PMID- 8173946
OWN - NLM
STAT- MEDLINE
DCOM- 19940609
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 635
IP  - 1-2
DP  - 1994 Jan 28
TI  - Intracerebroventricular neuropeptide Y increases gastric acid secretion by 
      decreasing tonic adrenergic inhibition of acid in dogs.
PG  - 118-24
AB  - Neuropeptide Y (NPY) has been shown to increase basal gastric acid secretion in 
      dogs. We examined the hypothesis that NPY might increase gastric acid secretion 
      by interaction with central catecholaminergic control of acid secretion in dogs. 
      Studies were performed in awake canines with gastric fistulas and 
      cerebroventricular guides which allowed injection into the lateral cerebral 
      ventricle. Intracerebroventricular (i.c.v.) injection of yohimbine (5 
      micrograms/kg) increased acid secretion compared to control (yohimbine: 9.1 +/- 
      3.3 mmol/h; control: 1.8 +/- 1.0 mmol/2 h P < 0.05), whereas prazosin and 
      propranolol (both 5 micrograms/kg i.c.v.) had no effect, suggesting that there is 
      tonic central alpha 2-adrenergic inhibition of acid secretion. NPY13-36 
      significantly increased acid secretion compared to control (NPY13-36 1000 pmol/kg 
      i.c.v.: 5.6 +/- 1.9 mmol/2 h; control: 1.3 +/- 0.8 mmol/2 h, P < 0.05), whereas 
      [Leu31,Pro34]-NPY had no effect, suggesting that the central effect of NPY is 
      mediated at a Y2, probably pre-synaptic receptor. Finally, i.c.v. 
      desmethylimipramine (DMI) inhibited the acid response to i.c.v. NPY when injected 
      before but not after NPY (i.c.v. DMI then i.c.v. NPY: control, 15.2 +/- 6.6 
      mmol/2 h; DMI, 3.5 +/- 1.2 mmol/2 h, P < 0.05; i.c.v. NPY followed by i.c.v. DMI: 
      control, 8.9 +/- 4.0 mmol/2 h; DMI, 9.9 +/- 2.9 mmol/2 h, P > 0.05). This 
      suggests that NPY acts by decreasing noradrenaline release. These findings are 
      compatible with the hypothesis that i.c.v. NPY increases acid secretion by 
      decreasing tonic central adrenergic inhibition of acid by decreasing release of 
      noradrenaline at a pre-synaptic level.
FAU - Geoghegan, J G
AU  - Geoghegan JG
AD  - Department of Surgery, Duke University Medical Center, Durham, NC 27710.
FAU - Lawson, D C
AU  - Lawson DC
FAU - Cheng, C A
AU  - Cheng CA
FAU - Pappas, T N
AU  - Pappas TN
LA  - eng
GR  - DK 38216/DK/NIDDK NIH HHS/United States
GR  - DK 40790-01/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Adrenergic Antagonists)
RN  - 0 (Neuropeptide Y)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, Neuropeptide Y)
RN  - 0 (neuropeptide Y (13-36))
RN  - 125580-28-1 (neuropeptide Y, Leu(31)-Pro(34)-)
RN  - TG537D343B (Desipramine)
SB  - IM
MH  - *Adrenergic Antagonists
MH  - Animals
MH  - Basal Metabolism
MH  - Desipramine/administration & dosage
MH  - Dogs
MH  - Female
MH  - Gastric Acid/*metabolism
MH  - Injections, Intraventricular
MH  - Male
MH  - Neuropeptide Y/*administration & dosage/analogs & derivatives
MH  - Peptide Fragments/administration & dosage
MH  - Receptors, Neuropeptide Y/analysis
EDAT- 1994/01/28 00:00
MHDA- 1994/01/28 00:01
CRDT- 1994/01/28 00:00
PHST- 1994/01/28 00:00 [pubmed]
PHST- 1994/01/28 00:01 [medline]
PHST- 1994/01/28 00:00 [entrez]
AID - 0006-8993(94)91430-3 [pii]
AID - 10.1016/0006-8993(94)91430-3 [doi]
PST - ppublish
SO  - Brain Res. 1994 Jan 28;635(1-2):118-24. doi: 10.1016/0006-8993(94)91430-3.