Differential sensitivity to ATP-sensitive potassium channel openers of norepinephrine-induced contraction of guinea pig and rat aorta

Saito, Wataru; Aida, Miwako; Sasaki, Masahiro; Saito, Yuuki; Tanaka, Yoshio; Tanaka, Hikaru; Shigenobu, Koki

doi:10.1016/s0024-3205(98)00194-5

Cited by 7 publications

(5 citation statements)

References 21 publications

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“…The sustained component of NA-produced contraction of guinea-pig aorta has a unique characteristic that it is resistant to the blockade by organic Ca 2+ entry blockers such as nifedipine, diltiazem and verapamil (Gouw et al 1990;Jenkin et al 1991;Saito et al 1998). By comparison, these Ca 2+ entry blockers have been shown to largely attenuate both sustained tension development and Ca 2+ entry produced by NA in rat aorta (Godfraind 1983;Sato et al 1988;Jenkin et al 1991;Saito et al 1998).…”

Section: Introductionmentioning

confidence: 99%

“…By comparison, these Ca 2+ entry blockers have been shown to largely attenuate both sustained tension development and Ca 2+ entry produced by NA in rat aorta (Godfraind 1983;Sato et al 1988;Jenkin et al 1991;Saito et al 1998). These pharmaco-mechanical and biochemical observations imply the existence of a plasma-membrane Ca 2+ -permeable channel in guinea-pig aortic smooth muscle cells, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Comparison of the Ca 2+ entry channels responsible for mechanical responses of guinea-pig aorta to noradrenaline and thapsigargin using SK&F 96365 and LOE 908

Tanaka

Imai

Igarashi

et al. 2000

Naunyn-Schmiedeberg's Archives of Pharmacology

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Noradrenaline (NA) produces sustained contractions in conduit arteries such as aorta isolated from various animal species. In guinea-pig aorta, NA-produced sustained contraction is largely dependent upon the influx of extracellular Ca2+, but is refractory to the treatment with organic Ca2+ entry blockers. In the present study, we attempted to characterize pharmacologically the Ca2+ entry channel responsible for NA-produced sustained contraction of guinea-pig aorta using SK&F 96365 (1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenylethyl]-1H-imi dazole) and LOE 908 ((R,S)-(3,4-dihydro-6,7-dimethoxy-isoquinoline-1-yl)-2-phenyl-N,N-di-[2- (2,3,4-trimethoxyphenyl)ethyl]-acetamide), both of which block voltage-independent Ca2+ channels. The effects of SK&F 96365 and LOE 908 on NA-produced contraction were compared with those on extracellular Ca2+-dependent contractile and endothelium-dependent relaxant responses to thapsigargin (TSG), an inhibitor of Ca2+-pump Ca2+-ATPase. NA (3x10(-6) M)-produced sustained contraction of guinea-pig aorta without endothelium exhibited a strong dependency on the extracellular Ca2+. Nicardipine (10(-7) M), diltiazem (10(-5) M) and verapamil (10(-5) M) did not show any appreciable inhibitory effects on NA-produced sustained contraction. SK&F 96365 concentration-dependently (10(-6)-10(-4) M) attenuated the NA-produced sustained contraction whereas LOE 908 did not affect it at concentrations up to 10(-4) M. Similarly, extracellular Ca2+-dependent contraction of guinea-pig aorta without endothelium in response to TSG was also diminished by SK&F 96365 but was unaffected by LOE 908. In fura-PE3-loaded vascular preparations, SK&F 96365 decreased both cytoplasmic Ca2+ level ([Ca2+]i) and muscle tension elevated by NA and TSG. Both SK&F 96365 and LOE 908 did not affect an endothelium-dependent relaxation of guinea-pig aorta in response to TSG. These findings suggest that in guinea-pig aortic smooth muscle cells, NA activates Ca2+ influx across the plasma-membrane through the Ca2+-permeable channel which is identical with or has similar properties to the store-operated Ca2+ channel (SOCC) stimulated by TSG, but is distinct from endothelial cell SOCC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Comparison of the Ca 2+ entry channels responsible for mechanical responses of guinea-pig aorta to noradrenaline and thapsigargin using SK&F 96365 and LOE 908

Tanaka

Imai

Igarashi

et al. 2000

Naunyn-Schmiedeberg's Archives of Pharmacology

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“…NIP-121 and cromakalim have been used as activators of potassium channels, and noradrenaline as vasoconstrictor. It was explained by low dependence of noradrenaline-induced contraction to calcium influx under such a condition in guinea pig aorta [9]. Our experiments have been performed with phenylephrine as a vasoconstrictor and we have not observed any significant differences in phenylephrine efficacy in all experimental groups.…”

Section: Resultsmentioning

confidence: 70%

Pinacidil relaxing effect on phenylephrine-precontracted guinea pig aorta was abolished by pretreatment with 17-β-estradiol

Kocić

Gruchała‐Niedoszytko²

2009

International Journal of Cardiology

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“…Potassium (K + ) channels play an important role in the regulation of vascular smooth *p < 0.05 versus control muscle cell membrane excitability and tonus (11). Activation of K + channels in vascular smooth muscle hyperpolarises cell membranes and closes voltage-dependent calcium channels.…”

Section: Discussionmentioning

confidence: 99%

The Mechanisms of the Direct Vascular Effects of Sevoflurane on Saphenous Veins in Vitro

et al. 2009

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Aim:The purpose of this study was to determine the mechanism of the directs effects of sevoflurane on human veins in vitro.Methods: Dose-response curves were obtained for cumulative doses of sevoflurane (0.5, 1, 1.5 and 2 MAC) on saphenous vein strips precontracted with 5-hydroxytryptamine ( 5-HT 10 -6 mol/L) incubated with either Nω-nitroL-arginine-methyl ester (L-NAME) (10 -4 mol/L), indomethacine (10 -5 mol/L), glibenclamide (10 -6 mol/L) or tetraethylammonium (10 -4 mol/L) Results: Preincubation of vein strips with tetraethylammonium (TEA, Ca ++ -activated K + channel blocker) did not influence the relaxant responses to sevoflurane (p>0.05). L-NAME, indomethacine and glibenclamide reduced the relaxation response to sevoflurane (p<0.05).Conclusion: Our results demonstrated that sevoflurane produces concentration dependent relaxation in human saphenous vein. The relaxant effects of sevoflurane are probably related with activation of nitric oxide synthase, cyclooxygenase and K ATP channels pathways.

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Differential sensitivity to ATP-sensitive potassium channel openers of norepinephrine-induced contraction of guinea pig and rat aorta

Cited by 7 publications

References 21 publications

Comparison of the Ca 2+ entry channels responsible for mechanical responses of guinea-pig aorta to noradrenaline and thapsigargin using SK&F 96365 and LOE 908

Comparison of the Ca 2+ entry channels responsible for mechanical responses of guinea-pig aorta to noradrenaline and thapsigargin using SK&F 96365 and LOE 908

Pinacidil relaxing effect on phenylephrine-precontracted guinea pig aorta was abolished by pretreatment with 17-β-estradiol

The Mechanisms of the Direct Vascular Effects of Sevoflurane on Saphenous Veins in Vitro

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