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• W2034182021 abstract "1 Transmembrane potentials were recorded from isolated carotid arteries of the guinea-pig supervised with modified Krebs-Ringer bicarbonate solution. Smooth muscle cells were impaled from the adventitial side with intracellular glass microelectrodes filled with KCl (30–80 MΩ). 2 Acetylcholine (1 μm) in the presence of inhibitors of nitric oxide synthase, (Nω-nitro-L-arginine (L-NOARG) 100 μm) and cyclo-oxygenase, (indomethacin 5 μm) induced an endothelium-dependent hyperpolarization (−18.9±1.6 mV, n = 15). 3 In the presence of these two inhibitors, S-nitroso-L-glutathione (10 μm), sodium nitroprusside (10 μm), 3-morphohnosydnonimine (SIN-1, 10 μm) and iloprost (0.1 μm) induced endothelium-independent hyperpolarizations of the smooth muscle cells (respectively: −16.0±2.3, −16.3±3.4, −12.8±2.0 and −14.5±1.5 mV, n = 4–6). 4 The addition of glibenclamide (1 μm) did not influence the acetylcholine-induced L-NOARG/indomethacin-resistant hyperpolarization (−18.0 ± 1.8 mV, n = 10). In contrast, the responses induced by S-nitroso-L-glutathione, sodium nitroprusside, SIN-1 and iloprost were abolished (changes in membrane potential: −0.8 ± 1.1, 1.3 ± 3.9, 4.5 ± 4.6 and 0.3 ± 0.8 mV respectively, n = 4–5). 5 In the presence of NO synthase and cyclo-oxygenase inhibitors, charybdotoxin (0.1 μm) or apamin (0.5 μm) did not influence the hyperpolarization produced by acetylcholine. However, in the presence of the combination of charybdotoxin and apamin, the acetylcholine-induced L-NOARG/indomethacin-resistant hyperpolarization was converted to a depolarization (4.4 ± 1.2mV, n = 20) while the endothelium-independent hyperpolarizations induced by S-nitroso-L-glutathione, sodium nitroprusside, SIN-1 and iloprost were not affected significantly (respectively: −20.4 ± 3.4, −22.5 ± 4.9, −14.5 ± 4.7 and −14.5 ± 0.5mV, n = 4–5). 6 In the presence of the combination of charybdotoxin and apamin and in the absence of L-NOARG and indomethacin, acetylcholine induced a hyperpolarization (−19.5 ± 3.7 mV, n = 4). This hyperpolarization induced by acetylcholine was not affected by the addition of indomethacin (−18.3 ± 4.6 mV, n = 3). In the presence of the combination of charybdotoxin, apamin and L-NOARG (in the absence of indomethacin), acetylcholine, in 5 out of 7 vessels, still produced hyperpolarization which was not significantly smaller (−9.1 ± 5.6 mV, n = 7) than the one observed in the absence of L-NOARG. 7 These findings suggest that, in the guinea-pig isolated carotid artery, the endothelium-independent hyperpolarizations induced by NO donors and iloprost involve the opening of KATP channels while the acetylcholine-induced endothelium-dependent hyperpolarization (resistant to the inhibition of NO-synthase and cyclo-oxygenase) involves the opening of Ca2+-activated potassium channel(s). Furthermore, in this tissue, acetylcholine induces the simultaneous release of various factors from endothelial origin: hyperpolarizing factors (NO, endothelium derived hyperpolarizing factor (EDHF) and prostaglandins) and possibly a depolarizing factor." @default.
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• W2034182021 date "1996-11-01" @default.
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• W2034182021 title "Endothelium-derived factors and hyperpolarization of the carotid artery of the guinea-pig" @default.
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• W2034182021 doi "https://doi.org/10.1111/j.1476-5381.1996.tb15765.x" @default.
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