Effects of adenosine analogs and ouabain on rhythmicity in human coronary artery

Sabouni, M H; Mustafa, S. Jamal

doi:10.1016/0014-2999(89)90787-5

Cited by 12 publications

(7 citation statements)

References 17 publications

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“…This suggestion is supported by the observation of several investigators that ouabain-mediated inhibition of Na + /K + -ATPase blocks vasomotion (23,24,28,29). However, how the Na + pumps of individual cells are entrained in this model to effect synchronized vasomotion in larger areas has not been discussed.…”

Section: Discussionsupporting

confidence: 57%

A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries

Giachini

Carneiro

Lima

et al. 2009

Braz J Med Biol Res

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Section: Discussionsupporting

confidence: 57%

A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries

Giachini

Carneiro

Lima

et al. 2009

Braz J Med Biol Res

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“…Some arteries show vasomotion spontaneously (e.g. Johansson & Bohr 1966) Changes in the activity of the Na+-K' pump (Sabouni & Mustafa 1989), as well as variation in movements of potassium or calcium across the cell membrane (Lamb et al 1985, Mulvany 1988) have been proposed to induce rhythmic activity. Such rhythmical changes in the transmembrane ion currents have been suggested to be secondary to oscillations in intermediary metabolism (Siege1 et al.…”

mentioning

confidence: 99%

Rhythmic contractions of isolated small arteries from rat: influence of the endothelium

Gustafsson¹,

Mulvany²,

Nilsson³

1993

Acta Physiologica Scandinavica

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Small arteries of the mesenteric arcade from Wistar rats display rhythmic oscillations superimposed on the tonic contractile response when exposed to submaximal doses of noradrenaline. We have previously shown that mechanical removal of the endothelium abolishes these oscillations. In the present study different methods to eliminate or modify the influence of the endothelium were used in order to further characterize the mechanisms behind rhythmic contractions in these vessels. Endothelium was removed either mechanically or chemically by perfusing the vessels with 0.3% CHAPS. The absence of functional endothelium enhanced noradrenaline sensitivity and simultaneously abolished oscillations in tension and membrane potential, but did not affect resting membrane potential. The rhythmic activity was also reduced or abolished by exposure to haemoglobin, methylene blue, LY83583 or L-NNA. Indomethacin and propranolol were without effect. Sodium nitroprusside or the permeant analogue of cyclic GMP, 8-bromo cyclic GMP, restored rhythmic activity in precontracted endothelium-denuded vessels. The data suggest that release of nitric oxide from the endothelium, and subsequent generation of cyclic GMP in the smooth muscle, activates oscillations in membrane potential and tension; the oscillator itself appears to be located within the smooth muscle cells.

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“…In vascular smooth muscle, most previous work has favoured a membrane-linked oscillator dependent on variations in membrane potential caused by variations in e.g. Na+K+-ATPase activity (Sabouni & Mustafa 1989, Siege1 et al 1989 or potassium conductance (Lamb et al 1985, Mulvany 1988). Previously, we have shown the rhythmic oscillations of mesenteric small arteries from rat to be endothelium-dependent (Gustafsson et al 1993).…”

mentioning

confidence: 99%

Rhythmic contractions of isolated small arteries from rat: role of calcium

Gustafsson

Nilsson

1993

Acta Physiologica Scandinavica

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In order to investigate the mechanisms behind rhythmic contractions in small arteries of the mesenteric arcade from Wistar rats, the calcium dependency of the oscillations in response to noradrenaline activation was tested on isolated vessels. Application of 1 microM ryanodine or 30 microM TMB-8 (procedures known to inhibit Ca2+ release from intracellular stores) totally abolished the rhythmic activity, even though the antagonists had opposite effects on the amplitude of the contractile response to noradrenaline. Verapamil (1 microM) or felodipine (1 nM) (agents known to inhibit influx of extracellular Ca2+) also abolished the oscillations and reduced the maximal noradrenaline response by about 40%. Reducing the extracellular Ca2+ concentration to 0.1 mM reduced the amplitude of the noradrenaline response to a similar extent as 1 nM felodipine, but did not eliminate the oscillations. This may indicate that the effect of calcium entry blockers was to eliminate the voltage-dependency of Ca2+ inflow rather than just reducing the Ca2+ level. Manoeuvres that would increase the cytosolic Ca2+ concentration (exposure to caffeine or to the calcium agonist BAY-K 8644) increased the frequency of the oscillations. These observations indicate an important role, not only for voltage-operating channels, but also for intracellular calcium stores in the generation of rhythmic contractions in these small arteries. Oscillations appear to be generated by an interplay between membrane activation and intracellular calcium stores.

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Effects of adenosine analogs and ouabain on rhythmicity in human coronary artery

Cited by 12 publications

References 17 publications

A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries

A key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries

Rhythmic contractions of isolated small arteries from rat: influence of the endothelium

Rhythmic contractions of isolated small arteries from rat: role of calcium

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