PMID- 7550548
OWN - NLM
STAT- MEDLINE
DCOM- 19951109
LR  - 20131121
IS  - 1230-6002 (Print)
IS  - 1230-6002 (Linking)
VI  - 47
IP  - 1
DP  - 1995 Jan-Feb
TI  - Dopaminergic neuronal systems modulate the central cardiovascular effects of TRH 
      in rats.
PG  - 43-52
AB  - Thyrotropin releasing hormone (pGlu-His-Pro-NH2-TRH) is a hypothalamic peptide 
      that exerts pharmacological actions on the mammalian central nervous and 
      circulatory systems independent of hormonal activity. In rats TRH produces an 
      increase in blood pressure, heart rate and respiratory rate, following its 
      intracerebroventricular (icv) administration. Because of a suspected role of the 
      central dopamine (DA) system in these effects, we examined the influence of 
      assorted DA receptor agonists and antagonists on the central cardiovascular and 
      respiratory effects of TRH. Adult male Wistar rats were anesthetized with 
      urethane (1.5 g/kg ip), implanted with an intracranial cannula for icv 
      injections, and continuously monitored for (a) mean arterial blood pressure via 
      an indwelling catheter in the right carotid artery, (b) heart rate via an ECG 
      lead II signal and (c) respiratory rate via a photoelectric transducer. TRH (100 
      nmol) produced a sustained increase in blood pressure (ca. 20 mm Hg), heart rate 
      (ca. 60 beats per min-bpm) and respiratory rate (< or = 200 breaths per min) 
      during a 30 min observation period. The DA D1 receptor agonist SKF 38393 HCl (0.3 
      or 3.0 mg/kg ip) attenuated the effects of TRH on blood pressure and heart rate 
      by > 50%, while the DA D2 receptor agonist quinpirole HCl (1.0 mg/kg ip) 
      potentiated the chronotropic response to TRH by > 50%. The predominant DA D2 
      receptor antagonist haloperidol lactate (1.0 mg/kg ip) potentiated the effects of 
      TRH on blood pressure and heart rate by > 50%, with the latter effect on heart 
      rate being mimicked by the D2 receptor antagonist spiperone HCl (1.0 mg/kg ip). 
      Chlorpromazine HCl (5.0 mg/kg ip), a low potency non-selective D2 receptor 
      antagonist, had effects opposite to that of haloperidol. The effect of TRH on 
      respiration was potentiated by quinpirole but not modified by other DA receptor 
      agonists or antagonists. These findings indicate that the DA system is involved 
      in a complex manner in the central cardiovascular actions of TRH, while DA D2 
      receptors alone appear to be involved in modulating respiratory effects of TRH.
FAU - Jedrusiak, J
AU  - Jedrusiak J
AD  - Department of Pharmacology, Medical Academy, Zabrze, Poland.
FAU - Brus, R
AU  - Brus R
FAU - Kostrzewa, R M
AU  - Kostrzewa RM
FAU - Slowinski, Z
AU  - Slowinski Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Poland
TA  - Pol J Pharmacol
JT  - Polish journal of pharmacology
JID - 9313882
RN  - 0 (Dopamine Agonists)
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Ergolines)
RN  - 20OP60125T (Quinpirole)
RN  - 5Y5F15120W (Thyrotropin-Releasing Hormone)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Dopamine/*physiology
MH  - Dopamine Agonists/pharmacology
MH  - Dopamine Antagonists/pharmacology
MH  - Ergolines/pharmacology
MH  - Heart Rate/drug effects
MH  - Hemodynamics/*drug effects/*physiology
MH  - Injections, Intraventricular
MH  - Male
MH  - Molecular Sequence Data
MH  - Neurons/*physiology
MH  - Quinpirole
MH  - Rats
MH  - Rats, Wistar
MH  - Respiratory Mechanics/drug effects
MH  - Thyrotropin-Releasing Hormone/administration & dosage/*pharmacology
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PST - ppublish
SO  - Pol J Pharmacol. 1995 Jan-Feb;47(1):43-52.