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Biomedical subjects

G Delitala

Publications and source records attributed to G Delitala.

At least 73 records · Page 4Linked to original sources
PubMed1983

Cholinergic receptor control mechanisms for L-dopa, apomorphine, and clonidine-induced growth hormone secretion in man.

The effect of pirenzepine, an anticholinergic agent, on GH release induced by L-dopa (500 mg po), apomorphine (0.75 mg sc), and clonidine (0.150 mg iv) administration was studied in a group of normal men. Pirenzepine, a cholinergic muscarinic antagonist, completely blocked the GH rise induced by dopamine- and adreno-receptor stimulation. In contrast, the PRL-inhibiting action of L-dopa was not modified by the cholinergic antagonist. The data suggest that acetylcholine and its receptors are important regulators of the neurosecretory mechanisms that control GH secretion in man.

Adult↗
PubMed1983

Participation of endogenous opiates in regulation of the hypothalamic-pituitary-testicular axis in normal men.

To assess the influence of endogenous opioids on human gonadotropin secretion, integrated concentrations of gonadotropins during 24-h naloxone infusion (2.08 mg/h) were examined in a group of six normal men. Naloxone significantly stimulated LH secretion in all subjects, whereas serum FSH levels were similar during both saline and naloxone infusion. Serum testosterone, dihydrotestosterone, and 17 alpha-hydroxyprogesterone levels increased during the infusion of naloxone, but the delta 4-androstenedione concentration was not modified. The frequency and amplitude of LH secretory episodes were clearly increased when an equal amount of the drug was given and LH concentrations were measured every 15 min for 6 h. The results suggest the endogenous opioids inhibit the hypothalamic-pituitary-gonadal axis in normal men.

17-alpha-Hydroxyprogesterone↗
PubMed1982

Effects of the H2 receptor antagonist ranitidine on anterior pituitary hormone secretion in man.

The effect of an i.v. bolus of the H2-receptor antagonist ranitidine 50, 100, 200 and 300 mg on serum levels of prolactin, TSH, GH, LH, FSH and cortisol was studied in 12 normal males. Ranitidine 200 and 300 mg significantly stimulated prolactin release without affecting any of the other hormones. Ranitidine 300 mg caused a rise in prolactin comparable to that observed following cimetidine 200 mg. The results show that ranitidine releases prolactin in man, but only when a large intravenous injection is given.

Adult↗
PubMed1982

Participation of cholinergic muscarinic receptors in glucagon- and arginine-mediated growth hormone secretion in man.

To investigate the participation of cholinergic receptors in glucagon- and arginine-induced GH and PRL secretion, glucagon (1 mg, sc) and arginine (30 mg over 30 min) were administered to a group of normal subjects. On a different occasion, both tests were repeated after premedication with 40 mg pirenzepine, a muscarinic blocker, given iv 5 min before the test substances. Pirenzepine completely suppressed the glucagon- and arginine-induced GH rise in all subjects. The PRL response to arginine was not altered by pirenzepine. The results suggest that cholinergic muscarinic receptors regulate the GH response to glucagon and arginine in man.

Adult↗
PubMed1982

Growth hormone, prolactin and cortisol nyctohemeral variations during naloxone-induced opiate receptor blockade in man.

To evaluate the role of endogenous opioid peptides in prolactin (Prl), growth hormone (GH) and cortisol neuroregulation, 50 mg of the opiate antagonist naloxone was infused over 24 h to 6 normal male volunteers. An additional naloxone dose (5 mg) was given iv as a bolus injection at 20.00 h. blood specimens were collected hourly by means of a portable constant withdrawal pump. Naloxone failed to alter 24 h secretion of GH and Prl. The sleep-related GH and Prl rise was also unaffected by the opiate blocker. Moreover, naloxone failed to alter the circadian rhythm of cortisol and its 24 h concentration. The results do not suggest, a major role of opiate receptors in spontaneous GH, Prl and cortisol secretion in man.

