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Biomedical subjects

F Labrie

Publications and source records attributed to F Labrie.

At least 595 records · Page 33Linked to original sources
PubMed1978

[Inhibitory effects of LHRH on ovarian LH receptors in rats].

The administration of LHRH or of its analog [D-Ala6, des-Gly-NH10(2)] LHRH ethylamide to the female rat on day 10 of gestation resulted in termination of pregnancy and in a marked decrease in ovarian LH receptors and plasma progesterone level. Asingle injection of either compound during diestrus I also led to a decrease in LH receptors. These data demonstrate the high sensitivity of the control of ovarian LH receptors by circulating gonadotrophins and suggest that the contraceptive action of pre- and postcoitally administered LHRH is mediated by negative control of LH receptors.

Animals↗
PubMed1978

[Luteolytic action of LHRH in women].

Several subcutaneous administrations of 250 microgram of LHRH (4 or 5 adminstrations at 4-hourly intervals per day) between the 2nd and 7th day post-ovulation in 4 normal women led to early luteolysis as demonstrated by a fall in serum progesterone concentration and early onset (2 to 3 days earlier) of menstruation.

Adult↗
PubMed1978

Evidence for a role of endorphins in stress- and suckling-induced prolactin release in the rat.

Injection of the opiate antagonist naloxone completely prevented the rise of serum prolactin induced by ether stress in intact male rats. Naloxone also led to a 50--95% inhibition of the marked elevation of plasma prolactin levels induced by suckling. These data suggest that endogenous opiates (endorphins) are involved in the stimulation of prolactin release induced by both stress and suckling in the rat.

Animals↗
PubMed1978

Inhibitory effect of a luteinizing hormone (LH)-releasing hormone agonist on rat ovarian LH and follicle-stimulating hormone receptor levels during pregnancy.

When injected at the daily dose of 100 microgram on days 7 through 12 of pregnancy, the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6, des-Gly-NH2(10)] LHRH ethylamide led to complete suppression of pregnancy and a 45% to 60% decrease in plasma progesterone concentration. The antifertility effect of the LHRH analog was accompanied by an early and almost complete inhibition of ovarian LH/human chorionic gonadotropin and follicle-stimulating hormone receptor levels. These data suggest that the antifertility effects of LHRH agonists are mediated by down-regulation of ovarian gonadotropin receptors and decreased luteal function.

Animals↗
PubMed1978

Inhibition of ovarian luteinizing hormone (LH) and follicle-stimulating hormone receptor levels with an LH-releasing hormone agonist during the estrous cycle in the rat.

A single injection of the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6,des-Gly-NH2(10)]LHRH ethylamide to female rats on diestrus I produced a marked reduction in ovarian LH/human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH) receptor levels, uterine weight, and plasma progesterone levels measured 2 days later on expected proestrus. A maximal inhibitory effect was seen after a dose of only 40 ng of the peptide. No consistent effect of the LHRH analog was seen on ovarian prolactin receptors. When the analog was injected on day 7 of pregnancy, the inhibition of ovarian LH/hCG receptors was of shorter duration and was much less sensitive than that in nonpregnant animals. These data indicate that ovarian LH and FSH receptors levels are highly sensitive to changes in endogenous gonadotropin secretion and suggest that the gonadotropin surge occurring spontaneously on proestrus may play an important role in the regulation of ovarian gonadotropin receptors during the estrous cycle.

Animals↗
PubMed1978

Enzymatic degradation of somatostatin by rat plasma and hypothalamus.

A highly sensitive and specific radioimmunoassay for somatostatin has been used to study inactivation of the neurohormone by plasma and hypothalamic peptidase(s). Specificity of the inactivation process was indicated by the absence of interference by addition of luteinizing hormone releasing hormone, thyrotropin-releasing hormone, oxytocin, or substance P. The inactivating ability of hypothalamic tissue and plasma was destroyed by heating and the protease inhibitor benzamidine prevented plasma activity, thus suggesting the enzymatic nature of the processes involved. The present data suggest that the inactivation of somatostatin by hypothalamus and plasma could be an important factor in the regulation of circulating somatostatin levels.

Animals↗
PubMed1978

Effect of gonadal steroids on the luteinizing hormone and follicle-stimulating hormone response to 8-bromo-adenosine 3',5'-monophosphate in anterior pituitary cells in culture.

