Relation of membrane potential to basolateral TEA transport in isolated snake proximal renal tubules

1995 ◽  
Vol 268 (6) ◽  
pp. R1539-R1545 ◽  
Author(s):  
Y. K. Kim ◽  
W. H. Dantzler

We measured the effects of changes in bath K+ concentration ([K+]) on basolateral membrane potential difference (PD) and [3H]tetraethylammonium (TEA) transport in isolated snake (Thamnophis) proximal renal tubules (25 degrees C; pH 7.4). Increasing bath [K+] from 3 to 65 mM decreased PD from -60 mV (inside of cells negative) to -20 mV and 2-min uptake of [3H]TEA by approximately 25%, indicating that PD influences TEA entry into the cells. Uptake of [3H]TEA was inhibited similarly at both K+ concentrations by unlabeled TEA, indicating that uptake is carrier mediated. Kt (approximately 18 microM) for 2-min uptake of [3H]TEA in 3 mM K+ increased significantly in 65 mM K+, suggesting that the decrease in PD or the increase in [K+] alters the affinity of the transporter for TEA. The steady-state cell-to-bath ratio for [3H]TEA with 3 mM K+ (-60 mV PD) was approximately 16, significantly above the ratio of 10 predicted for passive distribution at electrochemical equilibrium. With 65 mM K+ (-20 mV PD) this ratio decreased to approximately 6, again significantly above the predicted ratio of 2. These data suggest that the PD can account for much, but not all, of the steady-state uptake of TEA. Efflux of [3H]TEA across the basolateral membrane was identical with either 3 or 65 mM K+ in the bath but was almost completely inhibited in either case by tetrapentylammonium, a potent inhibitor of TEA uptake. These data indicate that virtually all TEA transport across the basolateral membrane is carrier mediated and that transport out of the cells is unaffected by PD.

1984 ◽  
Vol 246 (6) ◽  
pp. F889-F896 ◽  
Author(s):  
S. Sasaki ◽  
C. A. Berry

To clarify the mechanism(s) of HCO-3 movement across the basolateral membrane, rabbit proximal convoluted tubules were perfused in vitro. Two possible mechanisms were examined: neutral HCO-3 exit coupled to chloride and rheogenic HCO-3 exit. A complete C1- substitution with isethionate in the lumen and bath did not affect HCO-3 reabsorption, suggesting that HCO-3 exit is not coupled to chloride. Addition of 2 mM Ba2+ to the bath, which has been shown to depolarize the basolateral membrane potential difference, caused a 42% inhibition of HCO-3 reabsorption and a 32% inhibition of volume flux, suggesting that HCO-3 exit is rheogenic. Ba2+ did not affect the volume flux when HCO-3 reabsorption was inhibited by acetazolamide, suggesting that the Ba2+ effect is not due to a general inhibition of cell metabolism. From these data we propose that HCO-3 exits the basolateral membrane by a rheogenic, chloride-independent mechanism.


1988 ◽  
Vol 255 (3) ◽  
pp. R492-R499 ◽  
Author(s):  
P. M. Smith ◽  
J. B. Pritchard ◽  
D. S. Miller

The relationship between organic cation uptake and basolateral membrane potential was studied in renal tubules from two marine teleost fish, Southern flounder (Paralicthys lethostigma) and killifish (Fundulus heteroclitis). Carrier-mediated uptake of the model organic cation, tetraethylammonium (TEA), increased when K+ was changed from 2.5 to 0.2 mM and decreased when medium K+ was increased to 20 mM. Uptake was also reduced by the K+ channel blocker barium (1 mM). Furthermore, basolateral membrane potential hyperpolarized 15-25 mV in low-K+ medium and depolarized 30-40 mV in high-K+ medium. Barium also depolarized. Finally, basolateral membrane potential was depolarized in a concentration-dependent manner by addition of 100-500 microM TEA or Darstine. Thus treatments that hyperpolarize the basolateral membrane potential increase carrier-mediated TEA uptake, whereas those that depolarize basolateral membrane potential reduce uptake. Furthermore, organic cation transport into tubular cells involves the net influx of positive charge. Together, these findings support the argument that carrier-mediated organic cation uptake at the basolateral membrane is a potential-driven, electrogenic process.


