PMID- 2555871
OWN - NLM
STAT- MEDLINE
DCOM- 19900104
LR  - 20190908
IS  - 0300-9572 (Print)
IS  - 0300-9572 (Linking)
VI  - 18
IP  - 2-3
DP  - 1989 Dec
TI  - Beta-endorphin and central control of arterial blood pressure during challenge of 
      circulatory homeostasis.
PG  - 173-82
AB  - A variety of neurotransmitters and neuropeptides appear to participate in the 
      central control mechanisms of arterial blood pressure. Our knowledge of these 
      mechanisms is limited as yet. In the present study the involvement of the opioid 
      peptide beta-endorphin in circulatory homeostasis was studied. Under conditions 
      in which beta-endorphin does not affect basal blood pressure and heart rate this 
      peptide had a pronounced prohypotensive influence in normotensive rats. This was 
      found for two conditions during which circulatory homeostasis was challenged. 
      Firstly, during blood letting in a rat model employed to test blood pressure 
      regulation during hemorrhage, and secondly, for the central hypotensive action of 
      alpha-methyldopa. In the first model hypotension was produced by stepwise 
      bleeding to respectively 80, 60 and 40 mmHg mean arterial pressure. 
      Intracerebroventricular (i.c.v.) administration of an antiserum raised against 
      beta-endorphin or of naloxone (s.c. or i.c.v.) caused a significant increase in 
      the required bleeding volume, whereas an opposite action was observed after the 
      injection of morphine (s.c.) or of beta-endorphin (i.c.v.). The role of 
      beta-endorphin in the hypotensive action of alpha-methyldopa, given 
      intracisternally (i.c.) was evaluated in conscious rats equipped with chronic 
      cannulas. Pretreatment with the opiate antagonist naltrexone (i.c.) caused an 
      inhibition of the hypotension and bradycardia induced by alpha-methyldopa. This 
      effect of the receptor antagonist was mimicked by i.c. administration of a 
      beta-endorphin antiserum. Taken together, these data point to a hypotensive 
      influence exerted by endogenous beta-endorphin under conditions during which 
      circulatory homeostasis are challenged.
FAU - de Jong, W
AU  - de Jong W
AD  - Rudolf Magnus Institute for Pharmacology, State University of Utrecht, The 
      Netherlands.
FAU - Sandor, P
AU  - Sandor P
FAU - Cox-van Put, J
AU  - Cox-van Put J
FAU - van den Berg, M H
AU  - van den Berg MH
FAU - van Giersbergen, P L
AU  - van Giersbergen PL
LA  - eng
PT  - Journal Article
PL  - Ireland
TA  - Resuscitation
JT  - Resuscitation
JID - 0332173
RN  - 0 (Endorphins)
RN  - 36B82AMQ7N (Naloxone)
RN  - 56LH93261Y (Methyldopa)
RN  - 60617-12-1 (beta-Endorphin)
RN  - 76I7G6D29C (Morphine)
SB  - IM
MH  - Animals
MH  - Blood Pressure/drug effects/*physiology
MH  - Blood Volume/drug effects
MH  - Bloodletting
MH  - Dose-Response Relationship, Drug
MH  - Endorphins/antagonists & inhibitors
MH  - Homeostasis/*physiology
MH  - Male
MH  - Methyldopa/pharmacology
MH  - Morphine
MH  - Naloxone/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Shock/*physiopathology
MH  - beta-Endorphin/*physiology
EDAT- 1989/12/01 00:00
MHDA- 1989/12/01 00:01
CRDT- 1989/12/01 00:00
PHST- 1989/12/01 00:00 [pubmed]
PHST- 1989/12/01 00:01 [medline]
PHST- 1989/12/01 00:00 [entrez]
AID - 0300-9572(89)90020-8 [pii]
AID - 10.1016/0300-9572(89)90020-8 [doi]
PST - ppublish
SO  - Resuscitation. 1989 Dec;18(2-3):173-82. doi: 10.1016/0300-9572(89)90020-8.