RT Journal Article
SR Electronic
T1 ROLE OF THE AUTONOMIC NERVOUS SYSTEM IN THE RESTING TACHYCARDIA OF EXPERIMENTAL HYPERTHYROIDISM
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 55
OP 65
VO 158
IS 1
A1 Vincent J. Cairoli
A1 J. Richard Crout
YR 1967
UL http://jpet.aspetjournals.org/content/158/1/55.abstract
AB Resting heart rate was measured in unanesthetized rats treated with 100 µg of Na-L-thyroxin s.c. per day for 10 days and in comparable control rats. Propranolol (2 mg/kg i.v.) reduced the heart rate of control and thyroxin-treated animals to the same degree. In contrast, reserpine (5 mg/kg i.p.) caused a proportionately greater fall in heart rate in thyroxin-treated animals, so that heart rate in thyroxin-treated and control rats eventually reached the same base line. When atropine (5 mg/kg i.p.) was given after propranolol and/or reserpine, the heart rate increase was such that thyroxin-treated rats always had significantly higher rates than comparably treated controls. Vagus nerve stimulation was slightly less effective in slowing the heart in thyroxin-treated rats than in controls. It is concluded that the resting heart rate of unanesthetized thyroxin-treated rats is always higher than normal if adrenergic and cholinergic influences are withdrawn simultaneously from the sino-atrial node; this tachycardia is attributed to a direct effect of thyroxin on the pacemaker cells. The rate-normalizing action of reserpine is apparently due to a combination of increased vagal activity and reduced peripheral adrenergic activity. No evidence was obtained to suggest that excessive thyroid hormone enhances either adrenergic neural activity or the sensitivity of cardiac beta-receptors to norepinephrine. © 1967 by The Williams & Wilkins Company