Inhibition of Na-Ca Exchange by General Anesthetics

@article{Haworth1989InhibitionON,
  title={Inhibition of Na-Ca Exchange by General Anesthetics},
  author={R. Haworth and ATILLA B GOKNUR and H. Berkoff},
  journal={Circulation Research},
  year={1989},
  volume={65},
  pages={1021–1023}
}
General anesthetics, typically octanol, were found to inhibit the influx of calcium in isolated sodium-loaded adult rat heart cells, using 45Ca, quin 2, or indo 1. Inhibition by octanol, like inhibition by sodium, was competitive with calcium. Octanol and sodium together inhibited calcium influx synergistically. At physiological levels of extracellular calcium and sodium, the EC50 was 177 ± 37 μM for octanol and 48 ± 5 μM for decanol. These values are threefold to fourfold larger than those… Expand
Inhibition of Sodium/Calcium Exchange and Calcium Channels of Heart Cells by Volatile Anesthetics
TLDR
Halothane, isoflurane, and enflurane inhibit both Sodium sup +/Calcium2+ exchange and Cal calcium2+ channels at concentrations relevant to anesthesia, although they exhibit differences in potency and number of sites of action. Expand
The Effects of Halothane and Isoflurane on Slowly Inactivating Sodium Current in Canine Cardiac Purkinje Cells
TLDR
Inhibition of slow inward Na+ current may contribute to the marked decrease of action potential durationproduced by volatile anesthetics in false tendon Purkinje fibers but does not account for the larger decreases of duration produced by isoflurane than halothane. Expand
Control of the Na-Ca exchanger in isolated heart cells. II. Beat-dependent activation in normal cells by intracellular calcium.
Electrical stimulation of isolated adult rat heart cells in suspension at 4 Hz resulted in a fourfold increase in the rate of sodium influx and efflux across the sarcolemma, with no change in totalExpand
Sodium-calcium exchange in neonatal myocardium: reversible inhibition by halothane.
TLDR
Inhibition of sodium-calcium exchange current would be expected to have a magnified effect on contractility in neonatal as opposed to adult myocardium, and could theoretically ameliorate reperfusion injury due to influx of calcium via the calcium exchanger. Expand
Control of the Na-Ca exchanger in isolated heart cells. I. Induction of Na-Na exchange in sodium-loaded cells by intracellular calcium.
TLDR
It is concluded 1) that intracellular calcium induces Na-Na exchange through the Na-Ca exchanger in sodium-loaded cells exposed to calcium; and 2) that Na- Na exchange can be activated by calcium that enters the cell through calcium channels, and it is proposed that this Na- na exchange reflects the intrinsic activity of theNa- Ca exchanger. Expand
Regulation of Sodium‐Calcium Exchange in Intact Myocytes by ATP and Calcium
TLDR
The results suggest that ATP depletion after ischemia plus reperfusion is unlikely to limit the rate of Ca uptake by Na-Ca exchange in the whole heart if at least one quarter of the ATP is restored. Expand
The effects of quinidine on sodium-dependent calcium efflux in isolated rod photoreceptors of the salamander retina
TLDR
The incomplete block of the Na∶Ca,K exchange current by quinidine shows that it does not act by simple competition with external Na+, and suggests that the inhibition of the exchange by qu inidine may be non-specific. Expand
ATP dependence of calcium uptake by the Na-Ca exchanger of adult heart cells.
TLDR
It is concluded that ATP depletion after ischemia plus reperfusion is unlikely to limit the rate of calcium uptake through Na-Ca exchange in the whole heart if at least one quarter of the ATP is restored. Expand
The potential of Na+/Ca2+ exchange blockers in the treatment of cardiac disease
TLDR
The effects of NCX blockade are discussed, supporting its potential as a new cardiovascular therapeutic strategy and its reversibility and electrogenic properties must be taken into consideration when predicting the outcome. Expand
Nitrous oxide enhances Na+/Ca++ exchange in the neuroblastoma cell line SK-N-SH.
TLDR
Findings indicate that N2O suppresses carbachol-stimulated increases in [Ca++]i by enhancing Na+/Ca++ exchange activity, which may contribute to the anesthetic action of N 2O. Expand
...
1
2
3
4
...

References

SHOWING 1-10 OF 34 REFERENCES
Inhibition of Na+/Ca2+ exchange in pituitary plasma membrane vesicles by analogues of amiloride.
TLDR
Results suggest that the inhibitors function as Na+ analogues, interact at a Na+ binding site on the carrier, and reversibly tie up the transporter in an inactive complex, and are effective inhibitors of the bovine brain and porcine cardiac transport systems. Expand
Competitive interactions of sodium and calcium with the sodium-calcium exchange system of cardiac sarcolemmal vesicles.
TLDR
The results suggest that the exchange carrier contains two classes of cation binding sites: a divalent site which can bind either 1 Ca2+ or 1-2 Na+ ions and a second site which binds at least one additional Na+. Expand
Inhibition of Na+/Ca2+ exchange in membrane vesicle and papillary muscle preparations from guinea pig heart by analogs of amiloride.
TLDR
Structural/activity studies based on transport measurements in vesicles prepared from guinea pig left ventricle indicate that hydrophobic substitutions at the terminal nitrogen atom of the guanidinium moiety of amiloride improved the inhibitory potency almost 100-fold over that of the parent compound. Expand
Can Ca entry via Na-Ca exchange directly activate cardiac muscle contraction?
TLDR
Even in the absence of a functional SR and with Ca current blocked, Na-Ca exchange might bring sufficient Ca into the cell to activate appreciable contractions, but only when [Na]i is elevated. Expand
Inhibition of calcium influx in isolated adult rat heart cells by ATP depletion.
TLDR
It is concluded that ATP depletion per se does not quickly elevate cytoplasmic free calcium and that such an elevation is prevented by a very strong inhibition of the rate of calcium entry. Expand
Modulation of Na+-Ca2+ exchange in sarcolemmal vesicles by intravesicular Ca2+.
TLDR
The results suggest that an understanding of the kinetics of the Na-Ca exchange system may be hampered by the autoacceleration of exchange activity that occurs during initial rate measurements as Ca2+ accumulates within the vesicles. Expand
Membrane Electrical Properties of Vesicular Na‐Ca Exchange Inhibitors in Single Atrial Myocytes
TLDR
Both dodecylamine and 3′,4′-dichlorobenzamil were found to inhibit myocardial Ca and K currents over the same range of concentrations in which block of exchange activity occurs. Expand
Sodium-calcium exchange in heart: membrane currents and changes in [Ca2+]i.
TLDR
Guinea pig ventricular myocytes under voltage clamp were perfused internally with fura-2, a fluorescent Ca2+-indicator, and changes in [Ca2+]i and membrane current that resulted from Na-Ca exchange were identified through the use of various organic channel blockers and impermeant ions. Expand
Effects of Thiopental on Tension Development, Action Potential, and Exchange of Calcium and Potassium in Rabbit Ventricular Myocardium
TLDR
Thiopental in concentrations of 28 and 227 μmoles/liter reduced the tension developed by isolated rabbit ventricular myocardium by 50 and 80%, respectively, and the negative inotropic effect of thiopental appears to be due to reduced availability of calcium to the myofibrils. Expand
Na-Ca exchange in cardiac tissues.
  • D. Ellis
  • Chemistry, Medicine
  • Advances in myocardiology
  • 1985
TLDR
These studies confirmed earlier estimates of the approximate exchange ratio of the Na-Ca countertransport system and have demonstrated its large maximum transport rate capabilities. Expand
...
1
2
3
4
...