PMID- 2891452
OWN - NLM
STAT- MEDLINE
DCOM- 19880218
LR  - 20190706
IS  - 0009-7330 (Print)
IS  - 0009-7330 (Linking)
VI  - 62
IP  - 1
DP  - 1988 Jan
TI  - Hemodynamic and neural mechanisms of action of thyrotropin-releasing hormone in 
      the rat.
PG  - 139-54
AB  - The mechanisms mediating the effects of thyrotropin-releasing hormone (TRH) on 
      the cardiovascular system were studied in the conscious rat. 
      Intracerebroventricular (i.c.v.) injection of TRH (8 pmol-80 nmol/kg) induced 
      dose-dependent increases in mean arterial pressure, heart rate, and cardiac 
      index. Hindquarter blood flow increased due to vasodilation, while an increase in 
      renal and mesenteric vascular resistance caused a decrease in blood flow in the 
      respective organs. The plasma levels of norepinephrine and epinephrine were 
      increased by TRH, while there was no change in plasma renin activity or 
      vasopressin. The cardiovascular actions of i.c.v. TRH were not influenced by 
      blockade of the renin-angiotensin system or vasopressin receptors. The ganglion 
      blocker chlorisondamine and the alpha 1- and alpha 2-adrenoreceptor antagonist 
      phentolamine (2 mg/kg i.v.) abolished the increase in blood pressure and 
      mesenteric vasoconstriction after i.c.v. TRH. Propranolol (2 mg/kg i.v.) blocked 
      the TRH-induced increase in cardiac index, heart rate, and hindquarter blood 
      flow. The hindquarter vasodilation induced by TRH was also blocked by the 
      selective beta 2-adrenoceptor antagonist ICI 188,551 (1 or 2 mg/kg i.v.), while 
      the beta 1-adrenoceptor blocker practolol (10 mg/kg i.v.) had no effect on the 
      hindquarter vasodilation produced by TRH but totally blocked the increase in 
      cardiac index. In adrenal demedullated rats, the systemic hemodynamic effects of 
      i.c.v. TRH were diminished along with the decrease in renal blood flow and 
      increase in renal vascular resistance; however, the increase in hindquarter blood 
      flow was attenuated only in adrenal demedullated rats pretreated with the 
      sympathetic blocker bretylium. The renal vasoconstriction induced by i.c.v. TRH 
      was not abolished by renal denervation. In sinoaortic debuffered rats, the 
      pressor, tachycardic, and mesenteric vasoconstrictor responses to centrally 
      administered TRH were significantly potentiated. Taken together, these data 
      suggest that the putative neurotransmitter TRH may play a role in central 
      regulation of cardiac functions and organ blood flow distribution through both 
      the sympathetic nerves and the adrenal medulla. A pivotal role for beta 
      2-adrenoceptors in mediation of hindquarter vasodilation is also demonstrated.
FAU - Siren, A L
AU  - Siren AL
AD  - Department of Neurology, Uniformed Services University of the Health Sciences, 
      Bethesda, MD 20814-4799.
FAU - Lake, C R
AU  - Lake CR
FAU - Feuerstein, G
AU  - Feuerstein G
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Adrenergic alpha-Antagonists)
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 5Y5F15120W (Thyrotropin-Releasing Hormone)
RN  - 9G64RSX1XD (Captopril)
RN  - H2AFV2HE66 (Saralasin)
RN  - JD3M24F66I (Chlorisondamine)
SB  - IM
MH  - Adrenalectomy
MH  - Adrenergic alpha-Antagonists/pharmacology
MH  - Adrenergic beta-Antagonists/pharmacology
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Captopril/pharmacology
MH  - Cardiovascular System/*drug effects
MH  - Chlorisondamine/pharmacology
MH  - Denervation
MH  - Dose-Response Relationship, Drug
MH  - Hemodynamics/drug effects
MH  - Injections, Intraventricular
MH  - Kidney/innervation
MH  - Male
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Saralasin/pharmacology
MH  - Sympathetic Nervous System/*drug effects
MH  - Thyrotropin-Releasing Hormone/administration & dosage/*pharmacology
EDAT- 1988/01/01 00:00
MHDA- 1988/01/01 00:01
CRDT- 1988/01/01 00:00
PHST- 1988/01/01 00:00 [pubmed]
PHST- 1988/01/01 00:01 [medline]
PHST- 1988/01/01 00:00 [entrez]
AID - 10.1161/01.res.62.1.139 [doi]
PST - ppublish
SO  - Circ Res. 1988 Jan;62(1):139-54. doi: 10.1161/01.res.62.1.139.