scholarly journals Kinetics of Na+ transport in Necturus proximal tubule.

1977 ◽  
Vol 70 (3) ◽  
pp. 307-328 ◽  
Author(s):  
K R Spring ◽  
G Giebisch
Keyword(s):  
Proximal Tubule ◽  
Na Transport ◽  
Kinetics Of ◽  
Necturus Proximal Tubule

Dissociation of proximal tubular glucose and Na+ reabsorption by amphotericin B

1979 ◽  
Vol 236 (4) ◽  
pp. F392-F397
Author(s):  
P. S. Aronson ◽  
J. P. Hayslett ◽  
M. Kashgarian
Keyword(s):  
Proximal Tubule ◽  
Glucose Uptake ◽  
Amphotericin B ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Na Transport ◽  
Glucose Reabsorption ◽  
Tubular Lumen ◽  
Proximal Tubular ◽  
Necturus Proximal Tubule

The effect of amphotericin B on glucose and Na+ transport was studied in the Necturus proximal tubule and in microvillus membrane vesicles isolated from the rabbit renal cortex. In the Necturus experiments, the rate constants for disappearance of radiolabeled glucose (kG) and mannitol (kM) from the tubular lumen were determined by stop-flow microperfusion. Saturability and Na+-dependence of glucose reabsorption was confirmed, since kG was reduced by raising intratubular glucose from 1 to 5 mM or by replacing intratubular Na+ with choline. Neither maneuver affected kM. Intratubular amphotericin B (10 microgram/ml), previously shown to stimulate active Na+ reabsorption in the Necturus proximal tubule, inhibited kG with no effect on kM. In the membrane vesicle preparation, amphotericin inhibited the uphill glucose uptake which results from imposing a NaCl gradient from outside to inside, but had no effect on glucose uptake in either the absence of Na+ or in the presence of Na+ when there was no Na+ gradient. Amphotericin B stimulated the uptake of Na+ by the vesicles. The observed dissociation of glucose and Na+ transport by amphotericin B is consistent with the concept that proximal tubular glucose reabsorption is energized by the luminal membrane Na+ gradient and is not directly linked to active Na+ transport per se.

scholarly journals Organic substrate effects on and heterogeneity of Necturus proximal tubule function

1980 ◽  
Vol 17 (4) ◽  
pp. 479-490 ◽  
Author(s):  
Jameson Forster ◽  
Paul S. Steels ◽  
Emile L. Boulpaep
Keyword(s):  
Proximal Tubule ◽  
Organic Substrate ◽  
Substrate Effects ◽  
Necturus Proximal Tubule

Effect of norepinephrine on cellular sodium transport in Ambystoma kidney proximal tubule

1994 ◽  
Vol 267 (5) ◽  
pp. F725-F736 ◽  
Author(s):  
S. Abdulnour-Nakhoul ◽  
R. N. Khuri ◽  
N. L. Nakhoul
Keyword(s):  
Proximal Tubule ◽  
Ambystoma Tigrinum ◽  
Na Transport ◽  
Control Solution ◽  
Kidney Proximal Tubule ◽  
Luminal Membrane ◽  
Intracellular Na Activity ◽  
Beta Receptors ◽  
Membrane Potential Difference ◽  
External K

The effect of norepinephrine (NE) on mechanisms of cellular Na+ transport in the isolated, perfused proximal tubule of Ambystoma tigrinum was examined. Single-barreled voltage and ion-selective microelectrodes were used to determine basolateral (V1), luminal (V2), and transepithelial (V3) membrane potentials and intracellular Na+ activity (alpha Nai). In CO2/HCO3- control solution, addition of NE (10(-6) M) to the bath caused depolarizations of V1, V2, and V3 are decreased alpha Nai. These effects were mimicked by isoproterenol and inhibited by propranolol. Addition of NE in the absence of luminal Na+ and substrates did not cause any changes in V1, V2, V3, or alpha Nai. NE did not affect the changes in membrane potential difference (PD) or alpha Nai caused by removal and readdition of luminal substrates and/or Na+. To study the effect of NE on Na-K-adenosinetriphosphatase (Na-K-ATPase), the pump was inhibited by external K+ removal and then reactivated by readdition of 12 mM K+ to the bath in the presence and absence of NE. Reactivation of the pump caused hyperpolarization of membrane PDs, and alpha Nai recovered monotonically in 3-5 min. The peak hyperpolarizations of V1 and V2 (approximately 1 min) were significantly larger in the presence of NE. During the first 3 min, and also at the same alpha Nai, the rate of decrease of alpha Nai was significantly faster in the presence of NE. In conclusion, these results show a direct effect of NE on cell membrane PDs and alpha Nai in the kidney proximal tubule. Most likely, beta-receptors are involved in mediating the action of NE. Neither Na/H exchange nor Na-substrate cotransport at the luminal membrane are affected by NE. On the other hand, NE activates Na-K-ATPase.

