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Biomedical subjects

H Meunier

Publications and source records attributed to H Meunier.

At least 37 records · Page 2Linked to original sources
PubMed1988

Kinetics of a single dose combination of nifedipine/acebutolol in patients with chronic liver disease.

The plasma kinetics of a nifedipine/acebutolol fixed dose combination were estimated after a single oral dose in patients with chronic liver disease and in a healthy control group of the same age. The drug metabolism evidently slowed down in the group with chronic liver disease. The plasma elimination half-lives of acebutolol, diacetolol and nifedipine of these patients were about twice as long as that in the control group. Doses of these drugs should be accordingly reduced, particularly in cirrhosis.

Acebutolol↗
PubMed1987

Rat inhibin: molecular cloning of alpha- and beta-subunit complementary deoxyribonucleic acids and expression in the ovary.

Inhibin is a gonadal protein hormone that suppresses the secretion of FSH from pituitary gonadotrophs. It has previously been characterized as a heterodimer of two dissimilar subunits (alpha, 18 kilodaltons and beta, 14 kilodaltons) the smaller of which exists in two forms (beta A and beta B) and can form dimers that stimulate the secretion of FSH. In the present work, cDNA clones encoding the inhibin alpha- and beta A-subunits have been isolated from rat ovary and characterized. The alpha-inhibin cDNA predicts a precursor protein of 366 amino acids containing the 133 amino acid mature alpha-subunit at its COOH-terminus. The beta A-inhibin cDNA predicts a precursor protein of 424 amino acids containing the 116 amino acid beta A-subunit at its COOH-terminus. Analysis of rat ovarian RNA indicates that alpha-inhibin mRNA levels are stimulated by PMSG treatment in vivo. In cultured granulosa cells, FSH also stimulates alpha-inhibin mRNA, and the FSH effect is suppressed by cotreatment with GnRH. Hybridization in situ to rat ovarian tissue demonstrates that both the alpha-inhibin and beta A-inhibin mRNAs are specifically expressed in granulosa cells of the developing follicles.

Amino Acid Sequence↗
PubMed1985

Structure, sequence and polymorphism in the HLA-D region.

Molecular analysis of the HLA-D region has uncovered a complex array of related genes encompassing a minimum of 6 alpha and 7 beta chain sequences. A high level of polymorphism is characteristic of the DQ alpha and beta genes, as well as DR beta. The DP genes, both alpha and beta, are also polymorphic, though to a lesser extent. The genes fit into the previously established loci: DP, DQ and DR, except for a newly-discovered sequence, DZ alpha, which is approximately equally related to all of the other alpha chain genes. Analysis of the polymorphism and evolution of the HLA-D region, by examination of the sequences, calls for several independent duplication events in the generation of this family of genes.

Base Sequence↗
PubMed1983

Multiple factors involved in the control of ACTH and alpha-MSH secretion.

Alpha 1-adrenergic agents are potent stimulators of ACTH secretion directly at the pituitary level as observed using anterior pituitary cells in primary culture and by in vivo studies. On the other hand, beta-adrenergic as well as antidopaminergic agents are also potent stimulators of ACTH secretion but at a suprapituitary level, since no effect of these compounds are observed in vitro. CRF administration has been found to lead to rapid and parallel increases in ACTH and alpha-MSH concentrations in rat plasma and the mechanism of action of CRF has been studied in vitro using rat anterior and intermediate lobe of pituitary gland for ACTH and alpha-MSH secretion, respectively. In both cases, CRF stimulates adenylate cyclase activity at ED50 values of 70 and 350 nM for ACTH and alpha-MSH, respectively. CRF stimulates adenylate cyclase activity at least partly through a guanyl nucleotide-dependent mechanism. Using rat pars intermedia cells in culture, we have demonstrated the presence, in addition of a CRF receptor, of a beta 2-adrenergic receptor which stimulates cyclic AMP accumulation and alpha-MSH secretion and of a dopaminergic receptor which inhibits cellular activity. These results have been confirmed in in vivo studies where isoproterenol and thioproperazine (a dopamine antagonist) lead to a rapid increase of alpha-MSH secretion.

