piperidines and ozagrel

piperidines has been researched along with ozagrel* in 2 studies

Reviews

1 review(s) available for piperidines and ozagrel

ArticleYear
[Endothelin receptor antagonist, phosphodiesterase inhibitor, thromboxane inhibitor].
    Nihon rinsho. Japanese journal of clinical medicine, 2001, Volume: 59, Issue:6

    According to the advanced comprehension of pathophysiology of primary pulmonary hypertension (PPH), a therapeutical approach to PPH has changed recently. One of the breakthrough to the treatment of PPH is application of prostacyclin. It has been revealed that intravenous administration of prostacyclin has improved the prognosis and patient's quality of life. Another development of endothelin receptor antagonists and phosphodiesterase inhibitors have provided a novel pulmonary-specific effect. An endothelin receptor antagonist has a great inhibitory effect against pulmonary vasculature remodeling. In this regard, this regard, this receptor antagonist has superior effect to other medicines. Furthermore, a phosphodiesterase inhibitor shows a great decreasing effect on pulmonary hypertension with less effect on systemic blood pressure. These drugs will provide a great potential to the treatment of pulmonary hypertension.

    Topics: Animals; Endothelin Receptor Antagonists; Enzyme Inhibitors; Humans; Hypertension, Pulmonary; Methacrylates; Phosphodiesterase Inhibitors; Piperidines; Purinones; Quinazolines

2001

Other Studies

1 other study(ies) available for piperidines and ozagrel

ArticleYear
The induction of a biphasic bronchospasm by the ETB agonist, IRL 1620, due to thromboxane A2 generation and endothelin-1 release in guinea-pigs.
    British journal of pharmacology, 1996, Volume: 118, Issue:6

    1. IRL 1620 (0.01-0.1 mg kg-1, i.v.), a selective endothelin B (ETB) receptor agonist, induced a dose-dependent biphasic increase in total lung resistance and a decrease in dynamic compliance in anaesthetized and artificially ventilated guinea-pigs. After intravenous injection of IRL 1620 (0.03 mg kg-1), the first phase was observed within 2 min whereas the second phase started between 5 and 10 min after injection and was long lasting. 2. In order to characterize which endothelin receptors are involved in both phases of bronchoconstriction, we studied the effect of ETA and ETB receptor antagonists (BQ 123 and BQ 788, respectively). BQ 788 (0.1-1 mg kg-1, i.v.) inhibited, in a dose-dependent manner, both phases of bronchoconstriction. BQ 123 (3 mg kg-1, i.v.) markedly inhibited (by 76%) the second phase of bronchoconstriction but had no effect on the early component of the response. 3. The effect of atropine, neurokinin-I (NK1) and neurokinin-2 (NK2) receptor antagonists (SR140333 and SR48968, respectively) were tested to investigate the possible involvement of cholinergic and sensory nerve activation, respectively, in the response to IRL 1620. Likewise, the role of arachidonic acid metabolites (leukotriene D4 antagonist, ONO-1078 and thromboxane A2 (TXA2) inhibitor, OKY-046) in this response was also investigated. OKY-046 (1 mg kg-1, i.v.) and atropine (1 mg kg-1, i.v.) partially inhibited the first phase (by 80% and 20%, respectively) without affecting the late phase of bronchoconstriction. Neither ONO-1078 (1 mg kg-1, i.v.) nor the combination of SR140333 (0.2 mg kg-1, i.v.) and SR 48968 (0.2 mg kg-1, i.v.) modified IRL 1620-induced bronchoconstriction. 4. A low dose of IRL 1620 (0.005 mg kg-1, i.v.) induced a monophasic bronchoconstriction. Pretreatment by phosphoramidon (100 mumol kg-1, i.v.) restored the second phase of bronchoconstriction. In this condition, BQ 123 (3 mg kg-1, i.v.) was able to inhibit partially the second phase of bronchoconstriction. 5. These results suggest that both phases of bronchoconstriction induced by IRL 1620 were mediated primarily by ETB receptor activation, the first phase being a consequence of TXA2 and acetylcholine release. The inhibition by an ETA receptor antagonist and the restoration by a neutral endopeptidase (NEP) inhibitor of the second phase of bronchoconstriction suggests that primary activation of ETB receptors leads to autocrine/paracrine endothelin-1 (ET-1) release that would subsequently cause profound b

    Topics: Animals; Atropine; Bronchial Spasm; Bronchodilator Agents; Endothelin Receptor Antagonists; Endothelin-1; Endothelins; Female; Guinea Pigs; In Vitro Techniques; Male; Methacrylates; Neurokinin-1 Receptor Antagonists; Oligopeptides; Peptide Fragments; Peptides, Cyclic; Piperidines; Receptors, Endothelin; Receptors, Neurokinin-2; Thromboxane A2; Thromboxane-A Synthase

1996