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Biomedical subjects

M Gambacciani

Publications and source records attributed to M Gambacciani.

82 records · Page 5Linked to original sources
PubMed1986

Evidence of specific benzodiazepine binding to myometrial membrane preparations from human pregnant uterus.

The muscle relaxant effect of benzodiazepines (BDZ) is widely held to be mediated at central as well as at peripheral level. In this study we report that crude membrane preparations from the myometrium of pregnant women possess binding sites for [3H]-RO 5-4864, specific ligand for the peripheral type of BDZ receptor. Scatchard analysis shows a high affinity binding site (KD = 3.1 +/- 1.2 nM) and a class of low affinity binding sites (KD greater than 30 nM). Displacement experiments show that various BDZ are differently effective in inhibiting [3H]-RO 5-4864 binding: RO 5-4864 greater than diazepam greater than flunitrazepam greater than lorazepam greater than chlordiazepoxide. In conclusion, these data seem to demonstrate that human myometrium possesses specific binding sites of 'peripheral type' for BDZ. It may be suggested that these binding sites are involved in mediating the myometrial relaxant effect exerted by BDZ. Thus, peripherally active BDZ could be used as tocolytic agents, avoiding BDZ central effects.

Adult↗
PubMed1985

Sex steroids modulate prolactin response to naloxone in postmenopausal women.

To evaluate whether ovarian steroids modify the prolactin (PRL) response to opioid receptor blockade, the effects of naloxone infusion (1.6 mg/h for 4 h) on PRL secretion were studied in 5 postmenopausal women. Naloxone infusion was performed in basal conditions and after chronic oral treatment with conjugated estrogens (CE) (1.25 mg/day, for 20 days) or CE plus medroxyprogesterone acetate (MPA) (10 mg/day, for 20 days). Under basal conditions, 17 beta-estradiol, estrone, gonadotropin, and PRL plasma levels were in the normal range for postmenopausal women, and naloxone failed to affect PRL secretion. Naloxone induced a significant PRL increase after CE treatment alone (p less than 0.001) or in combination with MPA (p less than 0.001). The increase was significantly higher (p less than 0.05) after CE + MPA treatment than after CE treatment alone. These data suggest that steroids modulate the stimulatory effect of naloxone on PRL secretion in postmenopausal women.

Endorphins↗
PubMed1984

Some properties of a purinergic receptor solubilized from human uterus membranes.

A purinergic receptor was identified in human myometrium membranes using 5'-N-[3H]ethylcarboxamide-adenosine [( 3H] NECA) as radioligand. Scatchard analysis of the binding data gave a Kd of 123 nM with 2.3 pmol ligand bound/mg protein. Displacement studies indicated that the binding site had the characteristics of the A2 adenosine receptors and some of those of the P2 purinoceptors since it was inhibited by two slowly degradable ATP derivatives with IC50 values comparable to that of NECA. The receptor was solubilized with sodium cholate and its binding properties were the same as those of the membrane-bound form. No -SH group appeared to be essential for the binding activity. By density gradient centrifugation the purinergic receptor-detergent complex was estimated to have an apparent molecular mass of 95 kDa.

Adenosine↗
PubMed1984

Evidence that estrogens inhibit LH secretion through opioids in postmenopausal women using naloxone.

To evaluate whether ovarian steroid environment may modify endogenous opioid activity at hypothalamic-pituitary level, the effects of naloxone infusion (1.2 mg/h for 4 h) on gonadotropin secretion were studied in 5 postmenopausal women who had natural menopause 3-5 years before the study. In addition, naloxone infusion was repeated in the same subjects after chronic oral treatment with conjugated estrogens (1.25 mg/day in two divided doses for 20 days). Before treatment, both the circulating levels of estrogens and plasma gonadotropins were in the normal range for postmenopausal women and naloxone infusion did not induce any significant modification of gonadotropin secretion. In contrast, after estrogen therapy, and the consequent rise in estrogen plasma levels, naloxone infusion induced a significant LH increase (p less than 0.01) starting during the last hour of treatment. These findings seem to confirm that endogenous opioid peptides may modulate the inhibitory effect exerted by estrogens on LH secretion, in humans.

