Evidence for a synergistic effect of somatostatin on vasoactive intestinal polypeptide-induced prolactin release in the rat: comparison with its effect on thyrotropin (TSH)-releasing hormone-stimulated TSH release.
The present experiments were carried out to clarify the role of endogenous somatostatin (SRIF) in the regulation of PRL and TSH release. The effects of electrical stimulation of the hypothalamic periventricular nucleus (PE) on vasoactive intestinal polypeptide (VIP)-induced PRL and TRH-stimulated TSH secretion were studied using pentobarbital-anesthetized male rats bearing indwelling cannulae in the right atria. The animals were implanted in the PE with bipolar concentric stimulating electrodes 1 week before the experiments began. The effects of a bolus injection or a continuous infusion of SRIF-14 (iv, 7.6 or 10 nmol/100 g BW, respectively) on the PRL or TSH release induced by VIP or TRH were also examined. Electrical stimulation of the PE significantly enhanced VIP-induced PRL release 19 min after the bolus injection of VIP (from 29.3 +/- 7.2 to 59.7 +/- 14.9 ng/ml, P less than 0.05). A bolus injection of SRIF had a similar effect and increased the PRL response to VIP (from 29.3 +/- 7.2 to 114.7 +/- 22.4 ng/ml, P less than 0.01). Continuous infusion of SRIF did not decrease the stimulatory effect of VIP on PRL release; on the contrary it significantly increased the PRL response to a first VIP injection (10 min after the onset of SRIF-14 infusion) over that observed after a second administration of VIP. Neither electrical stimulation of the PE nor the bolus SRIF-14 injection modified basal PRL secretion. Electrical stimulation of the PE slightly but significantly increased the TSH response to a bolus injection of TRH, but had no effect on the basal TSH release. In contrast, both the bolus injection and the continuous infusion of SRIF-14 significantly and persistently inhibited the TRH-stimulated TSH release. These results suggest that 1) SRIF does not inhibit VIP-induced PRL secretion in vivo but rather enhances it through some unknown mechanism; 2) SRIF inhibits TRH-stimulated TSH secretion.