Endocrinologia experimentalis最新文献

The medial basal hypothalamic (MBH) tissues were taken from rat fetuses at day 17-18 of gestation and transplanted into the third ventricle of adult female rats. 2.5 S mouse nerve growth factor (NGF) was infused into the third ventricle of some hosts for 2 weeks using a mini-osmotic pump. The other hosts were implanted silastic capsules containing estradiol. Three weeks after the operation, the transplants were immunocytochemically stained with anti-tyrosine hydroxylase (TH) antibody. A number of immunoreactive neurons was obtained in all of NGF-treated, estrogen-exposed and control transplants. Immunoreactive axons distributed densely in NGF-treated transplants. However, the distribution of immunoreactive axons was less dense in estrogen-exposed and control MBH transplants. These results suggest that NGF infused into the host ventricle stimulates the growth and/or regeneration of axons of hypothalamic neurons. In contrast, action of estrogen on transplanted hypothalamic tissues was not evident in the present study.

Dopamine has a catechol group which can be easily oxidized by mild oxidizing agents. Ascorbic acid has been routinely added to a dopamine solution in order to protect it from oxidation. We have examined the effect of ascorbic acid on dopaminergic inhibition of prolactin release. Male rat pituitary cells were dispersed using trypsin and cultured for 5-7 days before experiments. Ascorbic acid did not stimulate nor inhibit prolactin release in both static monolayer culture and dynamic perifusion systems, but potentiated by approximately 100 times the inhibitory effect of dopamine on prolactin release. In order to differentiate chemical protection from potentiation, we tested the potentiation effect of isoascorbic acid which is an epimer of biologically active L-ascorbic acid but is biologically less active. Our results indicated that isoascorbic acid caused less potentiation of the dopaminergic effect on prolactin release than did ascorbic acid. In a perifusion system, a high concentration of dopamine (100 nmol/l) was unable to inhibit prolactin release for a 1 h experimental period, but a low concentration of dopamine (10 nmol/l) plus ascorbic acid (10 mumol/l) inhibited prolactin release for the entire 1 h perifusion period. There is a strong possibility that ascorbic acid may be a physiological supplementary agent for the prolactin-release inhibiting factor (PIF) since the blood concentration of ascorbic acid is rather high (23-85 mumol/l).

Changes in peripheral clinico-chemical parameters (packed cell volume (PCV), hemoglobin (HGB), serum glucose, carbamide nitrogen (CN), sodium, uric acid and creatinine) were investigated in mice during the development of acute morphine tolerance. Acute morphine treatment (in drug-naive organism) altered the PCV, HGB, serum glucose and CN levels in a naloxone-reversible manner. Acute tolerance developed in PVC, HGB, sodium and CN values. The data raise the possibility of a relationship between clinico-chemical and pharmacological tolerance.

Continuous exposure to foster pups elicits specific behavioural patterns in adult naive female or male rats. The first exposure induces active avoidance of young. By day 2 or 3 adults show neutral behaviour. Next day complete maternal behaviour begins to develop; e.g. retrieving of pups, nursing and crouching. The avoidance reaction activates stress mechanisms, and the developed maternal behaviour is associated with moderate prolactin release. The question is raised whether pup-induced catecholamine and prolactin release is able to alter enzyme activity in T-cells. Using Arg-Pro-; Leu-Pro; and Pro-Pro-4-nitroanilide as substrates the activity of a marker enzyme dipeptidyl peptidase IV, DP IV, EC. 3.4.14.5., was measured in T-cell suspension prepared from the thymi of adrenalectomized female and male Wistar rats. We found that changes of DP IV activity during the pup-induced avoidance phase could be prevented by propranolol pretreatment indicating the role of catecholamines in this phenomenon. Prolactin released during artificial maternal behaviour in female rats resulted in an elevation of DP IV activity which failed to develop, if they were given daily injections of bromocriptine or apomorphine. It is concluded that pup-exposure is the most physiological way to influence hormonal mechanisms and immune functions, which are highly responsive to sensory stimuli.

The effect of chronic administration of SMS 201-995, a long acting analogue of somatostatin, has been studied in 30 acromegalic patients (pts). CT-scan showed pituitary adenoma in 20/30 pts, empty sella in 9/30 pts and no sign of pituitary tumor in one case. SMS 201-995 was administered subcutaneously every 8 hours at the daily dose of 150-900 micrograms. Blood samples for GH, insulin and blood glucose were taken hourly from 04:00 to 20:00 h before treatment, after 15 days and then monthly or fortnightly. IGF-I plasma levels were assayed at 08:00 h in the same day as GH determinations. CT-scan controls were carried out after 12-24 months of treatment in 16/20 pts. GH plasma levels were normalized in 16/30 pts after 0.5-9 months of SMS treatment, whereas in 14/30 pts they were reduced by about 50%. In 10/16 pts the CT-scan examination showed a shrinkage of the tumor size of 20-55%, while no variation of the tumor mass was observed in the 2 pts. In conclusion our data show that SMS 201-995 is a very effective medical treatment in acromegalic patients.

A long-lasting decrease of the basal and stress-induced arterial blood pressure was obtained in rats with inherited emotional stress-induced hypertension by means of injections of the dopamine precursor L-DOPA during early postnatal ontogeny (21-25 days of the life). "Permanent" hypotensive effect of L-DOPA was caused by the elevation of the brain but not peripheral catecholamine levels and was not related to a stimulation of the hypothalamic-pituitary-adrenocortical system in response to administration of the dopamine precursor. The restoring effect of L-DOPA was produced through enhancement of synthesis of the brain noradrenaline and, perhaps, adrenaline. The effect was associated with a normalization of the response of the brain adrenergic system to noradrenaline.