Angiotensin II-dependent proximal tubule sodium transport requires receptor-mediated endocytosis

1994 ◽  
Vol 266 (3) ◽  
pp. C669-C675 ◽  
Author(s):  
J. R. Schelling ◽  
S. L. Linas
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Receptor Internalization ◽  
Ang Ii ◽  
Na Transport ◽  
Cellular Mechanisms ◽  
Transport Pathways ◽  
Proximal Tubule Cells ◽  
Receptor Mediated Endocytosis ◽  
Tubule Cells

Angiotensin II (ANG II) receptors are present on apical and basolateral surfaces of proximal tubule cells. To determine the cellular mechanisms of proximal tubule ANG II receptor-mediated Na transport, apical-to-basolateral 22Na flux was measured in cultured proximal tubule cells. Apical ANG II caused increases in 22Na flux (maximum response: 100 nM, 30 min). Basolateral ANG II resulted in 22Na flux that was 23-56% greater than 22Na flux observed with equimolar apical ANG II. Apical ANG II-induced 22Na flux was prevented by preincubation with amiloride, ouabain, and the AT1 receptor antagonist losartan. Because apical ANG II signaling was previously shown to be endocytosis dependent, we questioned whether endocytosis was required for ANG II-stimulated proximal tubule Na transport as well. Apical (but not basolateral) ANG II-dependent 22Na flux was inhibited by phenylarsine oxide, an agent which prevents ANG II receptor internalization. In conclusion, apical and basolateral ANG II caused proximal tubule Na transport. Apical ANG II-dependent Na flux was mediated by AT1 receptors, transcellular transport pathways, and receptor-mediated endocytosis.

Loss of epithelial polarity: A novel hypothesis for reduced proximal tubule Na+ transport following ischemic injury

1989 ◽  
Vol 107 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Bruce A. Molitoris ◽  
Laurence K. Chan ◽  
Joseph I. Shapiro ◽  
John D. Conger ◽  
Sandor A. Falk
Keyword(s):  
Proximal Tubule ◽  
Ischemic Injury ◽  
Epithelial Polarity ◽  
Na Transport

scholarly journals Basolateral Na(+)-H+ antiporter. Mechanisms of electroneutral and conductive ion transport.

1994 ◽  
Vol 103 (5) ◽  
pp. 895-916 ◽  
Author(s):  
M A Post ◽  
D C Dawson
Keyword(s):  
Cation Exchange ◽  
Current Flow ◽  
Relative Proportion ◽  
Extracellular Fluid ◽  
Proton Gradient ◽  
Na Transport ◽  
Activation Kinetics ◽  
High Affinity Site ◽  
Kinetics Of ◽  
Proton Currents

The basolateral Na-H antiporter of the turtle colon exhibits both conductive and electroneutral Na+ transport (Post and Dawson. 1992. American Journal of Physiology. 262:C1089-C1094). To explore the mechanism of antiporter-mediated current flow, we compared the conditions necessary to evoke conduction and exchange, and determined the kinetics of activation for both processes. Outward (cell to extracellular fluid) but not inward (extracellular fluid to cell) Na+ or Li+ gradients promoted antiporter-mediated Na+ or Li+ currents, whereas an outwardly directed proton gradient drove inward Na+ or Li+ currents. Proton gradient-driven, "counterflow" current is strong evidence for an exchange stoichiometry of > 1 Na+ or Li+ per proton. Consistent with this notion, outward Na+ and Li+ currents generated by outward Na+ or Li+ gradients displayed sigmoidal activation kinetics. Antiporter-mediated proton currents were never observed, suggesting that only a single proton was transported per turnover of the antiporter. In contrast to Na+ conduction, Na+ exchange was driven by either outwardly or inwardly directed Na+, Li+, or H+ gradients, and the activation of Na+/Na+ exchange was consistent with Michaelis-Menten kinetics (K1/2 = 5 mM). Raising the extracellular fluid Na+ or Li+ concentration, but not extracellular fluid proton concentration, inhibited antiporter-mediated conduction and activated Na+ exchange. These results are consistent with a model for the Na-H antiporter in which the binding of Na+ or Li+ to a high-affinity site gives rise to one-for-one cation exchange, but the binding of Na+ or Li+ ions to other, lower-affinity sites can give rise to a nonunity, cation exchange stoichiometry and, hence, the net translocation of charge. The relative proportion of conductive and nonconductive events is determined by the magnitude and orientation of the substrate gradient and by the serosal concentration of Na+ or Li+.

