Isotope Techniques to Study Kinetics of Na+ and K+ Transport Under Salinity Conditions

2012 ◽  
pp. 389-398 ◽  
Author(s):  
Dev T. Britto ◽  
Herbert J. Kronzucker
1978 ◽  
Vol 72 (3) ◽  
pp. 283-295 ◽  
Author(s):  
D B Rhoads ◽  
W Epstein

Kinetics of K exchange in the steady state and of net K uptake after osmotic upshock are reported for the four K transport systems of Escherichia coli: Kdp, TrkA, TrkD, and TrkF. Energy requirements for K exchange are reported for the Kdp and TrkA systems. For each system, kinetics of these two modes of K transport differ from those for net K uptake by K-depleted cells (Rhoads, D. B. F.B. Walters, and W. Epstein. 1976. J. Gen. Physiol. 67:325-341). The TrkA and TrkD systems are inhibited by high intracellular K, the TrkF system is stimulated by intracellular K, whereas the Kdp system is inhibited by external K when intracellular K is high. All four systems mediate net K uptake in response to osmotic upshock. Exchange by the Kdp and TrkA systems requires ATP but is not dependent on the protonmotive force. Energy requirements for the Kdp system are thus identical whether measured as net K uptake or K exchange, whereas the TrkA system differs in that it is dependent on the protonmotive force only for net K uptake. We suggest that in both the Kpd and TrkA systems formation of a phosphorylated intermediate is necessary for all K transport, although exchange transport may not consume energy. The protonmotive-force dependence of the TrkA system is interpreted as a regulatory influence, limiting this system to exchange except when the protonmotive force is high.


1984 ◽  
Vol 111 (1) ◽  
pp. 201-223
Author(s):  
J. W. HANRAHAN ◽  
J. E. PHILLIPS

The kinetics of 36C1 fluxes across cAMP-stimulated, short-circuited locust rectum were studied. Raising external K+ from 0 to 100 mM increased both Kt and Vmax for net Cl transport (JnetCl) by four- to six-fold. Hill plots of JnetCl indicated non-cooperative Cl interactions. The sequence for cation stimulation of JnetCl was K > Rb > Cs > Na > NH4. Low levels of K were stimulatory only when added to the mucosal side. Cyclic AMP (cAMP) caused a small active absorption of K, although this was minor compared to the four-fold increase in transepithelial K diffusion (PK). Neither cAMP stimulation of JnetK nor of PK was sensitive to Cl removal, suggesting that K-stimulated Cl absorption and K transport are not mediated by the same co-transport mechanism. Potassium is the counter-ion for electrogenic Cl transport because JnetK was less than 10% of the JnetK during cAMP exposure under Isc conditions, but JnetK equalled JnetCl at open-circuit.


1985 ◽  
Vol 249 (5) ◽  
pp. C490-C496 ◽  
Author(s):  
D. Kaji ◽  
T. Kahn

The majority of the ouabain-insensitive K influx in human erythrocytes is dependent on the presence of Cl. Recent studies have shown that a portion of the Cl-dependent K influx persists in the absence of external Na (Nao). It has been suggested that this Nao-independent component represents (K + Cl) cotransport, whereas the remainder of the Cl-dependent K influx seen on addition of external Na represents (Na + K + 2Cl) cotransport. In the present studies, the kinetics of Cl-dependent K influx were examined in the presence and absence of external Na, by varying external K and external Cl. Our studies suggest that the Nao-independent Cl-dependent pathway has a relatively low affinity for external K (Km 17-30 mM) in contrast to the high affinity of the Nao-augmented component (Km 3-4 mM). N-ethylmaleimide (NEM) stimulates the maximal velocity of the Nao-independent Cl-dependent K influx achievable without alteration of intracellular solutes but does not alter its Km for external K. In contrast, NEM has no stimulatory effect on the Nao-augmented component. The Cl dependence of the Nao-independent K influx is best described by a relatively flat curve with a mild upward concavity. The kinetic properties of the Nao-independent component of Cl-dependent K transport are very similar to those of the putative (K + Cl) cotransport pathway seen in low-K sheep erythrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)


2005 ◽  
Vol 46 (6) ◽  
pp. 1257-1265 ◽  
Author(s):  
Kajsa Bohlin ◽  
Bruce W. Patterson ◽  
Kimberly L. Spence ◽  
Assaad Merchak ◽  
James C. G. Zozobrado ◽  
...  

1979 ◽  
Vol 236 (2) ◽  
pp. F175-F183
Author(s):  
H. L. Wilkinson ◽  
D. G. Deeds ◽  
L. P. Sullivan ◽  
D. J. Welling

We studied the effect of ouabain on transepithelial and cellular potassium transport in the isolated perfused bullfrog kidney. We used recently developed techniques for estimating the unidirectional reabsorptive and secretory K fluxes (Jr and Js) and measuring the kinetics of cellular K transport. Two hours of perfusion with 1 X 10(-6) M ouabain did not affect GFR, reduced fractional Na reabsorption 57%, increased K excretion 41%, and inhibited Jr 34%. Js rose 68% at 60 min and then returned to the control level. Ninety minutes of perfusion with 5 X 10(-6) M ouabain reduced GFR 28% and fractional Na reabsorption 76%. K excretion rapidly increased 71% within 30 min and then fell to 60% of the control level, while Jr fell 64%. Js rose 42% in 30 min and then fell to 23% of the control level. Both doses reduced K uptake into cellular pools from the circulation and increased the rate coefficients for efflux into tubular fluid. The data indicate that ouabain inhibited reabsorption and transiently accelerated the rate of loss of K from the cells into the tubular fluid. This initially masked the ultimate inhibition of K secretion from the circulation into the tubular fluid.


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