The Experts below are selected from a list of 10104 Experts worldwide ranked by ideXlab platform
Hubert Vaudry - One of the best experts on this subject based on the ideXlab platform.
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Serotonin-induced stimulation of cortisol secretion from human adrenocortical tissue is mediated through activation of a Serotonin4 receptor subtype.
Neuroscience, 1992Co-Authors: Hervé Lefebvre, V. Contesse, Catherine Delarue, Marc G. J. Feuilloley, F. Hery, P. Grise, G. Raynaud, A.a.j. Verhofstad, L.m. Wolf, Hubert VaudryAbstract:Abstract The occurrence of Serotonin in the human adrenal gland was demonstrated both by immuno-histochemical and biochemical approaches. Using specific polyclonal antibodies to Serotonin, the presence of numerous immunoreactive cells was revealed by means of the peroxidase-antiperoxidase technique. These cells exhibited the morphological characteristics of mast cells. Combination of high performance liquid chromatography and electrochemical detection showed the presence of substantial amounts of both Serotonin and its metabolite 5-hydroxyindolacetic acid in adrenocortical extracts. The role of Serotonin in the regulation of steroidogenesis from human adrenocortical slices was studied in vitro using a perifusion system technique coupled to a specific radioimmunoassay for cortisol. Graded doses of Serotonin (from 10 −8 M to 3 × 10 −7 M) increased cortisol production in a dose-dependent manner. Prolonged exposure of adrenal fragments to Serotonin (10 −7 M) induced a biphasic response, i.e. a rapid and transient increase in cortisol secretion followed by a plateau phase, suggesting the existence of a desensitization phenomenon. The stimulatory effect of Serotonin (10 −7 M) was not altered during infusion of the Serotonin, and/or Serotonin 2 receptor antAgonists methysergide (10 −6 M) and ketanserin (10 −6 M), respectively. In contrast, ICS 205 930 (10 −6 M), a non-selective Serotonin 3 /Serotonin 4 antAgonist, totally abolished the response of adrenal slices to Serotonin (10 t7¯ M). The benzamide derivative zacopride, considered as a Serotonin 4 Agonist, induced a robust stimulation of cortisol secretion. In addition, the corticotropic effects of Serotonin (10 −7 M) and zacopride (10 −6 M) were not additive. Incubation of adrenocortical fragments with zacopride (10 −6 M) or Serotonin (10 −6 M) caused a significant increase in cAMP formation. Taken together, these data suggest that Serotonin, locally released by intra-adrenal mast-like cells, may act as a paracrine factor to stimulate cortisol secretion in man. Our results also indicate that Serotonin-induced corticosteroid production is mediated through activation of a Serotonin 4 receptor subtype positively coupled to adenylate cyclase.
Hervé Lefebvre - One of the best experts on this subject based on the ideXlab platform.
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Serotonin-induced stimulation of cortisol secretion from human adrenocortical tissue is mediated through activation of a Serotonin4 receptor subtype.
