Influence of Pituitary, Thyroid, and Adrenal Hormones on Norepinephrine Turnover and Metabolismin the Rat Heart

Norepinephrine turnover was estimated in the rat heart from the rate of release of tracer 3 H-norepinephrine and the depletion of endogenous norepinephrine after inhibition of synthesis. Cardiac norepinephrine turnover was markedly increased in chronically hypophysectomized rats. Thyroidectomy and adrenalectomy were also associated with increased cardiac norepinephrine turnover, whereas ovariectomy was not. Chronic treatment of hypophysectomized rats with thyroxine and ACTH restored the turnover to normal, the replacement of thyroxine being quantitatively more significant. Cardiac atrophy and decreased blood pressure occurred concomitantly with increased norepinephrine turnover in the hypophysectomized rat and were restored to normal with thyroid treatment. Ganglionic blockade of the hypophysectomized rat also restored the turnover toward normal. The metabolites of 3 H-norepinephrine were shifted with a decrease in O-methylated metabolites and an increase in deaminated products. This evidence suggests that thyroid deficiency and, to a lesser extent, adrenal deficiency are associated with an increase in cardiac norepinephrine turnover mediated by an increase in sympathetic nervous activity. The role of the increased turnover in relation to the hormonal deficiencies is discussed.