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Biomedical subjects

F Labrie

Publications and source records attributed to F Labrie.

At least 649 records · Page 36Linked to original sources
PubMed1976

Inhibition of luteinizing hormone release by analogs of luteinizing hormone-releasing hormone (LHRH) in vitro.

Sixteen synthetic analogs of LH-releasing hormone (LHRH) were tested for their ability to inhibit the stimulation of LH release induced by 3 X 10(-9)M LHRH in anterior pituitary cells in monolayer culture. Half-maximal inhibition of LHRH-induced LH release was obtained with 7 analogs at concentrations which ranged from 3 X 10(-6)M to 3 X 10(-5)M. None of these seven analogs had significant LH-releasing activity at concentrations up to 10-5M. Nine analogs had no detectable antagonistic activity when tested in up to a 3000-fold molar ratio of analog to LHRH.

Animals↗
PubMed1976

Characteristics of the interaction between thyrotropin-releasing hormone and somatostatin for thyrotropin and prolactin release.

Somatostatin, at concentrations up to 10(-7) M, does not inhibit the basal release of TSH from primary cultures of rat anterior pituitary cells. The TRH-induced TSH release is however 65% reduced by somatostatin, half-maximal inhibition being measured at 2.5 x 10(-10) M somatostatin. The concentration of TRH giving half-maximal stimulation (ED50) of TSH release is only slightly increased from 1 to 3 x 10(-9) M in the presence of 10(-8) M somatostatin. Somatostatin inhibits by 45-65% both the basal and TRH-induced PRL release of pituitary cells prepared from adult female rats, with half-maximal inhibition at approximately 5 x 10(-10) M somatostatin. The TRH ED50 for PRL release was not significantly affected by somatostatin. Somatostatin (200 mug) has no effect on the basal plasma levels of TSH or PRL in anesthetized male rats treated with estradiol benzoate (EB), hypothyroid rats, or hypothyroid animals treated with EB. The plasma TSH response to TRH is, however, reduced by approximately 75% by somatostatin while the plasma PRL response is not affected by injection of the peptide. The interaction between TRH and somatostatin for both TSH and PRL release is non-competitive and is thus likely to occur at a step subsequent to the binding of the peptides to their specific receptors in both thyrotrophs and mammotrophs.

Animals↗
PubMed1976

Selective effect of androgens on LH and FSH release in anterior pituitary cells in culture.

A possible direct effect of androgens at the pituitary level on gonadotropin release was studied using rat anterior pituitary cells in primary culture. The preincubation of cells with 3 X 10(-9)M testosterone (T) for 40 h increased the concentration of luteinizing hormone-releasing hormone (LHRH) required for half-maximal stimulation (ED50) of LH release from 3 X 10(-10)M to 1 X 10(-9)M. In the same experiment, the LHRH ED50 for FSH release (3 X 10(-10)M) was not affected by preincubation with T, while a slight stimulatory effect of the androgen was observed on balal FSH release and on the maximal FSH response to LHRH. Time-course experiments showed that the inhibitory effect of T on the LH response to LHRH was maximal after about 48 h of incubation and that 54 h after the removal of T, only 50% of the inhibition was reversed. 5 alpha-Dihydrotestosterone (DHT) and T led to the same maximal inhibition (15-20% of control) of the LH response to 10(-10)M LHRH. DHT was, however, about 3 times more potent than T, their ED50 values being 1.6 X 10(-10)M and 5 X 10(-10)M, respectively. In contrast to the effect on LH, the FSH response to 10(-10)M LHRH was only slightly, but not significantly, inhibited by increasing concentrations of DHT or T. The finding that total LH (medium + cell content) remained constant after incubation with T or DHT clearly indicates that the inhibition of the LH response to LHRH is really due to changes in the sensitivity of the releasing mechanisms in the LH-secreting cells. Androgens did, however, lead to increased total FSH. The present data indicate an independent control of LH and FSH secretion by a direct action of androgens at the pituitary level.

