prostaglandin-d2 and capsazepine

prostaglandin-d2 has been researched along with capsazepine* in 2 studies

Other Studies

2 other study(ies) available for prostaglandin-d2 and capsazepine

ArticleYear
Effects of capsazepine on human small airway responsiveness unravel a novel class of bronchorelaxants.
    Pulmonary pharmacology & therapeutics, 2007, Volume: 20, Issue:3

    Capsazepine is known as a transient receptor potential channel vanilloid subfamily 1 (TRPV(1)) antagonist that inhibits bronchoconstriction evoked in animals by TRPV(1) agonists. In this study, effects of capsazepine and chemically related analogues, so called capsazepinoids, were examined in vitro on contractile effects in human small airway preparations. Repeated cycles with 1h of LTD(4)-free physiological saline solution followed by 30min exposure to LTD(4) (10nM) demonstrated that the contractile responsiveness of the preparations exhibited little change over time despite repeated challenges (>12h). Capsazepine (1-100microM) reversibly and concentration-dependently inhibited the contractile response to LTD(4) with EC(50) approximately 10microM and approximately 90% relaxation at 100microM. Capsazepine (10microM) was approximately equally effective to attenuate the contractions evoked by several different inflammatory contractile agonists (LTD(4), PGD(2), histamine), and it relaxed preparations with established tonic contraction due to LTD(4). Higher concentrations of capsazepine were needed to relax ACh-contractions. The effect of capsazepine on LTD(4)-induced contractions was not significantly reduced by pre-treating the preparations with either of propranolol (10microM)+atropine (1microM), L-NAME (1mM), indomethacin (1microM), iberiotoxin (0.1microM), capsaicin (10microM), and nifedipine (10microM). Although the mechanism of action of the present capsazepine-induced bronchorelaxation remains unknown it emerged here that they represent a generally effective principle exerting a functional antagonism against contractile mediators but distinct from beta receptor agonists and inhibitors of L-type calcium channels. The inhibitory effect of capsazepine is shared by chemical analogues, but not with other TRPV(1) antagonists, suggesting the possibility that capsazepine represents a novel class of bronchorelaxants effective in human small airways. These findings were not predicted by previous observations that have concerned quite limited effects of capsazepine on airway tone in different animal test systems. If potency can be further increased and the results translated to in vivo, compounds representing the capsazepinoid class of bronchorelaxants might become useful in the treatment of patients suffering from asthma and COPD.

    Topics: Acetylcholine; Adrenergic beta-Antagonists; Atropine; Bronchi; Bronchodilator Agents; Capsaicin; Cholinergic Agents; Cyclooxygenase Inhibitors; Dose-Response Relationship, Drug; Enzyme Inhibitors; Histamine; Humans; In Vitro Techniques; Indomethacin; Leukotriene D4; Molecular Structure; Muscle Relaxation; Muscle, Smooth; NG-Nitroarginine Methyl Ester; Nifedipine; Peptides; Potassium Channels, Calcium-Activated; Propranolol; Prostaglandin D2; TRPV Cation Channels; Vasodilator Agents

2007
Direct activation of capsaicin receptors by products of lipoxygenases: endogenous capsaicin-like substances.
    Proceedings of the National Academy of Sciences of the United States of America, 2000, May-23, Volume: 97, Issue:11

    Capsaicin, a pungent ingredient of hot peppers, causes excitation of small sensory neurons, and thereby produces severe pain. A nonselective cation channel activated by capsaicin has been identified in sensory neurons and a cDNA encoding the channel has been cloned recently. However, an endogenous activator of the receptor has not yet been found. In this study, we show that several products of lipoxygenases directly activate the capsaicin-activated channel in isolated membrane patches of sensory neurons. Among them, 12- and 15-(S)-hydroperoxyeicosatetraenoic acids, 5- and 15-(S)-hydroxyeicosatetraenoic acids, and leukotriene B(4) possessed the highest potency. The eicosanoids also activated the cloned capsaicin receptor (VR1) expressed in HEK cells. Prostaglandins and unsaturated fatty acids failed to activate the channel. These results suggest a novel signaling mechanism underlying the pain sensory transduction.

    Topics: Animals; Capsaicin; Cell Line; Cells, Cultured; Dinoprostone; Eicosanoids; Ganglia, Spinal; Humans; Hydroxyeicosatetraenoic Acids; Inflammation; Ion Channel Gating; Leukotriene B4; Leukotrienes; Ligands; Lipid Peroxides; Lipoxygenase; Molecular Structure; Neurons, Afferent; Prostaglandin D2; Prostaglandin H2; Prostaglandins H; Rats; Receptors, Drug; Structure-Activity Relationship

2000