Document Detail


Sympathetic nerve stimulation versus pancreatic norepinephrine infusion in the dog: 2). Effects on basal release of somatostatin and pancreatic polypeptide.
MedLine Citation:
PMID:  2885175     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We compared the effects of sympathetic nerve stimulation to that of pancreatic norepinephrine (NE) infusion on pancreatic somatostatin-like immunoreactivity (SLI) and pancreatic polypeptide (PP) secretion in the halothane-anesthetized dog. During electrical stimulation (8 Hz, 1 msc, 10 mA, n = 6) of the sympathetic nerves surrounding the pancreatic artery, the pancreatic SLI output decreased from 827 +/- 340 fmol/min to 231 +/- 47 fmol/min (delta = -596 +/- 217 fmol/min, P less than 0.05) after 5 min, and PP output decreased from 11,972 +/- 374 pg/min to 5,518 +/- 774 pg/min (delta = -6,454 +/- 1,932 pg/min, P less than 0.02) after 3 min of stimulation. Arterial SLI or PP levels did not change. Sympathetic nerve stimulation also decreased pancreatic blood flow and increased pancreatic venous NE levels. To determine whether the NE, released locally during sympathetic nerve stimulation, is responsible for this inhibition of pancreatic SLI and PP outputs, exogenous NE was infused into the pancreatic artery at three different dose levels. The low dose of 12 ng/min (n = 6) increased pancreatic venous NE levels like sympathetic nerve stimulation. The medium dose of 120 ng/min (n = 6) reproduced the nerve stimulation-induced decrease of pancreatic blood flow. The high dose of 1,200 ng/min (n = 6) markedly exceeded both. It was found that neither the low nor the medium infusion rates of NE significantly affected pancreatic SLI or PP output. In contrast, infusion of NE at the very high dose level of 1,200 ng/min decreased pancreatic SLI output from 850 +/- 165 fmol/min to 318 +/- 59 fmol/min after 5 min of infusion (delta = -532 +/- 143 fmol/min, P less than 0.01) and decreased PP secretion from 22,777 +/- 7,082 pg/min to 12,764 +/- 6,100 pg/min after 3 min of infusion (delta = -10,013 +/- 2,399 pg/min, P less than 0.01). During this high dose rate NE infusion, both the increment of pancreatic venous SPV levels of NE and the decrement of pancreatic blood flow markedly exceeded the effects produced by sympathetic nerve stimulation. We conclude from this study in dogs: that selective electrical stimulation of the sympathetic nerves entering the pancreas decreases blood flow and inhibits pancreatic SLI and PP secretion, that NE infused into the pancreatic artery at moderate rates reproduces the decrease in blood flow yet does not reproduce the inhibition of pancreatic SLI and PP secretion, and that extremely high concentrations of NE, which markedly restrict pancreatic blood flow, decrease both pancreatic SLI and PP outputs.(ABSTRACT TRUNCATED AT 400 WORDS)
Authors:
B Ahrén; R C Veith; T L Paquette; G J Taborsky
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Endocrinology     Volume:  121     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1987 Jul 
Date Detail:
Created Date:  1987-07-27     Completed Date:  1987-07-27     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  332-9     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Arteries
Dogs
Electric Stimulation
Kinetics
Norepinephrine / blood,  pharmacology*
Pancreas / blood supply,  innervation,  secretion*
Pancreatic Polypeptide / secretion*
Regional Blood Flow / drug effects
Somatostatin / secretion*
Sympathetic Nervous System / physiology*
Veins
Grant Support
ID/Acronym/Agency:
AM-1289/AM/NIADDK NIH HHS; AM-17047/AM/NIADDK NIH HHS
Chemical
Reg. No./Substance:
51-41-2/Norepinephrine; 51110-01-1/Somatostatin; 59763-91-6/Pancreatic Polypeptide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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