Androgens↗
PubMed1976

Effect of pharmacological blockade of ACTH and TSH secretion on the acute stimulation of prolactin release by exposure to cold and ether stress.

Acute exposure of male rats to cold (5C)leads to a rapid increase of plasma levels of thyrotropin (TSH), prolactin (PRL), corticosterone, and L-thyroxine. Exposure to ether is similarly followed by a rapid increase of plasma levels of PRL and corticosterone, while TSH release is inhibited. Acute treatment with dexamethasone (500 mug) inhibits almost completely the PRL response to both exposure to cold and ether stress, while the plasma TSH response to cold is only delayed and the decrease of plasma TSH observed after ether stress is unchanged. Basal plasma levels of both TSH and PRL are lowered after treatment with the steroid. Thyroxine treatment lowers the plasma TSH concentration to undetectable levels without affecting the plasma PRL response to cold or ether exposure. The present data suggest that the rise of plasma PRL observed after cold exposure is not related to TRH and may suggest that common mechanisms control ACTH and PRL secretion during acute stress exposure.

Adrenocorticotropic Hormone↗
PubMed1976

Estradiol-induced increase of the LH responsive to LH releasing hormone (LHRH) in rat anterior pituitary cells in culture.

The effect of 17 beta-estradiol (E2) on LH secretion was studied using rat adenohypophyseal cells in primary culture. Preincubation of cells with 1 X 10(-9) M E2 for 40 h decreased the concentration of LHRH required for half-maximal stimulation (ED50) of LH release from 3.0 +/- 0.3 to 1.6 +/- 0.2 X 10(-10)M (P less than 0.01). Basal LH release was increased from 84 +/- 4 to 182 +/- 8 ng LH-RP-1/ml/4h (P less than 0.01) by E2 pretreatment. Time-course experiments showed that the stimulatory effect of 10(-8)M E2 on the LH response to LHRH can be first measured after 10 h of incubation in the presence of E2 and that this effect is maximal after 24 h of incubation with the steroid. While E2 increases the LH responsiveness to LHRH, androgens decrease the sensitivity of LH-secreting cells to the neurohormone. The LHRH ED50 value of testosterone-treated cells is of 7.2 +/- 0.4 vs. 3.7 +/- 0.3 X 10(-10)M for control cells (P less than 0.01). E2 can only partially reverse this inhibitory effect of androgens on the LH response to LHRH. These data show clearly that E2 can have a direct stimulatory effect on LH-secreting cells to increase the sensitivity of their response to LHRH.

Animals↗
PubMed1975

Changes of pituitary sensitivity to LH-RH during the rat estrous cycle.

The plasma LH (luteinizing hormone) response to 200 ng of LH-RH (LH-releasing hormone) injected subcutaneously at different stages of the estrous cycle in normal rats under Surital anesthisia was maximal during the afternoon of proestrus and lowest on diestrus I. The area under the plasma LH curve measured at 13:00 on proestrus was approximately 7-fold higher than that obtained at 15:30 h on diestrus I. Intermediate responses were found on diestrus II, estrus and morning of proestrus. An approsimately 2.5-fold higher LH response was observed on proestrus than on diestrus I after injection of [D-Ala2, des Gly-NH2-10] LH-RH ethylamide at 15:00 h. That these marked changes of LH response are not secondary to interference by endogenous LH-RH, changes of the metabolism or transport of exogenous LH-RH or modification of plasma LH clearance is ascertanied by the finding of similar changes of pituitary sensitivity to LH-RH under in vitro conditions using pituitaries collected at the same stag-s of the estrous cycle. As measured both in vivo and in vitro, not only the amplitude but also the speed of LH response are maximal during the afternoon of proestrus and minimal on diestrus I.

Animals↗
PubMed1975

Calcium requirement for stimulation of cyclic AMP accumulation in anterior pituitary gland by LH-RH.