Maturation of proximal tubule Na+/H+ antiporter activity in sheep during transition from fetus to newborn

1994 ◽  
Vol 267 (4) ◽  
pp. F537-F545 ◽  
Author(s):  
E. N. Guillery ◽  
L. P. Karniski ◽  
M. S. Mathews ◽  
J. E. Robillard
Keyword(s):  
Proximal Tubule ◽  
Developmental Change ◽  
Membrane Vesicles ◽  
Michaelis Constant ◽  
Maturational Change ◽  
Significant Difference ◽  
Microvillus Membrane ◽  
Renal Tubular ◽  
Definition Of ◽  
Kinetics Of

We have studied maturational changes in the kinetics of the proximal tubule Na+/H+ antiporter. Microvillus membrane vesicles were prepared from renal cortex of fetal and newborn lambs. Amiloride-sensitive uptake of 22Na+ by these vesicles was measured and Woolf-Augustinsson-Hofstee plots were used to determine the Michaelis constant (Km) and rate of maximal uptake (Vmax). Initial studies of fetal lambs at 130-132 days gestation (n = 5; term is 145 days) and 3- to 4-day-old lambs (n = 5) revealed no maturational change in Km (7.27 +/- 1.25 for fetuses and 9.01 +/- 1.03 mM for lambs); however, there was a 242% increase in Vmax (from 1.28 +/- 0.33 in the fetuses to 4.37 +/- 0.85 nmol.s-1.mg protein-1 in the lambs, P = 0.005). Further definition of the developmental change in Na+/H+ antiporter Vmax was obtained when 144-day-gestation fetuses (n = 5) were compared with 24-h-old sibling lambs (n = 5) that had been delivered by cesarean section at 144 days gestation. Again, no significant difference was seen in Na+/H+ antiporter Km (14.9 +/- 6.5 for fetuses and 12.5 +/- 3.4 mM for lambs); however, a significant increase in Na+/H+ antiporter Vmax occurred (from 1.41 +/- 0.51 in the fetuses to 3.32 +/- 0.37 nmol.s-1.mg protein-1 in the lambs, P < 0.01). This study shows that there is a maturational increase in renal cortical Na+/H+ antiporter Vmax during the transition from fetal to newborn life. This increase parallels the increase in renal tubular Na+ reabsorption that occurs at this time.

Nonelectrolyte permeability of the paracellular pathway in Necturus proximal tubule

1975 ◽  
Vol 228 (2) ◽  
pp. 581-595 ◽  
Author(s):  
CA Berry ◽  
EL Boulpaep
Keyword(s):  
Tight Junction ◽  
Proximal Tubule ◽  
Water Flow ◽  
Volume Flow ◽  
Osmotic Gradient ◽  
Osmotic Water ◽  
Net Flux ◽  
Gradient Measurements ◽  
Paracellular Shunt ◽  
Necturus Proximal Tubule

Micropuncture experiments were performed on Necturus proximal tubule using stationary microperfusion and microrecollection techniques. The transepithelial movement of the extracellular marker, sucrose, was used to investigate the passive permeability of the paracellular shunt pathway under steady-state conditions, during spontaneous reabsorption and water flow induced by an external osmotic gradient. Measurements were made of the sucrose permeability (P-s) efflux, net flux, and of net volume flow. True P-s determined in the absence of net volume flow and transepithelial gradient was 0.96 10-6 cm s-1. Both ouabain and isotonic volume expansion decreased shunt P-s. During reabsorption, solute-coupled water flow increased apparent P-s and net sucrose flux equalled efflux. Osmotic water flow from lumen to plasma decreased apparent P-s, with net sucrose flux equal to efflux; whereas osmotic flow from plasma to lumen increased apparent P-s but no net flux was observed. It is concluded that changes in P-s can be interpreted as relative alterations of the tight junction and the lateral spaces and that a portion of the volume flow from lumen to plasma proceeds via the tight junction.

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