-8-Bromo-cAMP stimulated the release of LH (approximately 20-fold) and FSH (approximately 2-fold) in control rat anterior pituitary cells in primary culture. 8-Bromo-cAMP-induced LH release was 2-3 times greater in cells preincubated for 48 h in the presence of 10(-8) M 17 beta-estradiol (E2). The LH response to 10(-10) M LHRH was similarly increased by E2 pretreatment whereas progesterone (P), which had no effect on the response to 8-bromo-cAMP, led to a reduction of the stimulatory effect of E2 on the LH response to the neurohormone. Preincubation with 10(-8) M testosterone (T) decreased the LH response to 8-bromo-cAMP by about 40%, whereas the response to LHRH was 80% inhibited. 8-Bromo-cAMP-induced FSH release was slightly increased in cells preincubated with E2 but was greatly augmented in cells treated with E2 + P. Basal FSH release was slightly increased (40%) after preincubation with P or T whereas the response to 8-bromo-cAMP was not significantly affected. The sensitivity of the FSH response to LHRH was increased by E2 whereas P and T led to a stimulation of the maximal FSH response to LHRH with no significant effect on the LHRH ED50 value. The present data indicate that P and E2 exert their effects on LH and FSH release at steps before and after cAMP formation, respectively. T appears to act at both steps on the release of the two gonadotropins.

Animals↗
PubMed1978

Inhibition of spermatogenesis in the rat by treatment with [D-Ala6, Des-Gly-NH210] LHRH ethylamide.

The effect of treatment with a potent LHRH agonist, [D-Ala6, Des-Gly-NH210]LHRH ethylamide, injected at the low dose of 100 ng, twice a week, was evaluated on spermatogenesis in the rat. Significant degenerative changes of seminiferous tubules could be observed after two weeks of treatment. These changes were progressive and led to a marked inhibition of spermatogenesis after four to eight weeks of treatment. Testis weight was decreased to approximately 50% of control after eight weeks of treatment.

Animals↗
PubMed1978

[Specific role of sex steroids on the pituitary level. Sex steroids and anterior pituitary secretion].

Although sex steroids were known to play a role in the control of LH, FSH, TSH and prolactin secretion, in vivo experiments could not discriminate between hypothalamic and pituitary sites of action. In this study, the specific action of sex steroids at the anterior pituitary level could be achieved using rat adenohypophyseal cells in primary culture. While estrogens stimulated the sensitivity of the LH and FSH responses to LHRH, androgens had differential effects on the secretion of the two gonadotropins: marked inhibition of LH and stimulation of FSH secretion. Progesterone, on the other hand, while having no effect in the absence of estrogens, could reverse the stimulatory effect of estrogens on LH release while it led to a stimulation of FSH secretion. Estrogens and thyroid hormone exert respective stimulatory and inhibitory effects on TSH secretion by a direct action at the pituitary level. These effects appear to be mediated changes of the level of adenohy-pophyseal TRH receptors. A close correlation was observed between the specificity of binding of the dopamine agonist (3H)dihydroergocryptine and the control of prolactin release in cells in culture, thus supporting the physiological importance of the dopamine receptor in the control of prolactin release. The high degree precision of this system permits assessment of activity of not only dopamine agonists and antagonists, but also of compounds having mixed agonist-antagonistic activity. Preincubation of anterior pituitary cells with 17beta-estradiol not only stimulated basal and TRH-induced prolactin release but, more unexpectedly, led to an almost complete reversal of the inhibitory effect of dopamine agonists on prolactin secretion. Besides its own interest, the adenohypophyseal cell culture system could well be used as a model system for study of the interaction between estrogens and dopaminergic action.

Androgens↗
PubMed1977

Effect of somatostatin on thyrotropin, prolactin, growth hormone and insulin responses to thyrotropin releasing hormone and arginine in healthy, hypothyroid and acromegalic subjects.

The effect of somatostatin on the thyrotropin (TSH), prolactin, growth hormone (GH) and insulin responses to the combined administration of thyrotropin releasing hormone (TRH) and arginine was studied in six healthy subjects, three hypothyroid patients and three acromegalic patients. Similar inhibition by somatostatin of the TSH and insulin responses was observed in the three groups. While the tetradecapeptide had no significant effect on the prolactin response in the healthy and acromegalic subjects, it caused an unexpected inhibition of the prolactin response in two of the hypothyroid subjects. Contrary to the findings in the healthy and hypothyroid subjects, somatostatin did not inhibit the GH response in the acromegalic patients. Normal inhibition by somatostatin of the insulin response, followed by a rebound in insulin secretion, was observed in all subjects. These preliminary data indicate increased sensitivity of the prolactin-secreting cells to somatostatin in hypothyroidism and suggest that decreased responsiveness of the somatotrophs to somatostatin could play a role in the pathogenesis of acromegaly.

Acromegaly↗