Last update 01 Nov 2024

Platelet-activating factor x endothelin receptor

Last update 01 Nov 2024

Basic Info

Drugs associated with Platelet-activating factor x endothelin receptor

CV-6209

Target

Platelet-activating factor x endothelin receptor

Mechanism

Platelet-activating factor inhibitors [+1]

Active Org.-

Originator Org.

Takeda Pharmaceutical Co., Ltd.

Active Indication-

Inactive Indication

Asthma [+2]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Platelet-activating factor x endothelin receptor

100 Translational Medicine associated with Platelet-activating factor x endothelin receptor

0 Patents (Medical) associated with Platelet-activating factor x endothelin receptor

Literatures (Medical) associated with Platelet-activating factor x endothelin receptor

01 Apr 2013·Inflammation ResearchQ3 · MEDICINE

Endothelin-3 at low concentrations attenuates inflammatory responses via the endothelin B2 receptor

Q3 · MEDICINE

Article

Author: Keiichi Ebina ; Akira Sato

OBJECTIVEThe aim of this study was to clarify a role of endothelins (ETs: ET-1, -2, and -3) and their receptors (ETA, ETB1, and ETB2) in inflammatory responses.METHODSMale Wistar rats (180-220 g) were used. The effects of ETs in the absence or presence of the ETA antagonist BQ-123/the selective ETB2 antagonist BQ-788, and the effect of the selective ETB1 agonist IRL-1620 and the nonselective ETB agonist BQ-3020, on rat hind paw oedema induced by several proinflammatory substances were examined. The involvement of nitric oxide (NO) in the effects of ETs on the paw oedema was investigated using the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME).RESULTSET-3, which acts mainly on ETB, at low concentrations specifically inhibited platelet-activating factor (PAF)-induced paw oedema, whereas neither ET-1 nor ET-2, both of which act on ETA and ETB, showed inhibitory activity. The inhibition by ET-1 and ET-3 (each 0.5 pmol/paw) in the presence of BQ-123 (66.4 ± 6.7 % and 65.4 ± 22.6 %, respectively), was comparable to that by ET-3 (0.5 pmol/paw) alone (65.4 ± 10.9 %), whereas neither ET-1 nor ET-3 in the presence of BQ-788 showed inhibitory activity. BQ-3020 (0.5 pmol/paw) inhibited the oedema by 50.9 ± 6.0 %, whereas IRL-1620 showed almost no activity. Additionally, L-NAME markedly attenuated the inhibitory effects of ET-3 on PAF-induced paw oedema. These results indicate that ETB2 may mediate NO production and attenuation of PAF-induced inflammatory responses. Moreover, ET-3 (0.5 pmol/paw) inhibited the oedema induced by ET-1 at higher dose and zymosan by 76.6 ± 11.0 and 85.4 ± 13.6 %, respectively, indicating that ET-3 at lower concentrations inhibits the paw oedema induced by various inflammatory substances.CONCLUSIONSET-3 at low concentrations may attenuate inflammatory responses via ETB2 activation and NO production.

01 Nov 2012·Reproductive SciencesQ3 · MEDICINE

The Significance of Endothelin in Platelet-Activating Factor-Induced Fetal Growth Restriction

Q3 · MEDICINE

Article

Author: Saira Khan ; Mark G. Neerhof ; Larry G. Thaete ; Sylvia Synowiec ; Xiao-Wu Qu

The significance of endothelin-1 (ET-1) in platelet-activating factor (PAF)-induced fetal growth restriction (FGR) was evaluated in timed-pregnant rats receiving intravenous carbamyl-PAF (c-PAF; 0.5, 1.0, or 2.5 µg/kg per h) or vehicle, with or without ET-1 receptor A (ET(A)) antagonist (10 or 20 mg/kg per d) for 7 days beginning on gestation day 14. Tissues were collected on day 21. Carbamyl-PAF reduced fetal weights dose dependently. Placental weights were significantly reduced but not dose dependently. ET(A) antagonism prevented FGR at the 0.5, but not the 1.0 and 2.5 µg/kg per h c-PAF doses. Correspondingly, placental, but not uterine, preproET-1 messenger RNA (mRNA) expression (determined by reverse transcription-polymerase chain reaction) was increased at 0.5 µg/kg per h but not at higher c-PAF doses. In summary, c-PAF infusion results in fetal and placental growth restriction in the rat. At low doses of c-PAF, ET-1 is central to the pathophysiology of PAF-induced FGR. At higher c-PAF doses, FGR is induced by mechanisms other than ET-1 action.

01 Jan 2008·World Journal of GastroenterologyQ3 · MEDICINE

Synthesis of platelet-activating factor and its receptor expression in Kupffer cells in rat carbon tetrachloride-induced cirrhosis

Q3 · MEDICINE

Article

Author: Wang ; Su ; Yan ; Yin-Ying ; Chun-Ping ; Zhou ; Yang ; Shu-Hui ; Chen ; Yong-Yi ; Lin ; Feng ; Lu ; Yong-Ping

AIMTo determine the platelet-activating factor (PAF) synthesis and its receptor expression in Kupffer cells in rat carbon tetrachloride-induced cirrhosis.METHODSKupffer cells, isolated from the livers of control and CCl4-induced cirrhotic rats, were placed in serum-free medium overnight. PAF saturation binding, ET-1 saturation and competition binding were assayed. ET-1 induced PAF synthesis, mRNA expression of PAF, preproendothelin-1, endothelin A (ETA) and endothelin B (ETB) receptors were also determined.RESULTSA two-fold increase of PAF synthesis (1.42 +/- 0.14 vs 0.66 +/- 0.04 pg/microg DNA) and a 1.48-fold increase of membrane-bound PAF (1.02 +/- 0.06 vs 0.69 +/- 0.07 pg/microg DNA) were observed in activated Kupffer cells of cirrhotic rats. The application of ET-1 to Kupffer cells induced PAF synthesis in a concentration-dependent manner in both cirrhotic and normal rats via ETB receptor, but PAF synthesis in the activated Kupffer cells was more effective than that in the normal Kupffer cells. In activated Kupffer cells, PAF receptor expression and PAF binding capacity were markedly enhanced. Activated Kupffer cells raised the [125 I]-ET-1 binding capacity, but changed neither the affinity of the receptors, nor the expression of ETA receptor.CONCLUSIONKupffer cells in the course of CCl4-induced cirrhosis are the main source of increased PAF. ET-1 is involved endogenously in stimulating the PAF synthesis in activated Kupffer cells via ETB receptor by paracrine. ETA receptor did not appear in activated Kupffer cells, which may exacerbate the hepatic and extrahepatic complications of cirrhosis.

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