Disease relevance of CBiol_001997

• Furthermore, pretreating lung preparations with 13-azaprostanoic acid, a TXA2 antagonist, before infusion of AGEPC and untreated platelets also reduced the pulmonary hypertension and blocked the lung edema [1].
• Elevated thromboxane levels in the rat during endotoxic shock: protective effects of imidazole, 13-azaprostanoic acid, or essential fatty acid deficiency [2].
• Antagonism of platelet aggregation by 13-azaprostanoic acid in acute myocardial ischemia and sudden death [3].

High impact information on CBiol_001997

• In vitro L636,499 and a third antagonist, 13-azaprostanoic acid, specifically reversed endoperoxide-induced platelet aggregation and vascular smooth muscle contraction [4].
• Preliminary results with the stable hydrazide 4 indicate that it inhibits arachidonic acid (AA) induced human platelet aggregation and that, unlike 13-azaprostanoic acid (1), its site of action is at the cyclooxygenase level [5].
• Antagonism of prostaglandin-mediated responses in platelets and vascular smooth muscle by 13-azaprostanoic acid analogs. Evidence for selective blockade of thromboxane A2 responses [6].
• A thromboxane/endoperoxide receptor antagonist 13-azaprostanoic acid prevented irreversible platelet aggregation induced by low AGEPC concentrations [7].
• The actions of STA2 were blocked by 13-azaprostanoic acid, a TXA2 receptor antagonist [8].

Chemical compound and disease context of CBiol_001997

• The effects of 13-azaprostanoic acid (13-APA) were studied during acute myocardial ischemia in cats and in rabbit sudden death induced by sodium arachidonate (Na-Ar) [3].

Biological context of CBiol_001997

• 13-Azaprostanoic acid, a receptor level antagonist of thromboxane A2 inhibited STA2-induced elevation of [Ca2+]i, phosphorylation of myosin light chain and serotonin release [9].

Anatomical context of CBiol_001997

• Specific binding of the thromboxane A2 antagonist 13-azaprostanoic acid to human platelet membranes [10].
• Arachidonate-induced efflux from microsomes was not inhibited by indomethacin, 13-azaprostanoic acid, or catalase and superoxide dismutase, indicating that the release was due to arachidonate and not a metabolite [11].

Associations of CBiol_001997 with other chemical compounds

• This release was blocked by inhibition of the cyclooxygenase with indomethacin (20 microM) or the specific TXA2/PGH2 antagonist, 13-azaprostanoic acid (13-APA, 100 microM) [12].

References