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Vasoactive intestinal polypeptide (VIP) was measured by RIA in the hypophysial portal blood of rats after total hypophysectomy. The mean (+/- SE) VIP concentrations were 1332 +/- 171 pg/ml (range, 300-3868 pg/ml) under urethane anesthesia and 1735 +/- 707 pg/ml under pentobarbital anesthesia. The concentrations of VIP in peripheral plasma were, in most animals, less than 100 pg/ml. The secretion rate of VIP was not considerably changed during the blood collection. Immunoreactive VIP in hypophysial portal blood was identical to authentic VIP on gel chromatography. These findings suggest that VIP secreted from the hypothalamus may modulate pituitary function via the portal circulation. (Endocrinology 108: 395, 1981)

The effects of synthetic enkephalin analog (FK 33–824) and β-endorphin on growth hormone (GH) secretion and their interaction with brain monoamines were investigated in unanesthetized male rats. Blood samples (0.4 ml each) were withdrawn every 10–20 min for 6 h from a catheter chronically implanted in the right atrium. In all control rats, immunoreactive GH secretion was pulsatile in nature and two major GH bursts were found to occur around 12.00 and 15.30.The opioid peptides were injected between bursts at 14.00. Following an intravenous administration of FK 33–824 (10 μg/100 g b.w.), there was an abrupt increase in plasma GH, which was significantly suppressed by naloxone (125 μg/ 100 g b.w., i.v.), a specific opiate antagonist. Pretreatment with reserpine (1 mg/100 g b.w., i.p.) abolished not only the natural GH burst but also the GH response to FK 33–824. Pretreatment with dopamine-β-hydroxylase inhibitors, diethyldithiocarbamate (DDC, 100 mg/100 g b.w., i.v.) and fusarate (10 mg/100 g b.w., i.v.) also inhibited the natural GH burst and GH rise induced by FK 33–824. Intravenous injection of clonidine (15 μg/100 g b.w.), an α-adrenergic stimulant, resulted in an increase in plasma GH in the rats pretreated with reserpine, DDC or fusarate. Phenoxybenzamine (1 mg/100g b.w., i.v.), an α-adrenergic blocking agent, inhibited the GH response to FK 33–824. On the other hand, GH release induced by FK 33–824 was not influenced by propranolol (1 mg/100 g b.w., i.v.), a β-adrenergic blocking agent, nor pimozide (0.1 mg/100g b.w., i.v.), a dopamine antagonist. Intraventricular administration of β-endorphin (5 μg/rat) also increased the plasma GH levels which were lowered by phenoxybenzamine. These findings suggest that α-adrenergic mechanisms are involved in GH release induced by opioid peptides in the rat.

The effect of serotonin (5-HT) on plasma vasoactive intestinal polypeptide (VIP) levels in hypophysial portal blood was studied in urethane-anesthetized rats. Portal blood was collected by the parapharyngeal approach and plasma VIP was determined by radioimmunoassay. Mean (+/- SE) basal plasma VIP level was 1799 +/- 232 pg/ml, which was slightly decreased during the control experiments in which physiological saline was injected either intraventricularly or intravenously. Intraventricular injection of 5-HT (2 and 10 micrograms/rat) resulted in a significant increase in plasma VIP concentrations within 20 min. Intravenous injection of L-5-hydroxytryptophan (5-HTP, 1 mg/100 g BW), a precursor of 5-HT, also caused an increase in VIP concentrations in hypophysial portal plasma. The flow rate of hypophysial portal blood did not change throughout the experiments. These findings suggest that 5-HT stimulates VIP release from the median eminence into the hypophysial portal vessels in the rat.

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Effects of the centrally acting α-adrenergic agonist, clonidine, on growth hormone (GH) secretion was studied in conscious male rats pretreated with monosodium glutamate (MSG) during the neonatal period. GH secretory profiles in individual adult rats were obtained by repeated blood samplings every 10–20 min from 10.00 to 17.00 h. GH secretion was pulsatile with mean peak values at around 12.40 and 15.20 h in control rats. When clonidine (15 µg/100 g body weight) was injected intravenously into control rats at 14.00 h in the interval between two anticipated spontaneous GH bursts, plasma GH was increased with a mean peak value 20 min after the injection, and the following anticipated spontaneous GH burst was not observed during the experiment. In the rats neonatally treated with MSG (4 mg/g body weight, s.α), which causes selective destruction of the hypothalamic arcuate nucleus, plasma GH response to clonidine as well as the spontaneous GH bursts were considerably blunted, whereas prostaglandin Ei (5 µg/100 g body weight, i.v.) caused an abrupt increase in plasma GH levels in these animals. These results suggest that clonidine stimulates rat GH secretion, possibly by acting within the hypothalamus to stimulate GH releasing factor neurons.

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