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R J Krieg

Publications and source records attributed to R J Krieg.

77 records · Page 5Linked to original sources

Luteinizing hormone secretion by male rat pituitary cells perifused in vitro: effect of experimental left varicocele and orchiectomy.

It has been shown previously that experimental left varicocele in the rat, results in a bilateral decrease in intratesticular testosterone. In the present work, pituitary responsiveness to GnRH as a possible mediator of this effect has been examined. Unilateral varicoceles were created in adult rats. A second group of animals underwent a sham operation and a third underwent bilateral orchiectomy. Thirty days after surgery, rats from all three groups were sacrificed and their pituitaries were removed. Dispersed pituitary cells were perifused in Bio-Gel columns with varying concentrations of GnRH. The concentration of LH in the collected eluent was determined by radioimmunoassay. The mean, overall GnRH-stimulated LH immunoreactive secretion rate (ng/min/10(7) cells) by pituitary cells from rats with varicocele (0.062 +/- 0.11) was no different from the overall release from the sham-operated controls (0.051 +/- 0.007). The dose-response curves for GnRH-stimulated release of LH by dispersed pituitary cells in the two groups also were not different. The overall GnRH-stimulated LH release by cells from the orchiectomized rats (0.171 +/- 0.032) was significantly greater than release by cells from the sham-operated and varicocele rats, and the concentration-response curve from the orchiectomy group was significantly elevated over those of the other two groups. These results indicate that GnRH-stimulated immunoreactive LH release is not altered in rats with experimental left varicocele and, thus, is not the source of an endocrinopathy that leads to decreased intratesticular testosterone concentrations in these animals.

Animals↗

Norepinephrine stimulates LH-RH secretion into the hypophysial portal blood of the rat.

The present study was designed to investigate the effect of intracerebroventricular infusion of norepinephrine (NE) on the secretion of luteinizing hormone-releasing hormone (LH-RH) into the hypophysial portal blood of steroid-primed ovariectomized rats. Saline infusion into the third ventricle caused no significant change in LH-RH levels. NE infusion (20 micrograms) resulted in a significant release of LH-RH (p less than 0.05) into the portal blood 10-30 min later. This endogenous LH-RH was similar to synthetic LH-RH when characterized by thin-layer chromatography. LH secretion in similarly treated rats but with intact portal vessels, also was significantly elevated (p less than 0.05) at 20 and 40 min after the start of NE infusion. These results show that NE stimulated the secretion of LH-RH into the hypophysial portal blood and this correlated with an enhanced release of LH.

Animals↗

Pathophysiology of growth retardation in chronic renal failure.

Data concerning the transcription of growth hormone and the various interactions between growth hormone/insulin-like growth factor (IGF) axis in uremia, acidosis and nutrition are presented. The recent evidence of tissue resistance to growth hormone in uremia provided the medical rationale for the use of growth hormone in chronic renal failure. The growth hormone receptor resistance in uremia and the decreased IGF-I by acidosis are additional rationale for the use of growth hormone. New findings of how acidosis causes the reduction of IGF-I expression at the growth plate of the long bone and the significant proteolysis after even small changes in serum bicarbonate content are presented to provide the pediatrician with an overview of these recent advances.

Acidosis↗