Adult↗
PubMed1981

The opioid control of LH and FSH release: effects of a met-enkephalin analogue and naloxone.

The effect of long-acting analogue of met-enkephalin (DAMME) and naloxone on gonadotrophin secretion has been investigated in man. In menopausal women DAMME induced a progressive fall in LH to approximately 60% of basal levels at 3 h, which was blocked by naloxone; there was a smaller fall in FSH that did not attain statistical significance. However, the LHRH-induced rise in LH and FSH in young male volunteers was unaffected by pretreatment with a high-dose DAMME infusion. Naloxone infusion in young male and female normal subjects produced a significant rise in both LH and FSH. Long-term infusion of naloxone appeared to increase the rate, and possibly the amplitude, of LH pulsatility. These results suggest that met-enkephalin-like opioid peptides exert a tonic inhibitory control of LH release in both menopausal and young subjects of both sexes. This control is most likely to be at the level of the hypothalamus, and involves modulation of pulsatile LHRH release.

Adolescent↗
PubMed1981

Studies off the opiate control of prolactin, GH and TSH.

Opiate peptides are known to influence the secretion of several anterior pituitary hormones under basal conditions. Further studies on prolactin, GH and TSH have therefore been performed in normal subjects, under basal and stimulated conditions, using an opiate agonist and antagonist. Sixteen mg naloxone had no effect on the basal release of prolactin or GH, but lowered TSH. An infusion of the met-enkephalin analogue DAMME (1 mg) increased GH, and produced an exaggerated response of both prolactin and TSH to 200 micrograms TRH i.v. The peak responses of both prolactin and GH to hypoglycaemia were unaffected by pretreatment with either low-dose (0.4 mg) or high-dose (25 mg) naloxone, or DAMME (0.25 mg). These results suggest that opiate peptides are unlikely to play a major role in the tonic or hypoglycaemia-stimulated release of prolactin and GH, although they may be of importance in the control of TSH.

Adolescent↗
PubMed1981

GABA and muscimol inhibit the release of prolactin from dispersed rat anterior pituitary cells.

Prolactin release from columns of dispersed rat anterior pituitary cells was inhibited by GABA and the GABA agonist muscimol. The log dose-response curves for GABA and muscimol appeared to be parallel, but were not parallel to that for dopamine. Two GABA antagonists, bicuculline and picrotoxin, blocked the action of both GABA and muscimol, but the dopamine antagonists metoclopramide and perphenazine did not. The data suggest that there are specific GABA receptors on pituitary lactotrophs.

Animals↗
PubMed1981

Effects of a Met-enkephalin analogue and naloxone infusion on anterior pituitary hormone secretion in acromegaly.

The effect of a long-acting analogue of Met-enkephalin (Damme) and naloxone on anterior pituitary hormone secretion has been investigated in 14 acromegalic patients. Damme produced a progressive fall in circulating LH and cortisol and stimulated prolactin release in normoprolactinaemic patients. Naloxone infusion significantly stimulated gonadotrophin and cortisol secretion without modifying basal prolactin release both in normo-and hyperprolactinamic patients. GH levels remained unchanged during naloxone and Damme infusion. The data suggest that endogenous opiate receptors do not play a major role in modulating GH hypersecretion in acromegaly.

Acromegaly↗
PubMed1981

Opiate receptors and anterior pituitary hormone secretion in man. Effect of naloxone infusion.

The role of endogenous opioid receptors on anterior pituitary hormone secretion was evaluated by the administration of the opioid receptor antagonist naloxone. The infusion of naloxone (8 mg iv followed by 4mg/h for 3 h) did not alter basal growth hormone (GH), prolactin (Prl) and thyrotrophin (TSH) secretion but produced a significant rise in cortisol and gonadotrophins in normal man. The infusion of the opiate antagonist appeared to increase the rate and amplitude of luteinizing hormone (LH) pulsatility. Naloxone pre-medication (10 mg iv 30 min before testing) did not alter the pituitary response to TRH and LRH stimulation. These results demonstrate that naloxone can modify basal anterior pituitary hormone secretion and strongly suggest an endogenous opioid modulation of some of these hormones.