Removal of Ca2+ from the incubation medium by addition of 2 mM ethylene glycol bis-(beta-aminoethyl ether)-N, N'tetraacetic acid (EGTA) leads to at least 75% inhibition of the luteinizing hormone-releasing hormone (LH-RH)-induced accululation of adenosine 3'5'-monophoshpate (cyclic AMP) in rat anterior pituitary gland in vitro. This inhibitory effect of EGTA is reversed by the addition of Ca2+. A half-maximal effect of Ca2+ on LH-RH--induced cyclic AMP accumulation is observed at 2-5 X 10-5 M free Ca2+. The LH-RH-induced LH and FSH release is completely dependent upon the presence of Ca2+ in the incubation medium, a half-maximal effect being measured at 1-2 X 10-4 M free Ca2+. The basal release release of LH is increased upon Ca2+ removal.

Animals↗
PubMed1975

Inhibitory activity of four analogs of luteinizing hormone-releasing hormone in vivo.

Four analogs of luteinizing hormone-releasing hormone (LH-RH), [des-His2,D-Ala6]-LH-RH, [des-His2,D-Ala6, des-Gly-NH2(10)1-LH-RH ethylamide, [des-His2,D-Leu6]-LH-RH, and [D-Phe2,D-Leu6]-LH-RH, at 300-fold molar ratios (analog/LH-RH) led to an almost complete inhibition of LH response to LH-RH in anesthetized 4-day cycling rats on the afternoon of proestrus. At a 75-fold molar ratio, [des-His2,D-Ala6]-LH-RH still inhibited the LH-RH-induced LH release by 50%. The ethylamide substitution at the COOH terminus of [des-His2,D-Ala6]-LH-RH did not significantly improve the inhibitory activity of the molecule.

Animals↗
PubMed1975

Characteristics of action of prostaglandins on cyclic AMP accumulation in rat anterior pituitary gland.

Prostaglandins (PGs) were found to lead to a marked stimulation of cyclic AMP accumulation in rat anterior pituitary gland in vitro in the following decreasing order of potency: PG E-1 E-2 GREATER THAN A-1 A-I GREATER THAN F-1ALPHA F-2ALPHA. The effect of PGs is potentiated by theophylline. The stimulatory effect of PGs on cyclic AMP accumulation is already detected 2min after the addition of 1-x 10-7 to 1-x 10-6 M PG E-2 and its maximal effect is reached after approximated 30 min of incubation, with a progressive decrease toward basal cyclic AMP levels at later time intervals. Increased intracellular cyclic AMP concentrations are accompanied by an increased release of the nucleotide into incubation medium. Complete removal of Ca-e+ from the incubation medium by addition of EGTA was found to increase the stimulatory effect of PG E-2 ON CYCLIC AMP accumulation. The action of PGs on hormonal release and cyclic AMP accumulation support the hypothesis of a role of PGs in the mechanism of anterior pituitary hormone (particularly growth hormone) release.

Animals↗
PubMed1975

Effect of exposure to cold on hypothalamic TRH activity and plasma levels of TSH and prolactin in the rat.

No significant change in hypothalamic TRH content was found in rats during acute (5-240 min) exposure to cold (5 degrees C), in spite of rapid and sustained elevations in plasma TSH and thyroxine. Plasma PRL rose markedly in the first 15 min, but returned to normal thereafter. Chronic exposure to cold (32 days) was characterized by elevated plasma and pituitary levels of both TSH and PRL in the presence of an unaltered hypothalamic TRH content. If increased TRH release from the hypothalamus occurs during exposure to cold, as suggested by the pituitary-thyroid stimulation, either it is compensated for by an equal rise in synthesis, or the extra amount released is negligible in comparison with the hypothalamic content of TRH. The acute PRL response to exposure to cold may be related to an acute TRH release but could also result from the accompanying stress response acting by a mechanism independent of TRH.

Animals↗
PubMed1975

Development of the hypothalamic-pituitary-thyroid axis in the neonatal rat.