1993 ◽  
Vol 265 (1) ◽  
pp. G1-G8 ◽  
Author(s):  
J. G. Fitz ◽  
S. D. Lidofsky ◽  
B. F. Scharschmidt

Hepatocytes possess several mechanisms for membrane acid-base transport, which work in concert to maintain intracellular pH (pHi) in a narrow physiological range, despite metabolic processes that produce and consume substantial quantities of H+ and HCO3-.Na(+)-H+ and Cl(-)-HCO3- exchangers contribute to recovery from intracellular acidosis and alkalosis, respectively, but are largely inoperative at physiological values of pHi. Recent studies indicate that hepatocytes also possess a mechanism for coupled transport of Na+ and HCO3- across the basolateral membrane. This appears to be the dominant pathway for membrane acid-base transport operative under basal conditions, mediates influx of Na+ and HCO3-, and is an important contributor to recovery from intracellular acidosis. In this review, the properties of hepatic Na(+)-HCO3- cotransport are described with emphasis on its effects on pHi and Na+ homeostasis and on the possible role of membrane potential difference as a signal modulating the rate of HCO3- influx and pHi of hepatocytes through effects on this transporter.


1979 ◽  
Vol 78 (1) ◽  
pp. 29-45
Author(s):  
MAURIZIO MIROLLI

1. The response of the coxal receptors of the crab Scylla serrata to step stretches consisted of a partial action potential, Vα, followed by a steady-state depolarization, V8. The input resistance of the fibre was reduced during V8. 2. In the absence of stimulation, the dendrites of the receptors depolarized when external Na+ was substituted with choline or Li+, and when the external K+ concentration was increased or decreased. The dendrites also depolarized when ouabain was added to the saline. 3. The amplitude of both Vα and V8 was dependent on external Na+. In cells which were depolarized by ouabain, the amplitude of V8 increased when the K+ concentration of the saline was reduced. 4. V8 was followed by a small, but long-lasting, after-potential which was depolarizing when the membrane potential was between −70 and −60 mV. In cells depolarized by ouabain or by low K+ saline, the after-potential became hyperpolarizing. 5. When trains of brief stretches (each 5 ms in duration) were used as stimuli, the cells responded with trains of Vα responses. During this tetanic stimulation the cells hyperpolarized; cessation of the stimulus train was followed by a long-lasting hyperpolarization (PTH). 6. PTH was abolished in Li+ saline, in low K+ saline, and in the presence of ouabain. In control or in low K+ saline, PTH was not accompanied by a decrease in the input resistance of the fibres. 7. It is concluded that an electrogenic Na+ pump (or equivalent process) contributes a substantial fraction of the membrane potential of the unstimulated coxal receptors. Pump activity could be increased by Na+-loading the distal part of the cells with trains of Vα responses. By contrast, during the steady-state response to stretch, the pump was not activated.


1976 ◽  
Vol 3 (5) ◽  
pp. 677
Author(s):  
C.J Doughty ◽  
A.B Hope

Effects of 254 nm ultraviolet irradiation on the plasmalemma potential difference and conductance in C, corallina have been further analysed. Following an increase in passive chloride permeability, revealed from previous studies, and which is manifested as a depolarization of membrane potential difference and an increase in membrane conductance, a secondary depolarization was prominent at pH 7 and is attributed to u.v.-induced inhibition of an electrogenic pump. The secondary depolarization was usually accompanied by a decrease in membrane conductance. For doses of u.v. of 1400 J m-2, these effects were almost reversible within about 1 h


1962 ◽  
Vol 46 (2) ◽  
pp. 189-199 ◽  
Author(s):  
Ernest Page

The steady state transmembrane resting potential difference (Vm) has been measured in quiescent papillary muscles. Vm was determined as a function of the external K concentration in Cl and SO4 solutions and compared with the K equilibrium potential. Other measurements were made after replacement of external Na by choline, K by Rb and Cs, and Cl by SO4, CH3SO4, and NO3. Effects on Vm of albumin, temperature, and variation in internal K concentration are described.


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