Sodium‐‐potassium pump current in rabbit sino‐atrial node cells.

Abstract

1. The Na+-K+ pump current (Ip) was studied in sino-atrial (SA) node cells of rabbits using the whole-cell patch-clamp technique. 4. The cation dependence of the K+ site of the Na+-K+ pump was examined using various monovalent cations. The sequence was K+ > Rb+ > Cs+ > > > Li+.5. Ip at 0 mV also increased as [Nae]p9p was increased from 10 to 150 mm at 5-4 mm K+, with a Ko.5 value of 14 mm and a nHof 1P3 (n = 54).6. Ip at 0 mV was reduced by lowering the temperature from 37 to 25°C with 30 mm Napip and 5-4 mm K+. The temperature coefficient (Qlo) for Ip was 2-1 (n = 27). 7. With 10 mM Nat1p and 5-4 mm K+, the half-activation voltage of Ip was -52 + 16 mV and the current at this voltage was 22 5 + 3 5 pA (n = 10), indicating that Ip contributes significantly to the background outward current during the normal pacemaker potential of SA node cells. Irisawa, Brown & Giles, 1993). Recently, however, the presence of a time-independent background current has been reported and it has been shown that a Na+-dependent inward current makes a significant contribution to pacemaker depolarization (Hagiwara, Irisawa, Kasanuki & Hosoda, 1992

Sodium‐potassium pump current in smooth muscle cells from mesenteric resistance arteries of the guinea‐pig

“…The basic characteristics of the Na¤-K¤ pump current in vascular smooth muscle cells are similar to those reported in other cells such as cardiac myocytes Gao et al 1995;Sakai et al 1996) and vascular endothelial cells (Oike et al 1993). …”

“…This value is similar to that observed in cardiac cells (1·1 ± 0·1 pA pF¢ at 40 mV, ; 1·5 ± 0·2 pA pF¢ at 0 mV, Sakai et al 1996), and in endothelial cells (approximately 1·4 pA pF¢; Oike et al 1993) under similar conditions. It is thus likely that the Na¤-K¤ pump makes an important contribution to cell function including the maintenance of membrane potential, as in these tissues.…”

Sodium-pump potentials and currents in guinea-pig ventricular muscles and myocytes

“…-90 mV (Eisner et al 1981b) and (ii) inhibition of the pump for ≤15 min triggers a near-linear increase of 0.4-1.3 mM/min in intracellular Na + activity (about 0.5-1.7 mM/min in [Na + ] i ) (Deitmer and Ellis 1978;Eisner et al 1981b;Glitsch et al 1982;Levi and Boyett 1991;Whalley et al 1993). On this basis, we assumed that resting [Na + ] i in depolarized muscles was~7 mM (versus 8-12 mM in normally polarized muscle (Cohen et al 1982;Sakai et al 1996;Whalley et al 1993)), and that [Na + ] i increased at 0.75 mM/min (75% Na + ) or 1 mM/min (100% Na + ) during K + -free exposure (Table 1, columns 1, 2, and 3). Maximal pump current (limiting I p ) generated by saturating Rb + and saturating [Na + ] i at positive potentials is taken as 1.2 µA/cm 2 (cf.…”

A mathematical model of pacemaker activity recorded from mouse small intestine

“…As the kinetics of the Na C /K C pump have not been studied well in ICCs, we employed the model of Sakai et al (1996) obtained from rabbit sino-atrial node cells. The P NaK was adjusted to maintain the [Na C ] i below 20 mM against the large Na C influx by I AI during the depolarizing phase of a pacemaker potential.…”