Adrenocorticotropic Hormone↗
PubMed1983

CRF stimulates adenylate cyclase activity in the intermediate lobe of the pituitary gland.

Ovine corticotropin-releasing factor (CRF) stimulates adenylate cyclase activity in homogenate of the intermediate lobe of the bovine pituitary gland at an ED50 value of 150 nM. GTP increases the stimulatory effect induced by CRF as well as by the beta-adrenergic agonist isoproterenol on [32P]cyclic AMP formation in rat pars intermedia homogenate. In addition, GTP is required for inhibition by dopamine of the stimulatory action of both CRF and isoproterenol. The present data show that CRF stimulates adenylate cyclase activity in the intermediate lobe of the pituitary gland at least partly through a GTP-dependent mechanism. Moreover, dopamine can interfere with the action of CRF as well as that of isoproterenol, thus indicating that the neurohormone could be involved, in addition to beta-adrenergic agents, as stimulator of pars intermedia cell activity.

Adenylyl Cyclases↗
PubMed1983

Multiple hormonal control of pars intermedia cell activity.

In rat pars intermedia cells, the rate of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion was so far known to result from a balance between the stimulatory effect of beta-adrenergic agonists and the inhibitory influence of dopaminergic substances. Recently, we have identified a second stimulatory substance, namely corticotropin-releasing factor (CRF). CRF is a potent stimulator of pars intermedia adenylate cyclase activity, cAMP accumulation and alpha-MSH release. A requirement for calcium ions was observed on basal as well as on CRF-induced alpha-MSH secretion. The beta-adrenergic and CRF effects on adenylate cyclase activity, as well as the dopamine inhibition of adenylate cyclase activity, are potentiated by guanine nucleotides (GTP). Stimulation of the beta-adrenergic receptor with isoproterenol causes a rapid loss in cAMP responsiveness, which can be completely blocked by beta-adrenergic antagonists and partially prevented by dopamine. These findings suggest that CRF should now be considered, in addition to beta-adrenergic agents, as a stimulator of the activity of pars intermedia cells and that cAMP is also involved as mediator of its action. Changes of receptor sensitivity, as well as interaction of the two stimulatory receptors with the inhibitory dopaminergic receptor, are involved in the fine control of pars intermedia cell activity. All three receptors appear to exert their action through a common pathway, namely changes of adenylate cyclase activity.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Specificity of the beta 2-adrenergic receptor stimulating cyclic AMP accumulation in the intermediate lobe of rat pituitary gland.

Changes of cyclic AMP levels were used to assess the specificity of the beta-adrenergic receptor in primary cultures of cells prepared from the intermediate lobe of rat pituitary gland. During a 4 min incubation, beta-adrenergic agonists led to a 4 to 6 fold stimulation of cyclic AMP concentration with the following order of potency (Kd values): zinterol (0.75 nM) greater than hydroxybenzylisoproterenol (1.0 nM) greater than (--)-isoproterenol (4.6 nM) greater than soterenol greater than (7.7 nM) greater than (--)-epinephrine (10 nM) greater than OPC 2009 (procaterol, 11 nM) much greater than (--)-norepinephrine (300 nM). The potent antagonists cyanopindolol, (--)-propranolol and hydroxybenzylpindolol reversed the stimulatory effect of (--)-isoproterenol at Kd values of 0.4-0.6 nM. Other beta-adrenergic antagonists had the following order of potency: pindolol = (--)-alprenolol = timolol (0.9-1.0 mM) much greater than metoprolol (100 nM) greater than dichloroisoproterenol (300 nM) greater than butoxamine (1100 nM). The beta 1-selective antagonist practolol had a low potency at 700 nM. The stereoselectivity of the receptor is indicated by the 400 to 70 fold higher potency of the (--)-isomers of isoproterenol, epinephrine and propranolol as compared to their (+)-stereoisomers. The data show that the beta-adrenergic receptor in the intermediate lobe of the rat pituitary gland is mainly of the bet 2-subtype. Study of this pure population of postsynaptic beta-adrenergic receptors where binding could be correlated with other parameters of cellular activity (cyclic AMP formation and alpha-MSH secretion) should yield useful information about the less accessible adrenergic systems of the brain.

