Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nicotine caused a contraction of the rat coronary artery in the presence of Nomega-nitro-L-arginine methyl ester (L-NAME) and arachidonic acid, and did not in the absence of these agents. The present experiments were undertaken to pharmacologically characterize the nicotine-induced contraction in ring preparations of the rat coronary artery. The contraction was abolished by chemical removal of endothelium saponin. Oxygen radical scavengers, superoxide dismutase and catalase, significantly attenuated the contraction. Cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen, ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction. A TXA2 synthetase inhibitor (OKY-046) attenuated the contraction to a small extent only at high concentrations. A TXA2 receptor antagonist (S-1452) attenuated the contraction in a concentration-dependent manner. A nicotinic receptor antagonist (hexamethonium) attenuated the contraction in part and an alpha-adrenoceptor antagonist (prazosin) nearly abolished the contraction. From these results, it was suggested that the contraction induced by nicotine in the rat coronary artery in the presence of L-NAME and arachidonic acid is endothelium dependent, and involves reactive oxygen species and endothelial COX-1 metabolites of arachidonic acid. Part of the contraction is probably due to release of norepinephrine.
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PMID:Nicotine-induced contraction in the rat coronary artery: possible involvement of the endothelium, reactive oxygen species and COX-1 metabolites. 1181 54

Noradrenaline-induced contraction of the rat coronary arteries was significantly augmented by the presence of NG-nitro-L-arginine methyl ester (L-NAME) and arachidonic acid. The experiments in the study presented here were undertaken to characterize pharmacologically the augmented noradrenaline-induced contraction in ring preparations of rat coronary arteries. The contraction was stopped by a chemical remover of endothelium (saponin). Oxygen radical scavengers, superoxide dismutase and catalase, significantly attenuated the contraction. Cyclooxygenase-1 inhibitors (flurbiprofen, 10(-7) M) attenuated the noradrenaline-induced contraction and cyclooxygenase-2 (nimesulide, 10(-7) M) slightly attenuated the contraction. A thromboxane A2 (TXA2) synthetase inhibitor (OKY-046) and a TXA2 receptor antagonist (S-1452) did not affect the contraction. Based on these results, it was suggested that the contraction induced by noradrenaline in the rat coronary artery in the presence of L-NAME and arachidonic acid is endothelium-dependent, and that it involves reactive oxygen species and endothelial cyclooxygenase-1 metabolites of arachidonic acid.
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PMID:Noradrenaline-induced contraction mediated by endothelial COX-1 metabolites in the rat coronary artery. 1487 Oct 27

To explore the hypothesis that DPP-IV are involved in the diabetes-induced vascular damage, we assessed the vascular effects of chronic administration of saxagliptin (Saxa) or metformin (Met) in db/db mice, a model of type 2 diabetes, evaluating vascular structure and endothelial function in mesenteric small arteries. The increases in media/lumen and media cross sectional area were prevented by Saxa. In db/db, the blunted response to acetylcholine was only marginally affected by L-NAME (NO-synthase inhibitor), improved by SC-560 (cyclooxygenase-1 inhibitor) or SQ-29548 (thromboxane receptor antagonist), and totally restored by Apocynin (NAD(P)H-oxidase inhibitor). DFU (cyclooxygenase-2 inhibitor) had no effect. Saxa improved acetylcholine-induced relaxation, which returned partially sensitive to the inhibition of L-NAME. Dihydroethidium staining revealed an increased intravascular superoxide production in db/db, attenuated by L-NAME and Saxa, and abrogated by apocynin. The dimer/monomer ratio of endothelial NOS was decreased in db/db mice and restored by Saxa. Cyclooxygenase-1 and thromboxane-A2 receptor expression, higher in db/db, was down-regulated by Saxa. Met treatment did not modify any of the abnormal vascular responses. Saxa reverses vascular hypertrophic remodeling and ameliorates NO availability in small arteries from db/db mice through the abrogation of NAD(P)H oxidase-driven eNOS uncoupling and by reducing the action of cyclooxygenase-1-derived vasoconstrictors downregulating the expression of thromboxane-prostanoid receptors.
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PMID:Saxagliptin prevents vascular remodeling and oxidative stress in db/db mice. Role of endothelial nitric oxide synthase uncoupling and cyclooxygenase. 2645 87