Endorphins↗
PubMed1984

Benzodiazepine binding sites in human myometrium.

We report that membrane preparations of human myometrium possess binding sites for [3H] RO 5-4864, a specific ligand for the peripheral type of benzodiazepine receptors. Scatchard analysis shows a high-affinity binding site (Kd = 3.1 +/- 1.1 nM) and a class of low-affinity binding sites (Kd greater than 30nM) with positive cooperativity. Displacement and tryptic digestion experiments indicate that both these benzodiazepine binding sites are specific and proteic in nature. So benzodiazepines might exert their relaxant activity on uterine muscle directly at peripheral level through specific binding sites.

Adult↗
PubMed1982

The effects of the gabaergic drug, sodium valproate, on prolactin secretion in normal and hyperprolactinemic subjects.

To find out whether the gamma-aminobutyric acid (GABA)ergic system affects PRL secretion in humans, sodium valproate (DPA or Na-dipropyl-acetate), a drug inducing increase of endogenous GABA, was administered to 20 normal and 15 hyperprolactinemic subjects. PRL circulating levels were measured by RIA in the samples obtained after acute oral treatment with 400 mg DPA. A significant decrease (P less than 0.01) in comparison with basal levels was observed in normal women from 30-180 min after drug administration. DPA treatment also lowered blood PRL levels in hyperprolactinemic subjects (seven females) without evidence of pituitary tumor. A decrease very similar to the one found in normal subjects (P less than 0.05 vs. basal levels) was observed within 180 min from drug ingestion. Conversely, no significant changes were found after the same treatment in hyperprolactinemic patients with evidence of prolactinoma (seven females and one male). Taken together, these data seem to demonstrate that pharmacological enhancement of endogenous GABAergic tone is followed by inhibition of PRL secretion. They also suggest that GABA may exert an inhibitory control on PRL release in humans. In hyperprolactinemic subjects, this GABAergic control appears to be present only when a pituitary tumor cannot be demonstrated.

Adenoma↗
PubMed1981

Inhibitory effect of the dopamine agonist bromocriptine on the postcastration gonadotrophin rise in women.

Basal or stimulated gonadotrophin plasma levels were measured after bilateral ovariectomy in untreated and bromocriptine (BCT)-treated normal women. BCT was orally administered from the 7th to the 14th day after ovariectomy at a dose of 3.75 mg/day. BCT significantly (P less than 0.05) inhibited LH release, both basally and after LRF stimulation. Plasma FSH levels were also reduced in treated subjects, but this decrease did not reach statistical significance relative to controls. The blunted postcastration gonadotrophin rise found with BCT administration suggests that pituitary gonadotropin secretion is, in part, under dopaminergic inhibitory control.

Adult↗
PubMedDate not supplied

Dose-related effects of gamma-amino beta-hydroxy butyric acid (GABOB) infusion on growth hormone secretion in normal women.

The effect of gamma-amino beta-hydroxy butyric acid (GABOB) infusion on GH secretion has been investigated in 3 groups of 6 normal women. Different doses (100 mg/min, 20 mg/min, 3.5 mg/min) of GABOB diluted with normal saline solution were infused iv over a 20 min period and compared with control tests performed using only saline solution. The infusions with GABOB at the doses of 100 mg/min and 20 mg/min were followed by a significant rise (p less than 0.01) in GH plasma levels, in comparison to control tests. The quantitative GH secretion after 100 mg/min GABOB infusion was significantly greater (p less than 0.05) in comparison with quantitative GH secretion after 20 mg/min GABOB infusion. After 3.5 mg/min infusion, only 3 out of 6 subjects showed an increase in the hormone concentrations. The acute injection with sulpiride (5 mg iv, bolus), performed either before or after the start of GABOB infusion, failed to affect GH response to GABOB. These results show that GABOB infusion induce a dose-dependent rise in GH plasma levels in normal women. The dopaminergic system does not seem to be involved in this effect.

Adult↗