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Intraperitoneal (i.p.) injection of C-terminal octapeptide of cholecystokinin (CCK-8) produced a dose-related increase in plasma corticosterone levels in intact rats, but not in vagotomized ones. Intracerebroventricular (i.c.v.) injection of CCK-8 was ineffective in stimulating the secretion of corticosterone, and in vitro experiment on ACTH release indicated that CCK-8 could not affect pituitary tissue directly. Since i.p. injection of non-sulfated CCK-8 failed to elevate plasma corticosterone levels, sulfated tyrosine residue in the CCK molecule is assumed to be indispensable for the stimulation of visceral organs. On the other hand, vasoactive intestinal polypeptide (VIP) was found to cause a dose-dependent increase in plasma corticosterone levels when administered centrally, but not after i.p. injection. However, VIP could not stimulate the release of ACTH from the pituitary tissue directly. The results suggest that VIP, but not CCK, stimulates the hypothalamic CRF neurons either directly or indirectly.

Effect of cholecystokinin octapeptide and vasoactive intestinal polypeptide on adrenocortical secretion in the rat.