The effects of cholinergic muscarinic receptor antagonist pirenzepine on the GHRH-induced GH release were studied in 10 adolescent females with anorexia nervosa at different stages of the disease, in 5 adolescent females with eating disorders and in 5 normal adolescents. The patients were characterized according to psychological (DSM III-R), endocrinological (GnRH test), nutritional (Somatomedin-C, T3), and clinical (% IBW, duration of the amenorrhoea) criteria. On two separate occasions, each subject received an i.v. bolus injection of GHRH 1-40 (1 microgram/kg) alone or preceded by pirenzepine (0.6 mg/kg i.v. 5 min before GHRH 1-40). GHRH 1-40 injection induced a significantly (P less than 0.05) higher GH increase in the patients with anorexia nervosa at the acute stage as compared with the controls. Pirenzepine did not abolish opportunely the exaggerated GH response to GHRH 1-40 in anorectic patients at the acute stage unlike the control, who showed the blockade of GHRH-induced GH release by the cholinergic muscarinic antagonist (P less than 0.05). The anorectic adolescents at the non acute stage and the adolescents with eating disorders showed varying reductions of GH response; however, pirenzepine produced a blunted suppression of GHRH-induced GH increase as compared to the controls, which was not statistically significant. Somatomedin-C values were significantly (P less than 0.05) lower in anorectic patients at the acute stage as compared with controls. The abnormal activity of cholinergic system in anorectic patients, as our data show, could induce the GH hypersecretion through an inhibitory influence on the somatostatinergic function. The reduced somatomedin-C levels, a specific malnutrition index in anorectic patients, produce a modified feed-back on the hypothalamic site (somatostatin) and/or directly on the pituitary, following the GH hypersecretion.

The adrenergic system is involved in the neural control of GH secretion with both stimulatory and inhibitory influences mainly mediated via GHRH and/or somatostatin modulation. To throw further light on adrenergic neuroregulation of somatotrophic function in man, the effect of various catecholamine agonists and antagonists on basal or GHRH-stimulated GH secretion was studied. Twenty-one adult males aged 20-30 years underwent the following studies: 1. clonidine (CLON), alpha 2-agonist, (15 micrograms/min infused i.v. from 0 to +10 min) alone and preceded by yohimbine (YOH), alpha 2-antagonist, (30 mg orally at -50 min); 2. GHRH (GHRH 44, 1 microgram/kg i.v. bolus at 0 min) alone and preceded by YOH; 3. CLON alone and combined with methoxamine (METHOX), alpha 1-agonist, (1 mg/min infused i.v. from -10 to +10 min); 4. GHRH alone and combined with i.v. infusion of phentolamine (PHEN), alpha 1/alpha 2-antagonist, (0.5 mg/min from -60 to +30 min); 5. GHRH alone and combined with i.v. infusion of salbutamol (SAL), beta 2-agonist, (10 micrograms/min from -5 to +15 min). The GH response to CLON was inhibited by YOH (area under the response curve, mean +/- S.E.: 672.6 +/- 143.0 vs. 219.6 +/- 16.7 micrograms/l/h, P less than 0.05) but was not modified by METHOX (278.4 +/- 94.1 vs. 216.7 +/- 115.5 micrograms/l/h). On the other hand, YOH was unable to affect the GH response to GHRH (339.3 +/- 19.1 vs. 518 +/- 172.8 micrograms/l/h).(ABSTRACT TRUNCATED AT 250 WORDS)

Studies were undertaken to compare and contrast the effects of the vasoactive peptides, angiotensins II and III, bradykinin and endothelin, on mobilization of intracellular calcium in isolated, cultured bovine adrenal medullary (chromaffin) cells. Calcium mobilization was studied using the Fura-2 technique. The potency for elevating intracellular calcium, compared on a molar basis, was bradykinin greater than angiotensin III greater than angiotensin II much greater than endothelin. When nicotine and angiotensin II were added together, a synergism was evident with prolonged elevation of intracellular calcium. However, concomitant addition of angiotensin II and endothelin was barely additive. Yet, combined addition of endothelin and depolarizing potassium chloride yielded a very marked synergism in calcium mobilization. We conclude that the multiplicity of vasoactive peptide receptors on chromaffin cells exert interactive modulation on calcium mobilization in these cells and this property may have functional significance.

The response of TSH, PRL, LH and FSH to combined test with LHRH (Relefact LH-RH, HOECHST; 0.1 mg) and TRH (Relefact TRH, HOECHST; 0.2 mg) was examined before (day I) and after naloxone (Narcanti, DUPONT) bolus of 0.8 mg (day III) in 8 patients with polycystic ovary syndrome (POC) diagnosed by established criteria (hirsutism, oligoamenorrhoea, ultrasound appearance of polycystic ovary and serum LH/FSH greater than 2.0). TSH (RIA-INEP), PRL (MAIA-SERONO), LH (MAIA-SERONO) and FSH (MAIA-SERONO) were determined at -15, 0, 10, 20, 30, 45, 60, 90 and 120 min. The hormone responses were calculated as the areas under hormone curves and tested with Wilcoxon sum rank test. No significant difference was found in the hormone responses before and after naloxone injection. In terms of absolute values lower TSH level was found at 30 min after naloxone administration (14.7 +/- 12.0 vs. 9.73 +/- 7.61; P less than 0.05). In conclusion, our data based on short term naloxone application argue against the significant alteration of the opioid activity in patients with POC.