PMID- 2142565
OWN - NLM
STAT- MEDLINE
DCOM- 19900817
LR  - 20190824
IS  - 0065-4299 (Print)
IS  - 0065-4299 (Linking)
VI  - 30
IP  - 1-2
DP  - 1990 Apr
TI  - Antagonistic effect of naloxone on the hypertensive response of 
      intraventricularly administered histamine.
PG  - 226-30
AB  - Intracerebroventricular (i.c.v.) injections of histamine (HA) to 
      Vetbutal-anaesthetized rats elicited a biphasic pressure response: a fall of 
      blood pressure (BP) in the first minute, followed by a rise in BP. The heart rate 
      (HR) response was also biphasic: bradycardia in the first minute, followed by 
      tachycardia. The H1-receptor agonist 2-pyridylethylamine (PEA) increased the fall 
      in BP in the first minute in comparison with the HA group, and then elicited a 
      rise in BP that was, however, much lower than that produced by HA. Throughout the 
      experiment PEA produced essentially only a bradycardia. The H2-receptor agonist 
      dimaprit elicited a single-phase pressor response, i.e. a rise in BP and did not 
      elicit tachycardia. Intraventricular pretreatment of rats with naloxone greatly 
      reduced the initial response (phase 1) in the first minute in HA groups by 77-83% 
      and PEA groups by 83-100%. Naloxone given in small doses also reduced the fall in 
      HR by 71-100% in those groups. The experimental results permit a conclusion that 
      the phase 1 response, i.e. the fall in BP, results from excitation of 
      H1-receptors. Thus we may propose that H1-receptors are involved in the action of 
      naloxone. Naloxone in a dose of 0.1 microgram inhibited the hypertensive 
      responses of HA after 25-30 min. The reduction reached 71%. Naloxone reduced the 
      small rise in BP induced by PEA (10 micrograms) but totally blocked the rise in 
      BP induced by dimaprit (50 micrograms). This blockade indicates that the central 
      opioid system may transmit the total stimulating response (rise in BP) of H2 
      receptors induced by dimaprit. Participation of central opioid receptors in 
      HA-stimulated responses has already been demonstrated in corticosterone 
      secretion.
FAU - Mlynarska, M S
AU  - Mlynarska MS
AD  - Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Agents Actions
JT  - Agents and actions
JID - 0213341
RN  - 0 (Pyridines)
RN  - 36B82AMQ7N (Naloxone)
RN  - 80061L1WGD (Cimetidine)
RN  - 820484N8I3 (Histamine)
RN  - ATW1AH7OJ5 (2-(2-aminoethyl)pyridine)
RN  - GYV9AM2QAG (Thiourea)
RN  - HPE317O9TL (Pyrilamine)
RN  - ZZQ699148P (Dimaprit)
SB  - IM
MH  - Animals
MH  - Blood Pressure/*drug effects
MH  - Cimetidine/pharmacology
MH  - Dimaprit
MH  - Hemodynamics/drug effects
MH  - Histamine/administration & dosage/*pharmacology
MH  - In Vitro Techniques
MH  - Injections, Intraventricular
MH  - Male
MH  - Naloxone/*pharmacology
MH  - Pyridines/pharmacology
MH  - Pyrilamine/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Thiourea/pharmacology
EDAT- 1990/04/01 00:00
MHDA- 1990/04/01 00:01
CRDT- 1990/04/01 00:00
PHST- 1990/04/01 00:00 [pubmed]
PHST- 1990/04/01 00:01 [medline]
PHST- 1990/04/01 00:00 [entrez]
AID - 10.1007/BF01969045 [doi]
PST - ppublish
SO  - Agents Actions. 1990 Apr;30(1-2):226-30. doi: 10.1007/BF01969045.