Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system

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

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Abstract

To determine if acute stress activates pancreatic noradrenergic nerves, pancreatic norepinehrine (NE) output (spillover) was measured in halothane-anesthetized dogs. Central neuroglucopenia, induced by intravenous 2-deoxy-D-glucose ([2-DG] 600 mg/kg + 13.5 mg/kg-1 per min-1) increased pancreatic NE output from a baseline of 380 ± 100 to 1,490 ± 340 pg/min (Δ = 1,110 ± 290 pg/min, P < 0.01). Surgical denervation of the pancreas reduced this response by 90% (Δ = +120 ± 50 pg/min, P < 0.01 vs. intact innervation), suggesting that 2-DG activated pancreatic nerves by increasing the central sympathetic outflow to the pancreas rather than by actin directly on nerves within the pancreas itself. These experiments provide the first direct evidence of stress-induced activation of pancreatic noradrenergic nerves in vivo. In contrast, neither hemorrhagic hypotension (50 mmHg) nor hypoxia (6-8% O2) increased pancreatic NE output (Δ = +80 ± 110 and -20 ± 60 pg/min, respectively, P < 0.01 vs. neuroglucopenia) despite both producing increases of arterial plasma NE and epinephrine similar to glucopenia. The activation of pancreatic noradrenergic nerves is thus stress specific. Furthermore, because both glucopenia and hypotension increased arterial NE, yet only glucopenia activated pancreatic nerves, it is suggested that a regionally selective pattern of sympathetic activation can be elicited by acute stress, a condition in which sympathetic activation has traditionally been thought to be generalized and nondiscrete.

Original languageEnglish (US)
Pages (from-to)1538-1545
Number of pages8
JournalJournal of Clinical Investigation
Volume82
Issue number5
StatePublished - 1988
Externally publishedYes

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Sympathetic Nervous System
Hypotension
Pancreas
Deoxyglucose
Dogs
Denervation
Halothane
Epinephrine
Actins
Hypoxia

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system",
abstract = "To determine if acute stress activates pancreatic noradrenergic nerves, pancreatic norepinehrine (NE) output (spillover) was measured in halothane-anesthetized dogs. Central neuroglucopenia, induced by intravenous 2-deoxy-D-glucose ([2-DG] 600 mg/kg + 13.5 mg/kg-1 per min-1) increased pancreatic NE output from a baseline of 380 ± 100 to 1,490 ± 340 pg/min (Δ = 1,110 ± 290 pg/min, P < 0.01). Surgical denervation of the pancreas reduced this response by 90{\%} (Δ = +120 ± 50 pg/min, P < 0.01 vs. intact innervation), suggesting that 2-DG activated pancreatic nerves by increasing the central sympathetic outflow to the pancreas rather than by actin directly on nerves within the pancreas itself. These experiments provide the first direct evidence of stress-induced activation of pancreatic noradrenergic nerves in vivo. In contrast, neither hemorrhagic hypotension (50 mmHg) nor hypoxia (6-8{\%} O2) increased pancreatic NE output (Δ = +80 ± 110 and -20 ± 60 pg/min, respectively, P < 0.01 vs. neuroglucopenia) despite both producing increases of arterial plasma NE and epinephrine similar to glucopenia. The activation of pancreatic noradrenergic nerves is thus stress specific. Furthermore, because both glucopenia and hypotension increased arterial NE, yet only glucopenia activated pancreatic nerves, it is suggested that a regionally selective pattern of sympathetic activation can be elicited by acute stress, a condition in which sympathetic activation has traditionally been thought to be generalized and nondiscrete.",
author = "Havel, {Peter J} and Veith, {R. C.} and Dunning, {B. E.} and Taborsky, {G. J.}",
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T1 - Pancreatic noradrenergic nerves are activated by neuroglucopenia but not by hypotension or hypoxia in the dog. Evidence for stress-specific and regionally selective activation of the sympathetic nervous system

AU - Havel, Peter J

AU - Veith, R. C.

AU - Dunning, B. E.

AU - Taborsky, G. J.

PY - 1988

Y1 - 1988

N2 - To determine if acute stress activates pancreatic noradrenergic nerves, pancreatic norepinehrine (NE) output (spillover) was measured in halothane-anesthetized dogs. Central neuroglucopenia, induced by intravenous 2-deoxy-D-glucose ([2-DG] 600 mg/kg + 13.5 mg/kg-1 per min-1) increased pancreatic NE output from a baseline of 380 ± 100 to 1,490 ± 340 pg/min (Δ = 1,110 ± 290 pg/min, P < 0.01). Surgical denervation of the pancreas reduced this response by 90% (Δ = +120 ± 50 pg/min, P < 0.01 vs. intact innervation), suggesting that 2-DG activated pancreatic nerves by increasing the central sympathetic outflow to the pancreas rather than by actin directly on nerves within the pancreas itself. These experiments provide the first direct evidence of stress-induced activation of pancreatic noradrenergic nerves in vivo. In contrast, neither hemorrhagic hypotension (50 mmHg) nor hypoxia (6-8% O2) increased pancreatic NE output (Δ = +80 ± 110 and -20 ± 60 pg/min, respectively, P < 0.01 vs. neuroglucopenia) despite both producing increases of arterial plasma NE and epinephrine similar to glucopenia. The activation of pancreatic noradrenergic nerves is thus stress specific. Furthermore, because both glucopenia and hypotension increased arterial NE, yet only glucopenia activated pancreatic nerves, it is suggested that a regionally selective pattern of sympathetic activation can be elicited by acute stress, a condition in which sympathetic activation has traditionally been thought to be generalized and nondiscrete.

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