Margaret Sweetland

Effect of Short-Term Castration and Starvation upon Hypothalamic Content of Luteinizing Hormone-Releasing Hormone in Adult Male Rats

Summary A sensitive and specific radio-immunoassay for hypothalamic LH-RH has been described. Within 7 days after castration there is a significant decline in hypothalamic content of LH-RH in adult male rats. Total starvation for 7 days does not affect hypothalamic content of LH-RH in either intact or castrated rats. The authors thank the Hormone Distribution Officer, NIAMDD, for reagents for the radioimmuno-assay of rat LH and rat FSH. They also thank Mrs. E. Morris for secretarial assistance.

Effects of drug and alcohol abuse upon pituitary-testicular function in adolescent males

To assess the effects of drug and alcohol abuse (DAA) on the physical changes and hormones of puberty in adolescents, 26 males (13 5/12-22 years) enrolled in a drug rehabilitation program were examined. In 22 subjects four timed blood samples were obtained sequentially at 15 minute intervals for measurement of serum concentrations of testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH) and dehydroepiandrosterone sulfate (DHAS). The mean duration of DAA was 3.7 years, with marijuana and alcohol being the most frequently abused substances. The study subjects were compared to a matched control group of non-substance-abusing teenagers. All heights and weights of the DAA subjects fell within two standard deviations of the mean on the Tanner Growth Charts and no statically significant differences in the Tanner stages of sexual maturation were found between the DAA and control groups. The mean (+/- SD) testosterone level of the DAA group (221 +/- 109 ng/dl) was less than half that of the control group (477 +/- 193 ng/dl, p less than 0.001). Mean LH concentration in the DAA group (3.9 +/- 3.0 mIU/ml) was significantly less than that of the control group (10 +/- 4.9 mIU/ml, p less than 0.01). In both the DAA and control populations there was a significant (p less than 0.01) correlation between serum concentrations of LH and testosterone. The mean FSH level of the DAA group (3.3 +/- 1.1 mIU/ml) was significantly less (p less than 0.02) than that of the control group (4.7 +/- 1.9 mIU/ml). To assess the effects of treatment, six boys underwent repeat blood sampling 7-12 months after drug and alcohol withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Clonidine Upon Anterior Pituitary Function and Plasma Catecholamine Concentrations in Short Children and Adolescents

The effects of the alpha-adrenergic agonist Clonidine (0.15 mg/m p.o.) upon serum concentrations of growth hormone (GH), Cortisol and prolactin (PRL) were determined in 50 children and adolescents with short stature in order to determine the efficacy of this agent in the evaluation of anterior pituitary function. Two groups of short children were studied: Group I — children with constitutional delay in growth and sexual development or genetic short stature; Group II — children with GH deficiency as defined by subnormal GH secretory responses to insulin hypoglycemia, L-dopa and/or arginine. The peak GH secretory response to Clonidine (22.5 ± 2.1 ng/mL, mean ± SEM) in 28 non-GH-deficient short subjects (Group I) was greater than those recorded after sequential insulin-L-dopa (12.6 ± 1 . 0 ng/mL) or insulin-arginine (15.5 ± 2.2 ng/mL) administration. GH concentrations did not significantly increase after any provocative agent in 22 GH-deficient subjects (Group II). Mean Cortisol concentrations in Group I declined from 13.8 ± 1.0 to 6.0 ± 0.7 ug/dL at 90 minutes (p < 0.01) and returned nearly to basal levels by 180 minutes after Clonidine ingestion. Mean Cortisol concentrations in Group II declined from 11.3 ± 1.4 to 5.9 ± 0.9 ug/dL at 90 minutes (p < 0.05) and also returned to basal levels by 180 minutes. Mean basal PRL levels declined significantly in Group I (11.8 ± 1.7 to 6.7 ±1.0 ng/mL; ρ < 0.01) by 60 minutes and returned to

493 EFFECTS OF HUMAN PANCREATIC GROWTH HORMONE RELEASING HORMONE (HPGRH) ON GROWTH HORMONE (GH) SECRETION IN PREGNANT AND FETAL RATS

Pregnant Holtzman rats were studied at 19 and 20 days gestation. Animals were anesthetized at -30 min with pentobarbitol 60 mg/kg IP. 5 ug HPGRH 1–44 or normal saline was administered IV at 0 min. Blood for maternal GH measurement was obtained via cardiac puncture at 0 min and following decapitation at 11 min. Fetuses were removed by C-section between 7 and 11 min and cardiac blood from littermates pooled for a single fetal GH determination. *x±SD **ng/mlMean maternal GH levels rose significantly (p < 0.005) in animals receiving HPGRH and were unchanged in those receiving saline. Mean fetal GH levels were significantly greater (p < 0.005) at 20 vs 19 days gestation. There were no significant differences between mean fetal GH concentrations of mothers receiving HPGRH and those receiving saline. HPGRH increases GH concentrations in the pregnant rat. HPGRH administration to the pregnant rat during late gestation does not increase GH concentrations in the fetus suggesting either that HPGRH does not cross the rat placenta or that the fetal rat pituitary is insensitive to HPGRH at this dosage.

HYPOTHYROIDISM BLUNTS THE GROWTH HORMONE |[lpar]|GH|[rpar]| RELEASING EFFECT OF HUMAN PANCREATIC GROWTH HOROMONE-RELEASING FACTOR |[lpar]|hpGRF|[rpar]| IN THE ADULT MALE RAT

The 44 amino acid peptide hpGRF (Bachem) was administered to 300 gram male control or hypothyroid rats under pentobarbital anesthesia. In euthyroid animals (T4=5.0±1.9(SD) ug/dl), intravenous bolus injection of 1.0 ug of hpGRF (N=4) increased serum concentrations of rat GH from 157±95 to a peak of 1871±1458 ng/ml (p<0.01 vs base) within 5-10 minutes. At a dosage of 10 ug (N=5) hpGRF increased rGH levels in control animals from 213±95 to a peak of 3123±923 ng/ml (p<0.01 vs base) in 5-15 minutes. In rats rendered hypothyroid by the ingestion of 0.05% propylthiouracil in drinking water for 21 days (T4-0.6±0.1 ug/dl, p<0.01 vs control) 1.0 ug of hpGRF (N=8) increased rGH concentrations from 39±24 to a peak of 79±37 ng/ml (p<0.01 vs base) in 5-30 minutes, while 10 ug of hpGRF (N=7) increased rGH values from 42±26 to a peak of 99±47 ng/ml (p<0.01 vs base) in 5 to 15 minutes. Basl and post hpGRF rGH concentrations were significantly (p<0.01) higher in control than in hypothyroid animals. We conclude that primary hypothyroidism blunts the GH-releasing effect of hpGRF in male rats in vivo.