spinal cord transection. We conclude that NE and galanin are coreleased from pancreatic sympathetic nerves when these nerves are centrally activated during severe hypoglycemia in halothane-anesthetized dogs.

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KW - spinal cord transection

KW - stress

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