Alterations in [Ca2+]i mediated by sodium‐calcium exchange in smooth muscle cells isolated from the guinea‐pig ureter.

Aaronson, Philip I.; Benham, Christopher D.

doi:10.1113/jphysiol.1989.sp017745

Cited by 39 publications

(30 citation statements)

References 48 publications

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“…5), or following incubation with ryanodine (Fleischmann et al 1994). These results are in contrast to observations made in smooth muscle cells isolated from the guinea-pig urinary bladder or coronary artery (Ganitkevich & Isenberg, 1992, 1995 (Ganitkevich & Isenberg, 1991, consistent with an additional source of calcium ions, whereas other preparations demonstrate increases in [Ca2+]i of the magnitude reported here (Aaronson & Benham, 1989). Finally, the relationship between the calcium flux and molar increase in calcium predicts a cytosolic buffering constant similar to that reported for smooth muscle cells (Guerrero et al 1994) and non-excitable cells (Neher & Augustine, 1992 (Callewaert, Cleemann & Morad, 1988).…”

Section: Discussioncontrasting

confidence: 56%

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Voltage‐dependent calcium currents and cytosolic calcium in equine airway myocytes.

Fleischmann

Wang

Pring

et al. 1996

The Journal of Physiology

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1. The relationship between voltage-dependent calcium channel current (Ica) and cytosolic free calcium concentration ([Ca2+],) was studied in fura-2 AM-loaded equine tracheal myocytes at 35°C and 1X8 mm Ca2' using the nystatin patch clamp method. The average cytosolic calcium buffering constant was 77 + 3 (n = 14), and the endogenous calcium buffering constant component is likely to be between 15 and 50. 4. We conclude that under near physiological conditions, neither CICR nor Na+-Ca2+ exchange play a substantial role in the regulation of Ica-induced increases in [Ca2+]i, and that, even following release of intracellular calcium by caffeine, Na+-Ca2+ exchange does not play an appreciable role in the removal of calcium ions from the cytosol.

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Section: Discussioncontrasting

confidence: 56%

“…Following a rise in [Ca2+]i, removal of calcium ions from the cytosol of smooth muscle cells occurs over a time scale greater than an order of magnitude slower than that observed in cardiac myocytes (Aaronson & Benham, 1989;Becker et at. 1989;Wier, 1990;Ganitkevich & Isenberg, 1991;McCarron et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Voltage‐dependent calcium currents and cytosolic calcium in equine airway myocytes.

Fleischmann

Wang

Pring

et al. 1996

The Journal of Physiology

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“…4B). This saturation differs from the continuous rise in [Ca2+]i up to 10 s at depolarizations to 0 mV reported for guineapig ureter myocytes or pituitary cells (Aaronson & Benham, 1989;Benham, 1989a Fig. 5A and B).…”

Section: Calcium Transients In Smooth Muscle Cellscontrasting

confidence: 41%

“…Instead there was an immediate transition to the slow recovery phase upon repolarization ( Fig. 2A; see also Aaronson & Benham, 1989).…”

Section: Calcium Transients In Smooth Muscle Cellsmentioning

confidence: 99%

“…Applying microspectrofluometry under voltage-clamp conditions allows the pathways for Ca2+ influx to be quantified, e.g. non-selective cation channels activated by purinergic receptors (Benham, 1989b), Ca2+ channels activated by depolarization (Becker et al 1989), and in smooth muscle cells from ureter, the Na+-Ca2+ exchanger (Aaronson & Benham, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Depolarization‐mediated intracellular calcium transients in isolated smooth muscle cells of guinea‐pig urinary bladder.

Ganitkevich

Isenberg

1991

The Journal of Physiology

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Cytoplasmic calcium transients due to single action potentials and voltage-clamp depolarizations in mouse pancreatic B-cells.

et al. 1992

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Changes in the cytoplasmic free calcium concentration ([Ca2+]i) in pancreatic B‐cells play an important role in the regulation of insulin secretion. We have recorded [Ca2+]i transients evoked by single action potentials and voltage‐clamp Ca2+ currents in isolated B‐cells by the combination of dual wavelength emission spectrofluorimetry and the patch‐clamp technique. A 500–1000 ms depolarization of the B‐cell from −70 to −10 mV evoked a transient rise in [Ca2+]i from a resting value of approximately 100 nM to a peak concentration of 550 nM. Similar [Ca2+]i changes were associated with individual action potentials. The depolarization‐induced [Ca2+]i transients were abolished by application of nifedipine, a blocker of L‐type Ca2+ channels, indicating their dependence on influx of extracellular Ca2+. Following the voltage‐clamp step, [Ca2+]i decayed with a time constant of approximately 2.5 s and summation of [Ca2+]i occurred whenever depolarizations were applied with an interval of less than 2 s. The importance of the Na(+)‐Ca2+ exchange for B‐cell [Ca2+]i maintenance was evidenced by the demonstration that basal [Ca2+]i rose to 200 nM and the magnitude of the depolarization‐evoked [Ca2+]i transients was markedly increased after omission of extracellular Na+. However, the rate by which [Ca2+]i returned to basal was not affected, suggesting the existence of additional [Ca2+]i buffering processes.

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Alterations in [Ca2+]i mediated by sodium‐calcium exchange in smooth muscle cells isolated from the guinea‐pig ureter.

Abstract: SUMMARY1. Sodium-calcium exchange was studied in single enzymatically isolated cells of the guinea-pig ureter using the Ca2+-sensitive fluorescent dye Indo-1 to monitor the intracellular Ca2+ concentration ([Ca2+]

Cited by 39 publications

References 48 publications

Voltage‐dependent calcium currents and cytosolic calcium in equine airway myocytes.

Voltage‐dependent calcium currents and cytosolic calcium in equine airway myocytes.

Depolarization‐mediated intracellular calcium transients in isolated smooth muscle cells of guinea‐pig urinary bladder.

Cytoplasmic calcium transients due to single action potentials and voltage-clamp depolarizations in mouse pancreatic B-cells.

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