Disease relevance of VAPIPROST

• In Group 3 rats GR 32191 failed to influence progressive proteinuria and severity of glomerulosclerosis which were comparable to those in Group 1 [1].
• The haemodynamic effects of GR 32191, a thromboxane A2 receptor antagonist, in patients with renal artery stenosis and hypertension [2].
• This study was designed to determine if GR 32191 a thromboxane A2 receptor antagonist, would lower blood pressure in patients with hypertension and renal artery stenosis [2].
• Treatment was given as an intravenous injection with GR 32191 of 1 mg/kg body weight [3].

High impact information on VAPIPROST

• Low affinity sites, which irreversibly bind the antagonist GR 32191, transduce platelet activation and aggregation [4].
• 2. 1-heptan-2-yl-5-heptenoic acid (I-BOP) with high affinity support platelet shape change, whereas low affinity sites that bind irreversibly the antagonist GR 32191 transduce platelet aggregation [5].
• Blockade of the low affinity TP sites with GR 32191 prevented I-BOP-induced TPalpha phosphorylation [4].
• To elucidate the respective role of the two classes of pharmacological binding sites of TPs in shape change, platelets were incubated with I-BOP at low concentrations or stimulated by I-BOP at high concentrations after pretreatment with GR 32191 or activated with low concentrations of 8-epi-prostaglandin F(2)alpha [5].
• 2. Eight prostaglandin E (PGE) analogues were compared against sulprostone for their effects on PAF-induced aggregation in human platelet-rich plasma (PRP) in the presence of GR 32191 and the DP-receptor antagonist, BW A868C [6].

Biological context of VAPIPROST

• The results show that, GR 32191, given orally, in doses of 20 mg and 40 mg, does not reduce the blood pressure to any clinically important degree [2].

Anatomical context of VAPIPROST

• EP-092 produced pA2 values against prostanoid agonists in the human bronchus similar to those seen in the guinea-pig trachea, as did GR-32191 [7].

Associations of VAPIPROST with other chemical compounds

• In contrast to platelets, studies of ligand dissociation only identified GRr sites in rat aortic SMC and GR 32191 failed to inactivate PGH2/TxA2 receptors as detected by the PGH2/TxA2 receptor antagonist, [3H]SQ 29548 [8].

Gene context of VAPIPROST

• The endothelin-1-induced contractions were similarly inhibited by GR 32191 ([1R-[1alpha(Z),2beta,3beta,5alpha]]-(+)-7-[5-([1,1'-b iphenyl]-4-ylmethoxy)-3-hydroxy-2-(1-piperidinyl)cyclopentyl]-4-++ +heptonoic acid, a thromboxane A2 receptor antagonist [9].

References