Cardiovascular and metabolic responses to thyroid hormones in animals after sympathectomy or treatment with nerve growth factor

Abstract

The cardiovascular and metabolic effects of thyroxine (T 4) and triiodothyronine (T 3) were examined in rats and mice with decreased or permanently enhanced adrenergic innervations to the heart. 6-Hydroxydopamine (6-OHDA) and the antiserum to the nerve growth factor (AS) were administered to damage sympathetic fibers; the density of the cardiac adrenergic plexus was increased through the use of the nerve growth factor (NGF). Some animals were additionally adrenal demedullated or treated with N, N-diisopropyl- N′-isoamyl- N′-diethylaminoethylurea (P-286) to reduce circulating catecholamine levels. The results of these experiments showed that the rise in heart phosphorylase a activity produced by thyroid hormones was absent after adrenal demedullation and significantly inhibited after chemical sympathectomy with 6-OHDA. Interference with adrenal medullary function by P-286 in combination with chemical or immunological sympathectomy similarly prevented the hormone-induced activation of myocardial phosphorylase a. While an increase in the density of the peripheral sympathetic fibres to the heart accentuated the tachycardia characteristic of hyperthyroidism, the high metabolic rate which accompanies thyrotoxicosis was unaltered either by proliferation of adrenergic fibres or sympathectomy.