ROLE OF THE AUTONOMIC NERVOUS SYSTEM IN THE RESTING TACHYCARDIA OF EXPERIMENTAL HYPERTHYROIDISM

¹ Department of Pharmacology, The University of Texas, Southwestern Medical School, Dallas, Texas

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rate of unanesthetized thyroxin-treated rats is always higher than normal if adrenergic and cholinergic influences are withdrawn simultaneously from the sino-atrial node; this tachycardia is attributed to a direct effect of thyroxin on the pacemaker cells.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.