Adult↗
PubMed1981

On the role of dopamine receptors in the central regulation of human TSH.

The effects of acute administration of haloperidol (4 mg im) and pimozide (4 mg orally) on TSH and Prl secretion were studied in normal and hypothyroid man. The TRH-induced TSH secretion before and after pre-medication with pimozide and domperidone, a peripheral dopamine (DA) blocker, was also evaluated in a group of normal subjects. Haloperidol and pimozide induced a marked increment in serum Prl; mean Prl levels were still significantly elevated 12 h following pimozide administration. A small but significant TSH increase was observed following haloperidol and pimozide in normal as well as hypothyroid subjects. Both domperidone and pimozide significantly enhanced TRH-induced TSH release. In another experiment 3 women with primary thyroid failure received an infusion of DA (4 micrograms/kg/min for 4 h) with and without domperidone administration. TSH and Prl levels were suppressed by DA, but the effect was completely abolished by domperidone. The results suggest that psychotrophic drugs, such as haloperidol and pimozide, can, like substituted benzamides, stimulate TSH release in man. Since domperidone and DA do not cross the blood-brain-barrier and domperidone significantly enhanced the TSH response to TRH, the data also support the hypothesis that human TSH is regulated by DA at the hypothalamus (median eminence) and/or pituitary level.

Adult↗
PubMed1981

In vitro studies on the effects of ranitidine on isolated anterior pituitary and adrenal cells.

The effects of ranitidine on anterior pituitary and adrenal function have been studied using isolated perfused rat anterior pituitary and zona glomerulosa cells. Ranitidine did not have pituitary hormone releasing activity with respect to LH, TSH, GH and ACTH. It also did not alter prolactin secretion in experiments designed to test whether it acted as a dopamine agonist or antagonist. In the adrenal cell studies ranitidine infusion stimulated basal aldosterone secretion and inhibited the release of aldosterone in response to angiotensin II, but not to ACTH. These experiments suggest that ranitidine is unlikely to alter pituitary hormone secretion by a direct action on the pituitary. The drug, however, can affect aldosterone secretion in vitro and further in vivo studies are required to elucidate the significance of this.

Adrenal Cortex↗
PubMed1980

Inhibition of prolactin secretion by nomifensine in man.

Serum prolactin, TSH and GH levels were measured in thirty healthy volunteers in fasting conditions and following oral administration of 200 mg nomifensine. In addition, the effect of the drug on serum prolactin and TSH response to synthetic TRH was studied in twenty normal subjects. Inhibition of endogenous catecholamine reuptake by nomifensine significantly inhibited prolactin release whereas it had no effect on TSH and GH levels. Nomifensine administration had no appreciable effect on the TRH-induced release of TSH and prolactin.

Adult↗
PubMed1980

TSH and prolactin stimulation by the decarboxylase inhibitor benserazide in primary hypothyroidism.

200 mg of the 4-aromatic amino acid decarboxylase inhibitor benserazide were administered orally to five patients with primary hypothyroidism. Benserazide induced a significant increase in prolactin and TSH plasma concentration in all subjects. Since the drug blocks the conversion of DOPA to dopamine, these hormonal changes may be due to a reduction in circulating and/or median eminence levels of dopamine.

Adult↗
PubMed1980

Dopamine inhibits the naloxone induced gonadotrophin rise in man.

Twenty milligrams of the opiate receptor antagonist naloxone were infused over 3 h to five young male volunteers. Naloxone produced a significant rise in both LH and FSH, but did not affect serum prolactin levels. The infusion of dopamine (4 microgram . kg-1 . min-1) completely abolished the naloxone effect on gonadotrophin release. The results suggest a possible interaction between dopamine, opioid receptors and gonadotrophin secretion in man.

Adult↗