![]() ![]() ![]() Since the action of ACTH on the epinephrineforming enzyme is known to be mediated by its stimulation of glucocorticoid secretion, these data suggest that the location of the adrenal medulla within the cortex, and the delivery to the medulla of venous blood which has already perfused the cortex, might provide important natural mechanisms for stimulating epinephrine biosynthesis. However, the doses of exogenous glucocorticoid needed for this effect are at least 100-fold greater than the usual steroid “replacement doses.” A dose of ACTH which is equally effective with a given amount of hydrocortisone in depressing splenic weight is much more effective in restoring PNMT activity. The doses of ACTH required to restore epinephrine biosynthesis are of the same order of magnitude as those needed to maintain adrenal weight. The PNMT activity of hypophysectomized rats is also elevated by glucocorticoids, but is unaffected by FSH, LH, prolactin, TSH, growth hormone, estrogen, or testosterone. ![]() This decline, as well as the consequent fall in adrenal epinephrine content, can be corrected by treatment with ACTH. Hypophysectomy in the rat is followed by a decline in the activity of phenylethanolamine- N-methyl transferase (PNMT), the adrenal medullary enzyme which synthesizes epinephrine.
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