1984
DOI: 10.1042/cs067028p
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Endothelium-Dep Endent Calcium Fluxes in Rabbit Aorta

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Cited by 2 publications
(3 citation statements)
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“…Calcium influx was slightly but significantly higher with than without endothelium both in the absence and presence of noradrenaline. As previously reported (Collins, Griffith, Henderson & Lewis, 1985), this endothelium-dependent increment was abolished by flurbiprofen but not by the EDRF inhibitors dithiothreitol, potassium borohydride or phenidone (Griffith et al 1984a) (data not shown). Acetylcholine reduced noradrenaline-stimulated calcium influx in the presence of endothelium but had no effect in the absence of endothelium (Fig.…”
Section: Effect Of Endothelium On Noradrenaline-stimulated Calcium Insupporting
confidence: 87%
See 1 more Smart Citation
“…Calcium influx was slightly but significantly higher with than without endothelium both in the absence and presence of noradrenaline. As previously reported (Collins, Griffith, Henderson & Lewis, 1985), this endothelium-dependent increment was abolished by flurbiprofen but not by the EDRF inhibitors dithiothreitol, potassium borohydride or phenidone (Griffith et al 1984a) (data not shown). Acetylcholine reduced noradrenaline-stimulated calcium influx in the presence of endothelium but had no effect in the absence of endothelium (Fig.…”
Section: Effect Of Endothelium On Noradrenaline-stimulated Calcium Insupporting
confidence: 87%
“…It is now apparent that endothelium produces a potent vasodilator agent which is likely to prove of major importance in mediating and co-ordinating many ofthe fundamental phenomena ofvascular control (Furchgott, 1983; Griffith, Edwards, Collins, Lewis & Henderson, 1985a). Although the responsible agent, endothelium-derived relaxing factor (EDRF), has yet to be chemically identified, it is known to be an unstable, novel biological compound which is continually produced in the resting state under experimental conditions (Griffith, Edwards, Lewis, Newby & Henderson, 1984a;Griffith, Henderson, Hughes-Edwards & Lewis, 1984b) and whose production can be stimulated by a number of physiologically relevant substances (for review see Furchgott, 1983;and Griffith et al 1985 a).…”
Section: Introductionmentioning
confidence: 99%
“…This suggests that cyclic GMP might also regulate the opening ofthe Ca2+ channel in smooth muscle thereby modulating the Ca2+ gating mechanism activated by noradrenaline. This interpretation is in agreement with observations on the role ofendothelium in Ca2+ fluxes where it has been shown that the presence of endothelium reduces noradrenaline-dependent Ca2+ influx in rat and rabbit aortae Collins et al, 1985;Malta et al, 1986b).…”
Section: Discussionsupporting
confidence: 81%