The effect of adrenocortical hormones alone and in combination with growth hormone on cardiac hypertrophy and blood pressure of hypophysectomized rats

Abstract

There is no cardiac hypertrophy or hypertension in hypophysectomized rats after narrowing of their descending aortae (Hajdu & Beznak, 1943. ACTH, in a dose that completely prevented the atrophy of the adrenals due to hypophysectomy, had no influence on the cardiac weight and blood pressure of such rats (Beznak, 1952b). Treatment with growth hormone, on the other hand, completely restored the cardiac weight and blood pressure of hypophysectomized rats to normal and on aortic narrowing the same degree of cardiac hypertrophy and hypertension resulted as in normal rats (Beznak, 1954 b). For this, however, very large daily doses of growth hormone (4-10 mg in terms of Armour standard 22KR2) were necessary. The question arose whether some other hormones, notably the adrenocortical and thyroid hormones, could potentiate the effect of growth hormone. The thyroids and adrenals are not indispensable for the production of cardiac hypertrophy and hypertension because cardiac hypertrophy and hypertension take place in thyroidectomized (Beznak & Hajdu, 1944 as well as in adrenalectomized rats on aortic narrowing (Beznik, 1952b). Hay (1946) observed that lyophilized anterior pituitary (LAP) caused an increase in the weight of the kidneys and the heart in normal and in thyroidectomized rats. Yet that these hormones may have some effect was shown by the circumstance that both cardiac hypertrophy and hypertension-though present-were somewhat smaller in thyroidectomized and adrenalectomized rats than in normal rats on similar aortic constriction. It is known that the thyroids influence growth hormone secretion and the reaction of the tissues to growth hormone (Schwann,

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“…After induction of myocardial ischemia, Lewis dwarf rats fail to develop compensatory hypertrophy of the noninfarcted posterior wall, which exacerbates the loss of myocardial function (55). These findings are congruent with the results of early studies on hypophysectomized rats, showing that GH was necessary for a normal compensatory hypertrophic response following experimental aortic constriction (56)(57)(58).…”