Neuroscience, 1992Co-Authors: Hervé Lefebvre, V. Contesse, Catherine Delarue, Marc G. J. Feuilloley, F. Hery, P. Grise, G. Raynaud, A.a.j. Verhofstad, L.m. Wolf, Hubert VaudryAbstract:Abstract The occurrence of Serotonin in the human adrenal gland was demonstrated both by immuno-histochemical and biochemical approaches. Using specific polyclonal antibodies to Serotonin, the presence of numerous immunoreactive cells was revealed by means of the peroxidase-antiperoxidase technique. These cells exhibited the morphological characteristics of mast cells. Combination of high performance liquid chromatography and electrochemical detection showed the presence of substantial amounts of both Serotonin and its metabolite 5-hydroxyindolacetic acid in adrenocortical extracts. The role of Serotonin in the regulation of steroidogenesis from human adrenocortical slices was studied in vitro using a perifusion system technique coupled to a specific radioimmunoassay for cortisol. Graded doses of Serotonin (from 10 −8 M to 3 × 10 −7 M) increased cortisol production in a dose-dependent manner. Prolonged exposure of adrenal fragments to Serotonin (10 −7 M) induced a biphasic response, i.e. a rapid and transient increase in cortisol secretion followed by a plateau phase, suggesting the existence of a desensitization phenomenon. The stimulatory effect of Serotonin (10 −7 M) was not altered during infusion of the Serotonin, and/or Serotonin 2 receptor antAgonists methysergide (10 −6 M) and ketanserin (10 −6 M), respectively. In contrast, ICS 205 930 (10 −6 M), a non-selective Serotonin 3 /Serotonin 4 antAgonist, totally abolished the response of adrenal slices to Serotonin (10 t7¯ M). The benzamide derivative zacopride, considered as a Serotonin 4 Agonist, induced a robust stimulation of cortisol secretion. In addition, the corticotropic effects of Serotonin (10 −7 M) and zacopride (10 −6 M) were not additive. Incubation of adrenocortical fragments with zacopride (10 −6 M) or Serotonin (10 −6 M) caused a significant increase in cAMP formation. Taken together, these data suggest that Serotonin, locally released by intra-adrenal mast-like cells, may act as a paracrine factor to stimulate cortisol secretion in man. Our results also indicate that Serotonin-induced corticosteroid production is mediated through activation of a Serotonin 4 receptor subtype positively coupled to adenylate cyclase.
Michael A. Kamm - One of the best experts on this subject based on the ideXlab platform.
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Prucalopride, a systemic enterokinetic, for the treatment of constipation.
Alimentary Pharmacology & Therapeutics, 2002Co-Authors: Anton Emmanuel, A J Roy, Tanya Nicholls, Michael A. KammAbstract:Summary Background : Laxatives are frequently ineffective in treating constipation. An alternative therapeutic approach is to target Serotonin-4 receptors, which are involved in initiating peristalsis. Aim : In a double-blind, placebo-controlled trial, to assess the efficacy and safety of a systemically active Serotonin-4 Agonist, prucalopride. Methods : Seventy-four women with constipation were stratified into slow or normal transit groups, and each group was randomized to receive either placebo or 1 mg prucalopride daily for 4 weeks. A bowel function diary was maintained. Whole-gut and orocaecal transit, visceral sensitivity, quality of life and psychological state were assessed before and after treatment. Results : Prucalopride, not placebo, increased spontaneous stool frequency (P=0.008) and reduced time to first stool (P
V. Contesse - One of the best experts on this subject based on the ideXlab platform.
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Serotonin-induced stimulation of cortisol secretion from human adrenocortical tissue is mediated through activation of a Serotonin4 receptor subtype.
