PMID- 11299207
OWN - NLM
STAT- MEDLINE
DCOM- 20010517
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 280
IP  - 5
DP  - 2001 May
TI  - Thyroid status influences baroreflex function and autonomic contributions to 
      arterial pressure and heart rate.
PG  - H2061-8
AB  - The effect of thyroid status on arterial baroreflex function and autonomic 
      contributions to resting blood pressure and heart rate (HR) were evaluated in 
      conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) 
      with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid 
      (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean 
      arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). 
      Baroreflex function was evaluated with the use of a logistic function that 
      relates LSNA or HR to MAP during infusion of phenylephrine and sodium 
      nitroprusside. Contributions of the autonomic nervous system to resting MAP and 
      HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, 
      the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo 
      animals exhibited blunted sympathoexcitatory and tachycardic responses to 
      decreases in MAP. Furthermore, the data suggest that in Hypo rats, the 
      sympathetic influence on HR was predominant and the autonomic contribution to 
      resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex 
      function generally was similar to that in Eut rats. The autonomic contribution to 
      resting MAP was not different between Hyper and Eut rats, but predominant 
      parasympathetic influence on HR was exhibited in Hyper rats. The results 
      demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper 
      rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in 
      the heart, and the Hypo state increases the autonomic contributions to resting 
      blood pressure.
FAU - Foley, C M
AU  - Foley CM
AD  - Department of Veterinary Biomedical Sciences and Dalton Cardiovascular Research 
      Center, University of Missouri at Columbia, Columbia, Missouri 65211, USA.
FAU - McAllister, R M
AU  - McAllister RM
FAU - Hasser, E M
AU  - Hasser EM
LA  - eng
GR  - HL-36088/HL/NHLBI NIH HHS/United States
GR  - HL-55306/HL/NHLBI NIH HHS/United States
GR  - HL-57226/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Antithyroid Agents)
RN  - 0 (Ganglionic Blockers)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - 6G8X656T45 (Trimethaphan)
RN  - 721M9407IY (Propylthiouracil)
SB  - IM
MH  - Animals
MH  - Antithyroid Agents
MH  - Baroreflex/drug effects/*physiology
MH  - Blood Pressure/drug effects/*physiology
MH  - Consciousness
MH  - Ganglionic Blockers/pharmacology
MH  - Heart Rate/drug effects/*physiology
MH  - Hyperthyroidism/chemically induced/*physiopathology
MH  - Hypothyroidism/chemically induced/*physiopathology
MH  - Male
MH  - Propylthiouracil
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sympathetic Nervous System/physiology
MH  - Thyroid Gland/physiology
MH  - Triiodothyronine
MH  - Trimethaphan/pharmacology
OTO - NASA
OT  - Non-programmatic
EDAT- 2001/04/12 10:00
MHDA- 2001/05/18 10:01
CRDT- 2001/04/12 10:00
PHST- 2001/04/12 10:00 [pubmed]
PHST- 2001/05/18 10:01 [medline]
PHST- 2001/04/12 10:00 [entrez]
AID - 10.1152/ajpheart.2001.280.5.H2061 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2001 May;280(5):H2061-8. doi: 
      10.1152/ajpheart.2001.280.5.H2061.