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S H Shin

Publications and source records attributed to S H Shin.

At least 127 records · Page 7Linked to original sources

Effect of ergocristine on prolactin secretion in the male rat with pituitaries grafted beneath the kidney capsule.

Male rats in which three pituitaries were grafted beneath the kidney capsule showed approximately a fourfold increase in circulating plasma prolactin concentration. The elevated plasma prolactin concentration did not remain at a constant level but fluctuated with time. The elevated prolactin concentration declined immediately after a single bolus injection of ergocristine (30 micrograms/kg). The slope of the prolactin decay curve, determined by sequential blood sampling, was parallel to a theoretical slope having a 7-min half-life. This result indicates that ergocristine blocked prolactin secretion immediately and completely as the decay curve (T 1/2 = 6.5 min, confidence interval 4.5--11.3) resulting from the administration of ergocristine is the same as the endogenous prolactin decay curve (T 1/2 = 7 min).

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Unsuppressed prolactin secretion in the male rat is pulsatile.

The pattern of prolactin (Prl) secretion was studied in several different situations. In normal and castrated male rats, the plasma Prl level gently fluctuated along the course of time. When the presumed hypothalamic Prl inhibitory factor was suppressed by treatment with a pharmacological agent, pimozide (Pim), the plasma Prl concentration was elevated and the elevated plasma level fluctuated in an irregular and pulsatile manner. Another situation was examined. First, baseline Prl concentration was elevated by implantation of estradiol, which also caused a moderate fluctuation of the circulating Prl level. The Prl level was then lowered from the elevated plateau level by administration of a dopaminergic receptor agonist, ergocristine. During this partial blockade, the plasma Prl level fluctuated in episodic bursts. It is suggested that the inherent, unsuppressed secretion of Prl is pulsatile in nature, but that this pulsatile pattern is normally suppressed under the inhibiting influence of the hypothalamus.

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Estradiol generates pulses of prolactin secretion in castrated male rats.

Unrestrained, freely moving rats implanted with an atrial indwelling cannula were used to inject estradiol and to take blood samples. The effect of estradiol on prolactin secretion was monitored by taking blood samples every 2 min. When a single bolus of estradiol (100 micrograms/kg) was injected, no response was seen for approximately 2 h. There then followed a pulsatile pattern of plasma prolactin and this lasted more than 24 h. The elevation of the prolactin concentration was not accomplished by a gradual change but through frequent pulsatile bursts of secretion. The major slopes of the decay curves of these bursts, plotted on a semilogarithmic scale, were parallel to a theoretical curve with a slope of 7 min half-life. Such consistency of decay slopes indicates that prolactin secretion is accomplished through discrete bursts of secretion.

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The effect of exposure to ether on prolactin secretion and the half-life of endogenous prolactin in normal and castrated male rats.

Normal and castrated male rats implanted with permanent right atrial cannulae were used, and sequential blood samples were taken every 2 min through the cannula. When the rats, both normal and castrated, were exposed to ether for 2 min, the prolactin (Prl) concentration in plasma was immediately and dramatically elevated. During 40 min of continuous ether anesthesia, plasma Prl concentration was not sustained. After the initial 'surge' of Prl secretion, which lasted about 15 min, the concentration returned to normal levels. Following the peak of the Prl 'surge', Prl disappeared from the circulation with a calculated half-life of 7 min (mean value: 6.9 min; confidence interval: 6.3-7.7).

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Evidence for the existence of LH-RH binding protein.

LH-RH in rat hypothalamic extract (HE) emerges in 2 peaks after gel filtration on Sephadex G-25 with pyridine acetate buffer (PAB), pH 5.8, 1 peak in the unretarded protein fraction and the other near the salt region. A synthetic LH-RH marker was found only in the peak near the salt region by elution with acid. Using a dialysis technique, a protein fraction, from which LH-RH and other small molecular weight material were dissociated by gel filtration on Sephadex G-25 with acid, showed affinity for synthetic LH-RH. Synthetic LH-RH in the hypothalamic protein solution was retained in the dialysis bags more effectively than other types of protein solutions. This binding protein is of relatively small molecular size according to gel filtration behavior on Sephadex G-75. Since the dialysis experiment showed extremely poor recovery of total LH-RH, we determined the rate of loss of LH-RH under several conditions. The rate of disappearance was significantly less in solutions containing protein derived from cerebellum and hypothalamus, compared to bovine serum albumin (BSA) solution or salt solution. The ability of the hypothalamic protein to retard the rate of disappearance of LH-RH is further evidence for a special affinity between LH-RH and the protein factor. It is concluded that the protein LH-RH complex is dissociated by lowering the pH and that the dissociated protein and synthetic LH-RH can be re-associated to form a protein-hormone (PrH) complex at neutral pH.

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Effect of testosterone on hypothalamic LH-RH content.

Hypothalamic LH-RH content in male rats is lowered after castration. The s.c. implantation of testosterone or testosterone propionate-packed Silastic tubing (from 0.5 to 6 cm in length) in a range which encompassed the normal circulating plasma testosterone concentration, prevented this lowered LH-RH content 21 days following castration and simultaneous implantation. The temporal response to implanted testosterone was then studied: rats were killed 1,2,4,8,14 and 21 days after castration and simultaneous implantation of 3 cm testosterone-packed Silastic tubing. The hypothalamic LH-RH content began to decrease in the castrated group after 4 days and fell progressively thereafter. However, the hypothalamic LH-RH content of the castrated group maintained with constant levels of testosterone showed no such reduction at any time following castration. These experiments indicate that circulating testosterone in physiological concentrations can maintain a normal hypothalamic LH-RH content and demonstrate an action of testosterone, in physiological concentrations, in the feedback regulation of LH-RH secretion.

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Generation of hypophysiotropic activity in hypothalamic extracts in vitro.

The luteinizing hormone (LH) and follicle stimulating hormone (FSH) releasing activity, as well as the prolactin (PRL) release-inhibiting activity were measured in both neutral aqueous, and acid ethanolic extracts of rat hypothalami. LH and FSH-releasing activities were detectable only in the latter type of extract, whereas PRL release-inhibiting activity appeared in both. Neutral ultrafiltrates of the neutral extracts contained no gonadotropin releasing activity, however, acidification of the filtration medium induced its appearance. PRL release was inhibited by both neutral and acid filtrates. These results suggest that LH and FSH releasing factor(s) may be stored in the hypothalamus in an inactive form from which the active peptide is generated in vitro under acid conditions; however, this does not appear to be true for the component(s) responsible for the inhibition of PRL release.

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