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INVOLVEMENT OF ENDOTHELIAL CYCLO-OXYGENASE METABOLITES IN NORADRENALINE-INDUCED CONTRACTION OF RAT CORONARY ARTERY (2005)

Wang, Aimin ; Nishihashi, Tsuyoshi ; Trandafir, Cristina C ; [et al.]

Oxford, UK : Blackwell Science Pty

Clinical and experimental pharmacology and physiology 32 (2005), S. 0

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ISSN: 1440-1681

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Medicine

Notes: 1. Noradrenaline (NA; 0.3 µmol/L) caused a contraction of the rat coronary artery that markedly increased in the presence of the nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine methyl ester (l-NAME; 100 µmol/L) and arachidonic acid (1 µmol/L; P 〈 0.05).2. The present experiments attempted to elucidate the endothelium dependency of the contraction and to pharmacologically characterize the factors involved in the contraction induced by NA (0.3 µmol/L) in the presence of l-NAME and arachidonic acid in ring preparations of the rat coronary artery.3. The NA (0.3 µmol/L)-induced contraction was attenuated by a chemical remover of the endothelium (saponin at concentrations of 0.1 and 0.4 mg/mL) in a concentration-dependent manner (P 〈 0.05).4. The cyclo-oxygenase (COX)-1 inhibitor flurbiprofen (0.01–1 µmol/L) and the COX-2 inhibitor nimesulide (0.01–1 µmol/L) attenuated the NA-induced contraction in a concentration-dependent manner and the inhibitory effect of flurbiprofen was significantly more potent than that of nimesulide (P 〈 0.05). The 5-lipoxigenase inhibitor ZM-230487 (1 µmol/L) did not affect the NA-induced contraction.5. The thromboxane A2 (TXA2) synthetase inhibitor OKY-046 (30 µmol/L) and the TXA2 antagonist S-1452 (0.1–10 µmol/L) did not attenuate the NA-induced contraction.6. These results indicate that the contraction induced by NA in the rat coronary artery in the presence of l-NAME and arachidonic acid is endothelium dependent and is due to endothelial COX metabolites of arachidonic acid.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.0305-1870.2005.04242.x

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