Cyproheptadine
Serotonin Antagonists
Methysergide
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Nelson Syndrome
A syndrome characterized by HYPERPIGMENTATION, enlarging pituitary mass, visual defects secondary to compression of the OPTIC CHIASM, and elevated serum ACTH. It is caused by the expansion of an underlying ACTH-SECRETING PITUITARY ADENOMA that grows in the absence of feedback inhibition by adrenal CORTICOSTEROIDS, usually after ADRENALECTOMY.
Appetite Stimulants
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Histamine H1 Antagonists
Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.
Serotonin
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
Diphenhydramine
Ketotifen
Receptors, Serotonin
Fenclonine
Metergoline
Quipazine
5-Hydroxytryptophan
Ketanserin
Pimozide
A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to HALOPERIDOL for the suppression of vocal and motor tics in patients with Tourette syndrome. Although the precise mechanism of action is unknown, blockade of postsynaptic dopamine receptors has been postulated. (From AMA Drug Evaluations Annual, 1994, p403)
Inhibitory effects of cyproheptadine on pituitary-thyroid axis and pancreatic beta cells in rats. (1/134)
AIM: To study the influences of cyproheptadine (Cyp) on the endocrine functions of pituitary-thyroid axis and pancreatic beta cells in rats. METHODS: The effects of Cyp on functions of pituitary-thyroid axis and pancreatic beta cells were observed by radioimmunoassay, biochemical analysis, and electron microscope. RESULTS: Cyp 2.3 mg.kg-1 ig for 10 d decreased serum thyroid stimulating hormone (TSH) from control groups (5.3 +/- 0.9) to (4.2 +/- 0.9) mU.L-1 and insulin levels from (64 +/- 8) to (50 +/- 9) kIU.L-1 (P < 0.05 and 0.01). Cyp 4.6 mg.kg-1 decreased serum TSH (3.8 +/- 0.5) mU.L-1, T3 (1.2 +/- 0.2) mmol.L-1, T4 (62 +/- 7) mmol.L-1, and insulin levels (42 +/- 8) kIU.L-1 decreased (P < 0.05 or 0.01). The retrograde changes of ultrastructure of pituitary TSH cells and pancreatic beta cells. CONCLUSION: Cyp has an inhibiting action on endocrine functions of pituitary-thyroid axis and pancreatic beta cells in rats. (+info)Effects of dexamethasone, cyproheptadine, anisodamine, and dinoprostone on TNF alpha production in endotoxic shock. (2/134)
AIM: To study the effects of dexamethasone (Dex), cyproheptadine (Cyp), anisodamine (Ani), and dinoprostone (Din) on lipopolysaccharides (LPS)-induced tumor necrosis factor alpha (TNF alpha) gene expression and antishock effects of inhibiting TNF alpha production. METHODS: Endotoxic shock in rats was produced by i.v. injection of LPS (E coli O111B4, 5 mg.kg-1). TNF alpha mRNA accumulation was assessed by Northern blot. Plasma TNF alpha contents were determined by radioimmunoassay. RESULTS: The TNF alpha mRNA levels in rat liver at 2 h after LPS challenge was increased obviously (autoradiograms analyzed by scanning were 38 +/- 10 vs saline control 11 +/- 8, P < 0.01). The plasma TNF alpha contents were markedly increased [(22 +/- 3) micrograms.L-1 vs saline control (2.2 +/- 1.0) micrograms.L-1, P < 0.01]. Dex 5, Cyp 5, Ani 10, or Din 2 mg.kg-1 immediately injected after i.v. LPS markedly decreased the TNF alpha mRNA levels in rat liver and plasma TNF alpha contents. The Dex, Cyp, Ani, and Din improved the mouse survival rate 24 h after LPS 20 mg.kg-1 challenge. CONCLUSION: Dex, Cyp, Ani, and Din strongly inhibit LPS-induced TNF alpha gene expression, and have a beneficial antishock effects. (+info)Effects of rupatadine, a new dual antagonist of histamine and platelet-activating factor receptors, on human cardiac kv1.5 channels. (3/134)
1. The effects of rupatadine, a new dual antagonist of both histamine H1 and platelet-activating factor receptors, were studied on human cloned hKv1.5 channels expressed in Ltk- cells using the whole-cell patch-clamp technique. 2. Rupatadine produced a use- and concentration-dependent block of hKv1.5 channels (KD=2.4+/-0.7 micronM) and slowed the deactivation of the tail currents, thus inducing the 'crossover' phenomenon. 3. Rupatadine-induced block was voltage-dependent increasing in the voltage range for channel opening suggesting an open channel interaction. At potentials positive to +10 mV the blockade decreased with a shallow voltage-dependence. Moreover, rupatadine also modified the voltage-dependence of hKv1.5 channel activation, which exhibited two components, the midpoint of the steeper component averaging -25. 2+/-2.7 mV. 4. When the intracellular K+ concentration ([K+]i) was lowered to 25% the voltage-dependent unblock observed at positive potentials was suppressed and the activation curve in the presence of rupatadine did not exhibit two components even when the midpoint of the activation curve was shifted to more negative potentials (-30. 3+/-1.3 mV). 5. On channels mutated on the residue R485 (R485Y) which is located on the external entryway of the pore the rupatadine-induced block did not decrease at potentials positive to +10 mV. In contrast, on V512M channels rupatadine reproduced all the features of the blockade observed on wild type channels. 6. All these results suggest that rupatadine blocks hKv1.5 channels binding to an external and to an internal binding site but only at concentrations much higher than therapeutic plasma levels in man. Efflux of K+ promotes the unbinding from the external site. Furthermore, rupatadine binds to an internal site and dramatically modifies the voltage-dependence of channel opening. (+info)5-HT1P receptor-mediated slow depolarization in neurons of guinea pig inferior mesenteric ganglion. (4/134)
