Pharmacology
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Pharmacokinetics of Wood Creosote: Glucuronic Acid and Sulfate Conjugation of Phenolic Compounds
Pharmacology - Tập 51 Số 3 - Trang 195-204 - 1995
Effects of 2,3-Butanedione Monoxime on Induction of Action Potential Bursts in Central Snail Neurons: Direct and Indirect Modulations of Ionic Currents The effects of 2,3-butanedione monoxime (BDM) on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of giant African snail (<i>Achatina fulica </i>Ferussac). The effect of okadaic acid on the neuron was also tested. The RP4 neuron showed a spontaneous firing of action potential. Okadaic acid (1 µmol/l) did not alter the frequency of spontaneous action potential while BDM (3 mmol/l) reversibly elicited bursts of potential (BoP) of the RP4 neuron. The BoP elicited by BDM (3 mmol/l) were reversed 20 min after incubation with diazoxide (500 µmol/l) while the BoP were not altered in preparations treated with okadaic acid and BDM. The BDM-elicited BoP were not inhibited after administration with (a) hexamethonium (100 µmol/l), (b) atropine (1 mmol/l), (c) <i>d</i>-tubocurarine (100 µmol/l), (d) prazosin (100 µmol/l), (e) propranolol (100 µmol/l), (f) calcium-free solution, (g) high K<sup>+</sup> (12 mmol/l) or (h) with high Mg<sup>2+</sup> (30 mmol/l) solutions. The BDM-elicited BoP were inhibited by pretreatment with KT-5720 (10 µmol/l) or H89 (10 µmol/l), the protein kinase A inhibitors. However, the BoP were not affected after application of chelerythrine (10 µmol/l) or Ro 31-8220 (10 µmol/l), the protein kinase C inhibitors. Voltage-clamped studies revealed that BDM elicited a negative slope resistance (NSR) at membrane potentials between –50 and –10 mV. The NSR was not detectable at the same membrane potential in control RP4 neuron. It is suggested that the BoP elicited by BDM were not due to (1) the synaptic effects of neurotransmitters; (2) the activation of cholinergic, adrenergic receptors, or (3) phosphatase activity of the neuron. The BDM-elicited BoP were dependent on the protein kinase A related cAMP in the neuron and the delayed outward K<sup>+</sup> current may contribute to the BDM-elicited BoP.
Pharmacology - Tập 73 Số 2 - Trang 57-69 - 2005
Involvement of Central Dopamine in the Hyperthermia in Rats Produced by d-Amphetamine
Pharmacology - Tập 13 Số 4 - Trang 309-316 - 1975
Classification of Angiotensin Receptors in Rat Isolated Uterus, Portal Vein, and Aorta with the Novel Competitive Antagonist Sarmesin
Pharmacology - Tập 37 Số 3 - Trang 137-147 - 1988
Regional Cerebral Glucose Utilization during Vasopressin-Induced Barrel Rotations or Bicuculline-Induced Seizures in Rats
Pharmacology - Tập 36 Số 1 - Trang 1-8 - 1988
Diazepam Stimulates Migration and Phagocytosis of Human Neutrophils: Possible Contribution of Peripheral-Type Benzodiazepine Receptors and Intracellular Calcium In isolated human neutrophils, diazepam (10 nmol/l to 10 µmol/l) concentration-dependently increased migration and phagocytosis. Diazepam-induced migration and phagocytosis were inhibited by the peripheral benzodiazepine receptor (PBR) antagonist PK11195 (10 µmol/l). The PBR agonist Ro5-4864 (10 nmol/l to 10 µmol/l) did not affect migration but slightly enhanced phagocytosis, while clonazepam, which binds to the central-type benzodiazepine receptors but has no affinity for PBRs, was ineffective on both parameters up to 10 µmol/l. Phagocytosis induced by diazepam or Ro5-4864 was inhibited by the Ca<sup>2+</sup> channel blocker <i>L</i>-verapamil (10 µmol/l), which however did not affect the action of diazepam on migration. Competition binding experiments performed by fluorescent staining of PBRs showed that diazepam directly interacts with PBRs on human neutrophils. Both diazepam and Ro5-4864 (10 nmol/l to 10 µmol/l) induced a rise of intracellular free Ca<sup>2+</sup> concentrations ([Ca<sup>2+</sup>]<sub>i</sub>), which was inhibited by PK11195 (10 µmol/l) and <i>L</i>-verapamil (10 µmol/l) and prevented by extracellular Ca<sup>2+</sup> chelation with EGTA (5 mmol/l). In conclusion, experimental evidence indicates that in human neutrophils diazepam stimulates both migration and phagocytosis through activation of PBRs. Diazepam-induced [Ca<sup>2+</sup>]<sub>i</sub> changes depend on a PBR-operated, <i>L</i>-verapamil-sensitive increase in the plasma membrane permeability and subsequent extracellular Ca<sup>2+</sup> entry, and contribute to diazepam-induced phagocytosis. On the contrary, the effect of diazepam on migration seems to occur through Ca<sup>2+</sup>-independent mechanisms.
Pharmacology - Tập 63 Số 1 - Trang 42-49 - 2001
CRTH2 and D-Type Prostanoid Receptor Antagonists as Novel Therapeutic Agents for Inflammatory Diseases Accumulation of type 2 T helper (Th2) lymphocytes and eosinophils is a hallmark of bronchial asthma and other allergic diseases, and it is believed that these cells play a crucial pathogenic role in allergic inflammation. Thus, Th2 cells and eosinophils are currently considered a major therapeutic target in allergic diseases and asthma. However, drugs that selectively target the accumulation and activation of Th2 cells and eosinophils in tissues are unavailable so far. Prostaglandin (PG)D<sub>2</sub> is a key mediator in various inflammatory diseases including allergy and asthma. It is generated by activated mast cells after allergen exposure and subsequently orchestrates the recruitment of inflammatory cells to the tissue. PGD<sub>2</sub> induces the chemotaxis of Th2 cells, basophils and eosinophils, stimulates cytokine release from these cells and prolongs their survival, and might hence indirectly promote IgE production. PGD<sub>2</sub> mediates its biologic functions via 2 distinct G protein-coupled receptors, D-type prostanoid receptor (DP), and the chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2). DP and CRTH2 receptors are currently being considered as highly promising therapeutic targets for combating allergic diseases and asthma. Here, we revisit the roles of PGD<sub>2</sub> receptors in the regulation of eosinophil and Th2 cell function and the efforts towards developing candidate compounds for clinical evaluation.
Pharmacology - Tập 85 Số 6 - Trang 372-382 - 2010
Calmodulin Antagonists Enhance Calcium Binding to Calmodulin
Pharmacology - Tập 27 Số 3 - Trang 125-129 - 1983
Calmodulin Antagonists&rsquo; Binding Sites on Calmodulin
Pharmacology - Tập 26 Số 5 - Trang 249-257 - 1983
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