The hypothalmic content of thyrotropin-releasing hormone (TRH), the pituitary concentration of thyroid-stimulating hormone (TSH), and the serum concentrations of TSH, thyroxine (T4), and triiodothyronine (T3) have been determined at different intervals during the first 50 days following birth in the rat. From a minimum concentration of 1 pg/mug protein at birth, the hypothalamic concentration of TRH increased to a maximum of 5 to 6 pg between 16 and 28 days of age. Serum and pituitary TSH concentrations increased to maximum levels by the end of the first post-natal week; the elevated hormone levels were then maintained to the end of the third post-natal week. Circulating thyroid hormone concentrations were very low at birth. T4 increased rapidly between days 4 and 16 to reach a peak concentration of 6 mug/100 ml, while T3 followed a parallel pattern with a peak concentration of 108 ng/100 ml obtained only at day 28. These data indicate that, in the rat, components of the hypothalamic-pituitary-thyroid axis develop simultaneously during the post-natal period.

Aging↗
PubMed1975

Distribution of radioactivity in the organs of the rat and mouse after injection of (125I)alpha-melanocyte-stimulating hormone.

The distribution of radioactivity after intrajugular injection of 125I-labelled alpha-melanocyte-stimulating hormone (alpha-MSH) was studied by whole-body autoradiography of the mouse and by direct measurement of radioactivity in individual organs of the rat. Very high uptake of radioactivity in the pineal gland was measured 5 min after the injection of (125I)alpha-MSH. Lower levels of accumulation of radioactivity were found in the kidney and in the posterior (including intermediate) lobe of the pituitary. High uptake was also found in the thyroid, stomach, and oesophagus. The specificity of uptake of (125I)alpha-MSH into the pineal and pituitary is suggested by the very low uptake of Na125I into those tissues.

Adrenal Glands↗
PubMed1975

Distribution of radioactivity in the organs of the rat and mouse after injection of L-(3H)prolyl-L-leucyl-glycinamide.

The distribution of radioactivity after intrajugular injection of L-(3H)-prolyl-L-leucyl-glycinamide has been studied by whole-body autoradiography in the mouse and by direct measurement of radioactivity in individual organs of the rat. There is good agreement between results obtained with the two techniques and animal species. High levels of radioactivity were found in the pineal gland, anterior pituitary, posterior (including intermediate) lobe of the pituitary, and epididymal and brown fat. Lower uptake of radioactivity occurred in the submaxillary gland, kidney, and adrenal gland. The preferential uptake of radioactivity by the pineal gland after injection of the labelled tripeptide suggests a role for this hypothalamic hormone in the control of pineal activity.

Adipose Tissue↗
PubMed1975

In vitro interactions of gastrointestinal hormones on cyclic adenosine 3':5'-monophosphate levels and amylase output in the rat pancreas.

Four-fold increases in cyclic AMP levels were observed 5 to 10 min after rat pancreatic fragments were incubated with 10-7 M secretin or 10-6 M vasoactive intestinal polypeptide (VIP), in addition to 10 mM theophylline. From dose-response curves it appears that, on a molar basis, the potency of secretin was 20 times higher than that of VIP. It is concluded that cyclic AMP is probably the intracellular messenger of both secretin and VIP in centroacinar cells. Pancreozymin, caerulein, and the C-terminal octapeptide of pancreozymin inhibited the production of cyclic AMP observed with secretin of VIP, suggesting that the first three peptides were acting at a binding site different from the agonists, but coupled with the same adenylate cyclase. In acinar cells, secretin was able to exert slight ecbolic effects, and was also able to potentiate the effect of maximal concentrations of pancreozymin, caerulein, or the C-terminal octapeptide of pancreozymin. There was no simple correlation between amylase output and cyclic AMP levels, and copious amylase secretion was elicited even at control levels of cyclic AMP. Glucagon was neither an agonist nor an antagonist of any of the other polypeptides tested.

Amylases↗