Measurement of intracellular Ca2+ in cultured arterial smooth muscle cells using Fura-2 and digital imaging microscopy

Goldman, W. F.; Bova, Sergio; Blaustein, Mordecai P.

doi:10.1016/0143-4160(90)90073-4

Cited by 83 publications

(37 citation statements)

References 18 publications

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“…A completely new finding was that norbormide behaved like the calcium entry blocker verapamil by relaxing these preparations contracted by high K + depolarization. Such blockers shift the concentration-response curve for calcium on depolarized rat aortic rings to the right, and inhibit intracellular calcium transients induced by depolarization in a stabilized cell line obtained from rat embryonic aorta (A7r5) (3,8). Norbormide was as effective as verapamil in relaxing these preparations, it also antagonized calcium transients elicited by a depolarizing stimulus in A7r5 cells.…”

Section: Effects Of Norbormide On Vascular Smooth Musclementioning

confidence: 99%

Norbormide: a Calcium Entry Blocker with Selective Vasoconstrictor Activity in Rat Peripheral Arteries

Bova

Cima

Golovina

et al. 2001

Cardiovascular Drug Reviews

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Norbormide is a unique vasoactive substance endowed with species-and tissue-specific, endothelium independent, vasoconstrictor activity that is restricted to the peripheral arteries of rat. In rat aorta and in all tested arteries of other species norbormide exhibits vasorelaxant property presumably due to the blockade of calcium channels. A calcium entry blocker effect of norbormide has also been described in isolated, perfused guinea pig hearts. In these preparations norbormide produced coronary vasodilator, as well as negative inotropic and dromotropic effects. In single ventricular myocytes of guinea pigs norbormide reduces L-type calcium current. The mechanism underlying the selective vasoconstrictor effect of norbormide is unknown. In rat caudal artery, a vessel contracted by norbormide, the drug activates phospholipase C (PLC) signal cascade which is the biochemical pathway involved in the contractile effect triggered by most receptor-activating vasoactive agents. Therefore, norbormide-induced contraction of rat peripheral vessels is likely to be due to the activation of a PLC-coupled receptor abundantly or selectively expressed in vascular smooth muscle cells. The identification of this putative receptor could facilitate the development of tissue-selective pharmacological agents.

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Section: Effects Of Norbormide On Vascular Smooth Musclementioning

confidence: 99%

Norbormide: a Calcium Entry Blocker with Selective Vasoconstrictor Activity in Rat Peripheral Arteries

Bova

Cima

Golovina

et al. 2001

Cardiovascular Drug Reviews

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“…A7r5 cells (American Type Culture Collection), derived from fetal rat aorta, were maintained in culture (35). Cells from passages 8-25 were dispersed by trypsinization and subcultured onto 25-mm glass coverslips and used within 7 days.…”

Section: Methodsmentioning

confidence: 99%

“…VSM cells were loaded with the acetoxymethyl ester of the fluorescent Ca2+ indicator fura-2 (Molecular Probes) and digital imaging was performed as described (35). The cells; the latter agent promotes Ca2+ release from the caffeine-sensitive Ca2+ store, whereas TG irreversibly blocks Ca2+ sequestration and, hence, refilling of Ins(1,4,5)P3-sensitive stores (13,14).…”

Section: Methodsmentioning

confidence: 99%

Functionally and spatially distinct Ca2+ stores are revealed in cultured vascular smooth muscle cells.

Tribe

Borin²,

Blaustein³

1994

Proc. Natl. Acad. Sci. U.S.A.

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sequester Ca2+ was inhibited. This suggests that the caffeinesensitive store may have a thapsigargin-insensitive Ca2+-sequestration mechanism. To complement these fura-2 experiments, chlortetracycline was used to visualize the Ca2+ stores directly. The latter studies revealed spatial differences in the location of the thapsigargin-sensitive and caffeine-sensitive Ca2+ stores (measured as thapsigargin-sensitive and caffeinesensitive chlortetracyclin fluorescence). Thus, these two types of stores appear to be both functionally and spatially distinct.

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“…Continuing vessel perfusion for a further 10 min washed out the extraneous dye. The tissue was then left for an equilibration time of at least 20 min, thus allowing the intracellular esterase to cleave fura-2/AM into active fura-2 (Goldman et al, 1990). The tissue was viewed with an inverted microscope using an Â 40 oil-immersion objective (NA 1.3).…”

mentioning

confidence: 99%

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

Zhao

Helden

2003

British J Pharmacology

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1 In vitro experiments were performed to investigate the actions of endothelin-1 (ET-1) on vasomotion and vasospasm in guinea-pig mesenteric lymphatics. 2 ET-1 modulated lymphatic vasomotion independent of the endothelium, with lower concentrations (p10 nM) increasing lymphatic vasomotion and higher concentrations (X100 nM) causing vasospasm. 3 ET-1-induced increases in vasomotion were accompanied by an increase in tonic [Ca 2 þ ] i . 4 These actions were inhibited by the ET A receptor antagonist BQ-123 (1 mM), the phospholipase C (PLC) inhibitor U73122 (5 mM), removal of extracellular Ca 2 þ , chelation of intracellular Ca 2 þ with BAPTA/AM (10 mM), the store Ca 2 þ -ATPase inhibitor thapsigargin (1 mM), caffeine (10 mM) and the inositol 1,4,5-trisphosphate (IP 3 ) receptor blocker heparin and 2-APB (30 mM). In contrast, the ET B receptor antagonist BQ-788 (1 mM), ryanodine (1 & 20 mM), pertussis toxin (PTx) or Cs þ had no significant actions on vasomotion or the magnitude of increase in tonic [Ca 2 þ ] i . 5 ET-1-induced vasospasm was accompanied by a transient increase in smooth muscle [Ca 2 þ ] i followed by a sustained plateau, an action that was abolished by removal of extracellular Ca 2 þ , but only marginally inhibited by nifedipine (1 mM). 6 Caffeine (10 mM), SKF 96165 (30 mM) or U73122 (5 mM) together with nifedipine (1 mM) abolished ET-1-induced vasospasm and increase in [Ca 2 þ ] i . 7 These results indicate that ET-1 increases lymphatic vasomotion by acting on smooth muscle ET A receptors and activation of G-protein-PLC-IP 3 cascade, which is known to cause pacemaker Ca 2 þ release and resultant pacemaker potentials. High concentrations of ET-1 cause a failure in Ca 2 þ homeostasis causing vasospasm, triggered by excessive Ca 2 þ influx primarily through store-operated channels (SOCs) with L-Ca 2 þ voltage-operated channels (VOCs) also contributing, but to a much lesser extent.

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Measurement of intracellular Ca2+ in cultured arterial smooth muscle cells using Fura-2 and digital imaging microscopy

Cited by 83 publications

References 18 publications

Norbormide: a Calcium Entry Blocker with Selective Vasoconstrictor Activity in Rat Peripheral Arteries

Norbormide: a Calcium Entry Blocker with Selective Vasoconstrictor Activity in Rat Peripheral Arteries

Functionally and spatially distinct Ca2+ stores are revealed in cultured vascular smooth muscle cells.

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

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