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Titolo:
ENDOTHELIUM-DEPENDENT CONTRACTION IN INTRAPULMONARY ARTERIES - MEDIATION BY ENDOTHELIAL NK1 RECEPTORS AND TXA(2)
Autore:
SHIRAHASE H; KANDA M; KURAHASHI K; NAKAMURA S; USUI H; SHIMIZU Y;
Indirizzi:
KYOTO UNIV,RADIOISOTOPE RES CTR,DIV PHARMACOL KYOTO 606 JAPAN TOKAI UNIV,SCH MED,DEPT COMMUNITY HLTH KANAGAWA 25911 JAPAN
Titolo Testata:
British Journal of Pharmacology
fascicolo: 7, volume: 115, anno: 1995,
pagine: 1215 - 1220
SICI:
0007-1188(1995)115:7<1215:ECIIA->2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
CANINE BASILAR ARTERY; SUBSTANCE-P; PULMONARY VASCULATURE; CEREBRAL-ARTERIES; ACETYLCHOLINE; ANTAGONIST; THROMBOXANE-A2; DERIVATIVES; PEPTIDES; RELEASE;
Keywords:
SUBSTANCE P; INTRAPULMONARY ARTERY; ENDOTHELIUM-DEPENDENT CONTRACTION (EDC); NK1 RECEPTOR; THROMBOXANE A(2) (TXA(2)); NEUROKININ A; NEUROKININ B; NK2 RECEPTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
H. Shirahase et al., "ENDOTHELIUM-DEPENDENT CONTRACTION IN INTRAPULMONARY ARTERIES - MEDIATION BY ENDOTHELIAL NK1 RECEPTORS AND TXA(2)", British Journal of Pharmacology, 115(7), 1995, pp. 1215-1220

Abstract

1 We have examined whether three natural tachykinins, substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) induce an endothelium-dependent contraction (EDC) in the rabbit isolated intrapulmonary artery.2 Removal of the endothelium almost abolished the contraction inducedby SP (10(-8) M) while it did not attenuate the contraction induced by SP (10(-7) M), NKA (10(-9)-10(-7) M) or NKB (10(-8) and 10(-7) M). 3The EDC induced by SP (10(-8) M) was abolished by M(1 antagonists (FK-888, CP-96345, CP-99994 and SR-140333) but not by an NK2 antagonist (SR-48968). 4 The EDC induced by SP was attenuated by cyclo-oxygenase inhibitors (aspirin and indomethacin), thromboxane A(2) (TXA(2)) synthetase inhibitors (OKY-046, KY-234 and KY-063) and a TXA(2) antagonist (S-1452). 5 The rank order of potency causing endothelium-independent contraction (EIC) was NKA > NKB > SP. The EIC induced by SP (10(-7) M) was attenuated by an NK2 antagonist but not by NK1 antagonists, cyclo-oxygenase inhibitors, TXA(2) synthetase inhibitors or a TXA(2) antagonist. 6 In conclusion, SP at 10(-8) M induces EDC via endothelial NK1 receptors and TXA(2) production, and SP at 10(-7) M induces EIC via NK2receptors in the rabbit intrapulmonary artery.

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Documento generato il 29/09/20 alle ore 19:57:12