PMID- 11033318
OWN - NLM
STAT- MEDLINE
DCOM- 20010108
LR  - 20190624
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 405
IP  - 1-3
DP  - 2000 Sep 29
TI  - The role of atrial natriuretic peptide in alcohol withdrawal: a peripheral 
      indicator and central modulator?
PG  - 103-12
AB  - Changes in fluid and electrolyte homeostasis may accompany and are likely to 
      modify the clinical symptoms of alcohol-withdrawal reactions. It was of obvious 
      theoretical and practical interest therefore to investigate the changes in the 
      secretion of hormones, which regulate the fluid and electrolyte homeostasis 
      (atrial natriuretic peptide, aldosterone and plasma renin activity) during 
      alcohol withdrawal in chronic alcoholic patients. In a phase of severe 
      withdrawal, there were increased plasma renin activity and aldosterone levels 
      observed. In a phase of partial recovery, on the other hand, the elevated plasma 
      renin activity and aldosterone levels were back to the normal range. In 60% of 
      the patients, delirium tremens was gradually developing during the observation 
      period. In these patients, an elevated level of atrial natriuretic peptide was 
      observed at the time of hospital admission, i.e. days before the actual onset of 
      delirium tremens. It is concluded that the disturbed volume homeostasis and the 
      consequently altered plasma atrial natriuretic peptide secretion might be 
      associated with, and therefore used as an indicator of the onset of delirium 
      tremens. To study the role of central nervous atrial natriuretic peptide, mice 
      were rendered tolerant to and dependent on alcohol with an alcohol-liquid diet 
      for 14 days. Five hours after withdrawal from alcohol, withdrawal 
      hyperexcitability symptoms were analyzed. Intracerebroventricular (i.c.v.) 
      injection of atrial natriuretic peptide attenuated, whereas that of an antiserum 
      against atrial natriuretic peptide intensified the severity of handling-induced 
      convulsions. N-methyl-D-aspartate induced behavioral seizures in a dose-dependent 
      manner, whose effect was more intensive during the alcohol-withdrawal period than 
      in alcohol-naive animals. I.c.v. injections of atrial natriuretic peptide 
      dose-dependently inhibited, whereas that of antiserum against atrial natriuretic 
      peptide potentiated the seizure-inducing effect of N-methyl-D-aspartate in 
      alcohol-dependent mice. Although tentatively, it is concluded that peripheral 
      secretion of atrial natriuretic peptide may be an indicator, whereas central 
      nervous atrial natriuretic peptide a neuropeptide modulator of alcohol-withdrawal 
      symptomatology.
FAU - Kovacs, G L
AU  - Kovacs GL
AD  - Central Laboratory, Markusovszky Teaching Hospital, Markusovszky St. 3, H-9700, 
      Szombathely, Hungary. glkovacs@mail.matav.hu
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Biomarkers)
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (Neurotransmitter Agents)
RN  - 3K9958V90M (Ethanol)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
SB  - IM
MH  - Animals
MH  - Atrial Natriuretic Factor/blood/*physiology
MH  - Biomarkers
MH  - Central Nervous System Depressants/*adverse effects
MH  - Ethanol/*adverse effects
MH  - Humans
MH  - Neurotransmitter Agents/*physiology
MH  - Substance Withdrawal Syndrome/metabolism/*physiopathology
RF  - 66
EDAT- 2000/10/18 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/10/18 11:00
PHST- 2000/10/18 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/10/18 11:00 [entrez]
AID - S0014299900005458 [pii]
AID - 10.1016/s0014-2999(00)00545-8 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2000 Sep 29;405(1-3):103-12. doi: 10.1016/s0014-2999(00)00545-8.