AIM: To study the effects of several 5-hydroxytryptamine (5-HT) receptor subtype antagonists on 5-HT-induced depolarization and the effects of 5-HT1P receptor agonist on the membrane potential in the neurons of guinea pig inferior mesenteric ganglion (IMG). METHODS: Intracellular recordings were made from neurons of the isolated guinea pig IMG. RESULTS: Cyproheptadine (5-HT1/2 antagonist 10 mumol.L-1, n = 7) and BRL 24924 (5-HT1P antagonist 10 mumol.L-1, n = 19) reversibly suppressed 5-HT slow response; pressure ejection of MCPP (5-HT1P agonist 10 mmol.L-1) induced a slow depolarization in most of 5-HT sensitive neurons (10/14). CONCLUSION: 5-HT-induced slow depolarization is mediated by 5-HT1P receptor. (+info)A double blind controlled study of propranolol and cyproheptadine in migraine prophylaxis. (5/134)
Role of propranolol and cyproheptadine in the prophylaxis of migraine was studied in a controlled double blind trial. Two hundred fifty-nine patients were divided into four groups. Each group was either given a placebo, cyproheptadine, propranolol or a combination of the latter two drugs. The patients were followed for a period of three months. Significant relief in frequency, duration and severity from migranous attacks was seen in all drug treated groups over placebo. Significant correlation in response was seen in frequency, duration and severity in all the groups which received drugs. Statistically more significant relief was seen in cyproheptadine and propranolol treated group as compared to individual drug treated groups. In cyproheptadine and propranolol treated groups, the dropout rate was lower and associated symptoms were better relieved than in other groups. The study shows efficacy of combination of cyproheptadine and propranolol in migraine prophylaxis. (+info)Verapamil, cyproheptadine, and anisodamine antagonized [Ca2+]i elevation induced by TNFalpha in a single endothelial cell. (6/134)
AIM: To study the effect of tumor necrosis factor alpha (TNFalpha) on intracellular free Ca2+ concentration ([Ca2+]i) and the effects of verapamil (Ver), cyproheptadine (Cyp), and anisodamine (Ani) on TNFalpha-induced [Ca2+]i changes in single endothelial cell, and to explore the mechanisms of TNFalpha-mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains (ECV304) were seeded in 35-mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca2+]i in single endothelial cell were determined by laser scanning confocal microscopy. RESULTS: After stimulation with TNFalpha, [Ca2+]i in single endothelial cell rapidly increased in a concentration-dependent manner and arrived at the peak value within 60 s, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca2+]i elevation was more obvious in nuclear than in cytoplasma and decreased slowly. Ver (1, 2 micromol/L), Cyp (30, 60 micromol/L), and Ani (20, 40 micromol/L) markedly inhibited TNFalpha 1.2 nmol/L-induced [Ca2+]i elevation. CONCLUSION: TNFalpha markedly induces elevation of [Ca2+]i in a single endothelial cell, it may be an important mechanism of TNFalpha-induced shock and tissue injury. That Cyp and Ani obviously suppress TNFalpha-induced [Ca2+]i elevation probably is one of the mechanisms of their antishock effects. (+info)Anti-endotoxic shock effects of cyproheptadine in rats. (7/134)
OBJECTIVE: To investigate the antagonistic effect and mechanism of the effect of cyproheptadine (Cyp) on endotoxic shock in rats. METHODS: Endotoxic shock was produced in rats by i.v. injection of lipopolysaccharides (LPS) (5 mg/kg). Tumor necrosis factor (TNF(alpha)) mRNA expression was assessed by Northern blot. Plasma TNF(alpha) content was measured by radioimmunoassay. Plasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. The intracellular free calcium concentration ([Ca(2+)](i)) in single endothelial cells was determined by laser scanning confocal microscopy (LSCM). RESULTS: Cyp 5 mg/kg injected immediately after i.v. LPS raised the mean arterial blood pressure (MABP) of shocked rats and improved their 24 h survival rate. Meanwhile, Cyp markedly decreased TNF(alpha) mRNA levels in rat liver (18 +/- 10 vs. LPS + saline 38 +/- 10, P < 0.01) as well as plasma TNF(alpha) content [(7.8 +/- 2.4) microg/L vs. LPS + saline (21.5 +/- 3.2) microg/L, P < 0.01)]. It enhanced plasma SOD activity [(1037.2 +/- 112.8) NU/L vs LPS + saline (615.4 +/- 92.6) NU/L, P < 0.01], reduced the MDA content [(5.2 +/- 1.1) micromol/L vs. LPS + saline (9.8 +/- 1.5) micromol/L, P < 0.01], and inhibited TNF(alpha)-induced [Ca(2+)](i) elevation. CONCLUSION: Cyp exerts an anti-endotoxic shock effect by inhibiting TNF(alpha) gene expression, enhancing SOD activity, reducing lipid peroxidation, and preventing [Ca(2+)](i) overload. (+info)Suppressive effect of cyproheptadine on L-DOPA-induced growth hormone release in man. (8/134)
In order to elucidate the relationship between dopaminergic and serotoninergic mechanisms in regulating secretion of human growth hormone (hGH), the effect of cyproheptadine, an antiserotoninergic agent, on l-DOPA-induced hGH secretion was studied in normal subjects. Oral administration of 500 mg of l-DOPA caused a rise in plasma hGH in 6 of 7 subjects studied. This rise in plasma hGH was significantly blunted by the intravenous infusion of 5 mg of cyproheptadine. These results suggest the close relationship between dopamine and serotonin in the control of hGH secretion. (+info)
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