Sho Yunoki

Effects of 2-bromo-α-ergocryptine on β-endorphin-induced growth hormone, prolactin and luteining hormone release in urethane anesthetized rats

Abstract Adult male rats were injected intraperitoneally either with saline or 2-Br- α-ergocryptine(CB-154)(10 ng/0.5 ml/rat) 30 min prior to an intraventricular injection of saline or β-endorphin (1 μg/10 μl or 5 μg/10 μl) and 30 min after β-endorphin, they were sacrificed by decapitation. Intraventricular injection of β-endorphin elicited significant increases in serum GH, prolactin and LH levels in a dose-related manner. Pretreatment with CB-154 inhibited the release of GH, prolactin and LH induced by β-endorphin. These results indicate that the stimulatory effects of β-endorphin on GH, prolactin and LH may be involved in an inhibition of dopaminergic mechanism in the central nervous system.

Vasopressin and CRF-ACTH in Adrenalectomized and Dexamethasone-Treated Rats

Median eminence corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) and pituitary and peripheral plasma adrenocorticotropin (ACTH) and AVP were measured in male Wistar rats 1 and 2 weeks after bilateral adrenalectomy (ADX), sham operation (SHAM) or dexamethasone-treatment (DEX). Median eminence AVP content was unchanged 1 week after ADX but was significantly elevated 2 weeks after ADX, whereas CRF activity was reduced at 1 week after ADX and returned to control range at 2 weeks. Anterior pituitary ACTH content was elevated but posterior pituitary AVP content was reduced at 1 and 2 weeks after ADX. Plasma ACTH was greatly elevated in ADX rats and reduced in DEX rats, whereas plasma AVP did not differ significantly between these two groups or the control group. When ADX and SHAM rats were laparotomized under ether, plasma ACTH increased greatly, but this elevation was prevented by DEX treatment. The plasma AVP level was elevated in all three groups 2.5 min after onset of stress but returned to the basal range at 20 min. Median eminence CRF and AVP and pituitary ACTH and AVP were not significantly changed after onset of stress. These results indicate that the vasopressin and CRF-ACTH responses were not consistent in the median eminence, pituitary and peripheral plasma and suggest that vasopression is not involved in the feedback and acute stress mechanism of CRF-ACTH secretion. However, we have to measure CRF activity and AVP concentration in the hypophysial portal blood to confirm this conclusion.

Effects of nifedipine on prolactin, growth hormone, and luteinizing hormone release by rat anterior pituitary in vitro.

Summary The release of prolactin, GH, and LH was monitored by radioimmunoas-say in rat anterior pituitary tissue incubated in Krebs-Ringer bicarbonate medium. Nife-dipine, a strong Ca2+ blocker, at 10, 100, and 1000 ng/ml inhibited the release of prolactin in a dose-related manner, but did not inhibit the release of GH and LH. This drug also blocked the TRH-induced GH release and the LH-RH-induced LH release. These results indicate that the release of prolactin may be more closely tied to Ca2+ influx from extracellular fluid and with stimulus-secretion coupling than the release of GH and LH and that Ca2+ may also play a role in the release of anterior pituitary hormones induced by releasing hormones.

Inhibitory effects of substance P on the gamma-amino-butyric acid and gamma-hydroxybutyric acid-induced growth hormone and prolactin release in male rats

Abstract Gamma-aminobutyric acid (GABA) at 50 μg/10 μ1 was injected into the lateral ventricle after pretreatment with intraventricular injection of 1 μg of substance P in urethane anesthetized male rats. Thirty minutes after GABA injection the animals were decapitated and blood samples were collected from the trunk. Serum GH and prolactin were determined by radioimmunoassays. The intraventricular GABA elicited a significant increase in both serum GH and prolactin levels. Intraventricular substance P itself had no effect on serum GH and prolactin, but it inhibited the GABA-induced increases in serum GH and prolactin. Gamma-hydroxybutyric acid (GHB) was intraperitoneally injected with and without an intraventricular injection of substance P in urethane anesthetized rats. The GHB injection significantly increased serum GH and prolactin levels. Pretreatment with substance P completely inhibited the GHB-induced GH and prolactin responses. These results suggest that substance P might interact with GABA in the central nervous system.

Factor (s) Controlling the Secretion of Adrenocorticotropin (ACTH) in Peripheral Plasma

The factor(s) controlling the secretion of ACTH in peripheral plasma are not well known. The effects of non-extracted and extracted plasma on ACTH secretion were investigated using rat anterior pituitary cell cultures. Medium ACTH was assayed by radioimmunoassay, and the corticotropin releasing activity (CRA) was expressed as ACTH released. One hundred ul of non-extracted plasma showed significant CRA, whereas greater volumes of plasma showed reduced activity. Non-extracted plasma (250 approximately 500 microliter) rather reduced the secretion of ACTH evoked by hypothalamic extract (HE). When plasma was extracted with 0.2 N-acetic acid-acetone and divided into an acid phase and an acetone-ether phase by adding ether, the CRA was recovered in the acid phase while no significant activity was observed in the acetone-ether phase. The acid phase extract of plasma showed a positive dose-response relationship between the amount of plasma extract (50 approximately 800 microliter plasma equivalent) and ACTH release in pituitary cell cultures. The organic phase of plasma extract inhibited HE-induced release of ACTH, and this ACTH-release inhibiting activity was presumed to be corticosterone. When the acid phase extract of 20 ml plasma was applied to a Sephadex G-25 (fine) and eluted with 0.2 N acetic acid, two peaks of CRA were observed. One eluted in the region of void volume and another eluted in the retarded region where no activity was found in chromatography of HE. HE increased both ACTH and cyclic AMP release, but the plasma extract reduced cyclic AMP release. These results suggest that plasma contains both CRA and ACTH release inhibiting activity which can be extracted separately, and that plasma CRA is different from the hypothalamic corticotropin releasing factor.