Animals↗
PubMed1982

The dopamine receptor in the intermediate lobe of the rat pituitary gland is negatively coupled to adenylate cyclase.

The potency of a series of drugs to inhibit cyclic AMP accumulation in cells of the intermediate lobe of the rat pituitary gland in culture is typically dopaminergic. Dopaminergic antagonists reverse the inhibition of cyclic AMP levels according to their known pharmacological activity. The present data show that activation of the dopamine receptor in pars intermedia cells leads to inhibition of basal cyclic AMP accumulation and thus suggest that this receptor is negatively coupled to adenylate cyclase.

Adenylyl Cyclases↗
PubMed1982

beta-Adrenergic, CRF-ergic and dopaminergic mechanisms controlling alpha-MSH secretion in rat pars intermedia cells in primary culture.

1. A pure population of pars intermedia cells in primary culture was used to study changes in alpha-MSH secretion and cyclic AMP accumulation. 2. Beta-adrenergic agonists and CRF (corticotropin-releasing factor) stimulate alpha-MSH secretion and cyclic AMP accumulation. 3. Dopaminergic agonists inhibit basal as well as (-)isoproterenol- and CRF-induced alpha-MSH secretion and cyclic AMP accumulation. 4. Beta-adrenergic, dopaminergic and CRF receptors regulate pars intermedia cell activity probably through the adenylate cyclase system.

Adrenocorticotropic Hormone↗
PubMed1982

Direct effects of sex steroids on prolactin release at the anterior pituitary level: interactions with dopamine, thyrotropin-releasing hormone, and isobutylmethylxanthine.

When present alone for 4 or 8 days, 5 alpha-dihydrotestosterone (DHT) or the pure progestin R5020 (17,21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione) inhibits spontaneous PRL release by 33--50% in rat anterior pituitary cells in primary culture. This inhibitory effect of DHT and R5020 can only be partially reversed by 17 beta-estradiol (E alpha). DHT and R5020 inhibit spontaneous PRL release in E2-primed cells at ED50 values of 0.5 and 3 nM, respectively. While E2 diminishes by 30--60% the maximal inhibitory effect of dopamine on PRL release and increases by 10-fold the ED50 value of dopamine action, DHT and R5020 can prevent by 30--60% the action of E2 and thus increase the potency of dopamine to inhibit PRL release. The inhibitory action of DHT and R5020 as well as the stimulatory action of E2 on spontaneous PRL release are similarly expressed on TRH- and 3-isobutyl-1-methylxanthine-induced PRL release, thus suggesting that at least part of the highly effective modulatory effects of sex steroids are exerted at a step after cAMP formation.

1-Methyl-3-isobutylxanthine↗
PubMed1981

Cefotaxime kinetics after multiple-dose intramuscular study in healthy volunteers.

The pharmacokinetics of cefotaxime after repeated doses of intramuscular injections were studied in 8 healthy volunteers receiving 1 g cefotaxime every 8 h for 6 days. Mean peak serum level after the first 1 g intramuscular dose was 26.8 +/- 6.4 micrograms/ml and the peak serum concentration was reached within 75 min. The half-life of cefotaxime was 1.35 +/- 0.33 h and the total apparent clearance 263 +/- 63 ml/min. After the last injection (day 6), the mean peak serum level reached 19.1 +/- 3.2 micrograms/ml and the areas under the curve were significantly lower than on day 1. No body accumulation of the drug could be detected. Serum levels of cefotaxime monitored throughout the study 5 min prior to and 30 min after the intramuscular injection were found above the minimum inhibitory concentration for most aerobic gram-positive and gram-negative sensitive organisms.

Adult↗