The possible involvement of adrenergic mechanisms in regulating the secretion of growth hormone (GH)-releasing factor (GRF) from the rat hypothalamus was examined in vitro with a perifusion system. A high potassium concentration (56 mM) stimulated GRF release from the hypothalamus. The infusion of clonidine (10(-4) M), an alpha 2-adrenergic stimulant, resulted in an increase in the spontaneous release of GRF. In the presence of propranolol (10(-5) M), a beta-adrenergic blocking agent, clonidine (10(-5) and 10(-4) M) stimulated GRF release more prominently in a dose-related manner, whereas propranolol (10(-5) and 10(-4) M) by itself did not affect the spontaneous GRF release. The stimulatory effect of clonidine (10(-4) M) on GRF release in the presence of propranolol was inhibited by yohimbine (10(-4) M), an alpha 2-adrenergic blocking agent. These findings suggest that alpha 2-adrenergic mechanisms play a role in stimulating GRF release from the hypothalamus in rats.
Intracerebroventricular (icv) injection of somatostatin-14 (SRIF-14, 5 micrograms/rat) caused an increase in plasma GH in urethane-anesthetized rats and in conscious freely moving rats. Antiserum specific for rat GH-releasing factor (GRF) (0.5 ml/rat, iv) blunted GH release induced by SRIF-14 in these animals. The antiserum also suppressed spontaneous GH surges in conscious rats. In contrast, GH release induced by prostaglandin E2 (5 micrograms/100 g BW, iv) was not affected by the antiserum. SRIF-14 (5 micrograms/rat, icv) also raised plasma GH levels in conscious rats during the constant iv infusion of SRIF-14 (55 ng/55 microliter X min) which suppressed spontaneous GH secretion. Neither plasma TSH levels nor TSH release induced by a TRH analog were affected by icv injection of SRIF-14. These results suggest that the central stimulating effect of SRIF-14 on rat GH secretion is mediated, at least in part, by hypothalamic GRF and not due to a direct action on the pituitary.
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