Poisson–Fermi Modeling of the Ion Exchange Mechanism of the Sodium/Calcium Exchanger

In this work, nanosized calcium deficient hydroxyapatite (nCDHA) was synthesized by the precipitation method, and then utilized as an adsorbent for removal of Fe (II), Cu (II), Ni (II) and Cr (VI) ions from aqueous solutions after characterizing it by various techniques as scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), energy-dispersive X-ray spectroscopy (EDX) and BET method. A possible structure of synthesized nCDHA was proposed. The adsorption study indicated that the adsorption equilibrium is well fitted with Langmuir isotherm model with the maximum adsorption capacities followed the order of Fe (II) > Cu (II) > Ni (II) > Cr (VI) with the values of 137.23, 128.02, 83.19 and 2.92 mg/g, respectively. The ion-exchange mechanism was dominant for the adsorption of metal ions onto nCDHA at initial metal concentrations lower than 0.01 mol/L. Along with the ion-exchange mechanism, there was an additional precipitation occurred on the surface of nCDHA in the case of Fe (II) and Cu (II) at initial concentrations higher than 0.01 mol/L.

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Sodium-calcium exchange-mediated contractions in feline ventricular myocytes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.4.h1161 ◽

1992 ◽

Vol 263 (4) ◽

pp. H1161-H1169 ◽

Cited By ~ 25

Author(s):

H. B. Nuss ◽

S. R. Houser

Keyword(s):

Sarcoplasmic Reticulum ◽

Ventricular Myocytes ◽

Membrane Potentials ◽

Exchange Mechanism ◽

Ca Channel ◽

Ca Current ◽

Voltage Step ◽

Reverse Mode ◽

Sodium Calcium ◽

Calcium Exchange

The hypothesis that Ca entry by the sarcolemmal Na-Ca exchange mechanism induces sarcoplasmic reticulum (SR) Ca release, loads the SR with Ca, and/or directly induces contractions by elevating cytosolic free Ca was tested in voltage-clamped feline ventricular myocytes. Intracellular Na concentration was increased by cellular dialysis to enhance Ca influx via "reverse-mode" Na-Ca exchange at positive membrane potentials, at which the "L-type" Ca current (ICa) should be small. Contractions were induced in the presence of Ca channel antagonists by depolarization to these potentials, suggesting that Ca influx via reverse-mode Na-Ca exchange was involved. These contractions had both phasic (SR related) and tonic components of shortening. They were smaller and began with more delay after depolarization than contractions which involved ICa. The magnitude of shortening was graded by the amount and duration of depolarization, suggesting that Ca influx via reverse-mode Na-Ca exchange has the capacity to induce and grade SR Ca release. Small slow contractions could be evoked in the presence of ryanodine (to impair SR function) and verapamil (to block ICa), supporting the idea that Ca influx via Na-Ca exchange is sufficient to directly activate the contractile proteins. Contractions induced by voltage steps to +10 mV, which were usually small when ICa was blocked, were potentiated if preceded by a voltage step to strongly positive potentials. This potentiation was inhibited by ryanodine, suggesting that Ca entry that occurs by Na-Ca exchange may be important for normal SR Ca loading.(ABSTRACT TRUNCATED AT 250 WORDS)

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