Neuroscience, 1992Co-Authors: Hervé Lefebvre, V. Contesse, Catherine Delarue, Marc G. J. Feuilloley, F. Hery, P. Grise, G. Raynaud, A.a.j. Verhofstad, L.m. Wolf, Hubert VaudryAbstract:Abstract The occurrence of Serotonin in the human adrenal gland was demonstrated both by immuno-histochemical and biochemical approaches. Using specific polyclonal antibodies to Serotonin, the presence of numerous immunoreactive cells was revealed by means of the peroxidase-antiperoxidase technique. These cells exhibited the morphological characteristics of mast cells. Combination of high performance liquid chromatography and electrochemical detection showed the presence of substantial amounts of both Serotonin and its metabolite 5-hydroxyindolacetic acid in adrenocortical extracts. The role of Serotonin in the regulation of steroidogenesis from human adrenocortical slices was studied in vitro using a perifusion system technique coupled to a specific radioimmunoassay for cortisol. Graded doses of Serotonin (from 10 −8 M to 3 × 10 −7 M) increased cortisol production in a dose-dependent manner. Prolonged exposure of adrenal fragments to Serotonin (10 −7 M) induced a biphasic response, i.e. a rapid and transient increase in cortisol secretion followed by a plateau phase, suggesting the existence of a desensitization phenomenon. The stimulatory effect of Serotonin (10 −7 M) was not altered during infusion of the Serotonin, and/or Serotonin 2 receptor antAgonists methysergide (10 −6 M) and ketanserin (10 −6 M), respectively. In contrast, ICS 205 930 (10 −6 M), a non-selective Serotonin 3 /Serotonin 4 antAgonist, totally abolished the response of adrenal slices to Serotonin (10 t7¯ M). The benzamide derivative zacopride, considered as a Serotonin 4 Agonist, induced a robust stimulation of cortisol secretion. In addition, the corticotropic effects of Serotonin (10 −7 M) and zacopride (10 −6 M) were not additive. Incubation of adrenocortical fragments with zacopride (10 −6 M) or Serotonin (10 −6 M) caused a significant increase in cAMP formation. Taken together, these data suggest that Serotonin, locally released by intra-adrenal mast-like cells, may act as a paracrine factor to stimulate cortisol secretion in man. Our results also indicate that Serotonin-induced corticosteroid production is mediated through activation of a Serotonin 4 receptor subtype positively coupled to adenylate cyclase.
Catherine Delarue - One of the best experts on this subject based on the ideXlab platform.
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Serotonin-induced stimulation of cortisol secretion from human adrenocortical tissue is mediated through activation of a Serotonin4 receptor subtype.
Neuroscience, 1992Co-Authors: Hervé Lefebvre, V. Contesse, Catherine Delarue, Marc G. J. Feuilloley, F. Hery, P. Grise, G. Raynaud, A.a.j. Verhofstad, L.m. Wolf, Hubert VaudryAbstract:Abstract The occurrence of Serotonin in the human adrenal gland was demonstrated both by immuno-histochemical and biochemical approaches. Using specific polyclonal antibodies to Serotonin, the presence of numerous immunoreactive cells was revealed by means of the peroxidase-antiperoxidase technique. These cells exhibited the morphological characteristics of mast cells. Combination of high performance liquid chromatography and electrochemical detection showed the presence of substantial amounts of both Serotonin and its metabolite 5-hydroxyindolacetic acid in adrenocortical extracts. The role of Serotonin in the regulation of steroidogenesis from human adrenocortical slices was studied in vitro using a perifusion system technique coupled to a specific radioimmunoassay for cortisol. Graded doses of Serotonin (from 10 −8 M to 3 × 10 −7 M) increased cortisol production in a dose-dependent manner. Prolonged exposure of adrenal fragments to Serotonin (10 −7 M) induced a biphasic response, i.e. a rapid and transient increase in cortisol secretion followed by a plateau phase, suggesting the existence of a desensitization phenomenon. The stimulatory effect of Serotonin (10 −7 M) was not altered during infusion of the Serotonin, and/or Serotonin 2 receptor antAgonists methysergide (10 −6 M) and ketanserin (10 −6 M), respectively. In contrast, ICS 205 930 (10 −6 M), a non-selective Serotonin 3 /Serotonin 4 antAgonist, totally abolished the response of adrenal slices to Serotonin (10 t7¯ M). The benzamide derivative zacopride, considered as a Serotonin 4 Agonist, induced a robust stimulation of cortisol secretion. In addition, the corticotropic effects of Serotonin (10 −7 M) and zacopride (10 −6 M) were not additive. Incubation of adrenocortical fragments with zacopride (10 −6 M) or Serotonin (10 −6 M) caused a significant increase in cAMP formation. Taken together, these data suggest that Serotonin, locally released by intra-adrenal mast-like cells, may act as a paracrine factor to stimulate cortisol secretion in man. Our results also indicate that Serotonin-induced corticosteroid production is mediated through activation of a Serotonin 4 receptor subtype positively coupled to adenylate cyclase.
