Passive driving forces of proximal tubular fluid and bicarbonate transport: gradient dependence of H+ secretion

1983 ◽  
Vol 245 (5) ◽  
pp. F622-F633 ◽  
Author(s):  
Y. L. Chan ◽  
G. Malnic ◽  
G. Giebisch
Keyword(s):  
Driving Forces ◽  
Potential Gradient ◽  
Glass Electrode ◽  
Bicarbonate Transport ◽  
Oncotic Pressure ◽  
Luminal Membrane ◽  
Peritubular Capillaries ◽  
Proximal Tubular ◽  
Luminal Flow ◽  
Pressure Changes

The effect of oncotic pressure changes on fluid (Jv) and net bicarbonate transport (JHCO-3) and the transepithelial bicarbonate permeability (PHCO-3) were measured by an improved luminal and capillary microperfusion method that allows paired experiments on the same tubule. Rat proximal tubules were pump-perfused and Jv and [HCO-3] measured with [14C]inulin and a pH glass electrode. Raising peritubular protein (0-8-15 g/100 ml bovine serum albumin) stimulated Jv and HCO-3 reabsorption. The response to oncotic pressure changes was asymmetrical since changes of the luminal protein concentration had no significant effects. Whereas transepithelial solvent drag effects on HCO-3 must be minimal, peritubular protein most likely stimulates translocation of fluid and bicarbonate from intercellular spaces into peritubular capillaries. PHCO-3 was measured from HCO-3 net flux along a lumen-to-capillary-directed electrochemical potential gradient. In these experiments active H+ transport and Jv were minimized by 10(-4) M acetazolamide and luminal raffinose. PHCO-3 was 1.77 X 10(-5) cm X s-1 and was unaffected by increasing luminal flow rate from 10 to 45 nl X min-1. Since bicarbonate backflux is only a small fraction of physiological rates of JHCO-3, net transport alterations at varying [HCO-3] in the lumen must be due to changes in active HCO-3 (H+) transport. Thus, active H+ ion secretion across the luminal membrane of the proximal tubule is gradient dependent.

Control mechanisms of bicarbonate transport across the rat proximal convoluted tubule

1982 ◽  
Vol 242 (5) ◽  
pp. F532-F543 ◽  
Author(s):  
Y. L. Chan ◽  
B. Biagi ◽  
G. Giebisch
Keyword(s):  
Glass Electrode ◽  
Disulfonic Acid ◽  
Bicarbonate Transport ◽  
Control Mechanisms ◽  
Capillary Perfusion ◽  
Perfusion Rate ◽  
Luminal Perfusion ◽  
Luminal Flow ◽  
Acute Changes ◽  
Convoluted Tubules

Bicarbonate transport (JHCO3) was studied in rat proximal convoluted tubules by luminal and peritubular microperfusion, and the effects on tubular bicarbonate transport of selective changes in luminal and peritubular bicarbonate concentrations and of changes in luminal flow rate were evaluated. A pH glass electrode was used to measure [HCO3(-)] and gave results similar to those of a microcalorimetric method. Increasing the tubular and peritubular [HCO3(-)] at constant luminal perfusion rate (10 nl.min-1) augmented JHCO3, but JHCO3 increased more when pH changes were prevented by PCO2 adjustments (constant peritubular pH) than when pH was allowed to rise with the increase in [HCO3(-)] (constant PCO2). Elevation of the tubular HCO3(-) load by raising [HCO3(-)] stimulated JHCO3 more than when the HCO3(-) load was raised by enhancing luminal perfusion rate at constant [HCO3(-)] An increase in PCO2 at constant peritubular pH increased JHCO3. Diamox and benzolamide inhibited JHCO3 at luminal concentrations of 2-4 X 10(-4) M, yet a small but significant fraction of JHCO3 remained intact. Capillary perfusion with 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (5 X 10(-4) M) depressed JHCO3 by 70%. Acute changes in luminal and peritubular potassium concentrations (range, 2-6 meq/liter) had no effect on JHCO3, but JHCO3 increased moderately but significantly in severe dietary hypokalemia.

Low-affinity transport of pyroglutamyl-histidine in renal brush-border membrane vesicles

1989 ◽  
Vol 257 (5) ◽  
pp. C971-C975 ◽  
Author(s):  
H. A. Skopicki ◽  
K. Fisher ◽  
D. Zikos ◽  
G. Flouret ◽  
D. R. Peterson
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Brush Border Membrane Vesicles ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Luminal Membrane ◽  
Renal Brush Border Membrane ◽  
Proximal Tubular ◽  
Renal Brush Border

These studies were performed to determine if a low-affinity carrier is present in the luminal membrane of proximal tubular cells for the transport of the dipeptide, pyroglutamyl-histidine (pGlu-His). We have previously described the existence of a specific, high-affinity, low-capacity [transport constant (Kt) = 9.3 X 10(-8) M, Vmax = 6.1 X 10(-12) mol.mg-1.min-1] carrier for pGlu-His in renal brush-border membrane vesicles. In the present study, we sought to demonstrate that multiple carriers exist for the transport of a single dipeptide by determining whether a low-affinity carrier also exists for the uptake of pGlu-His. Transport of pGlu-His into brush-border membrane vesicles was saturable over the concentration range of 10(-5)-10(-3) M, yielding a Kt of 6.3 X 10(-5) M and a Vmax of 2.2 X 10(-10) mol.mg-1.min-1. Uptake was inhibited by the dipeptides glycyl-proline, glycyl-sarcosine, and carnosine but not by the tripeptide pyroglutamyl-histidyl-prolinamide. We conclude that 1) pGlu-His is transported across the luminal membrane of the proximal tubule by multiple carriers and 2) the lower affinity carrier, unlike the higher affinity carrier, is nonspecific with respect to other dipeptides.

Studies of the urinary acidification defect induced by lithium

1982 ◽  
Vol 242 (1) ◽  
pp. F23-F29 ◽  
Author(s):  
N. Bank ◽  
P. D. Lief ◽  
H. S. Aynedjian ◽  
B. F. Mutz
Keyword(s):  
Proximal Tubule ◽  
Renal Tubular Acidosis ◽  
Electrical Potential ◽  
Distal Renal Tubular Acidosis ◽  
Distal Nephron ◽  
Luminal Membrane ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Convoluted Tubules

Experiments were carried out in rats and isolated turtle bladders to study the defect in H+ transport induced by LiCl. After 3-4 days of intraperitoneal LiCl, rats developed urinary findings of "distal" renal tubular acidosis. Proximal tubular fluid pH measured in situ by glass microelectrodes was higher in lithium-treated rats than in acidotic controls. Proximal fluid total CO2 [tCO2] was also higher, and the fraction of tCO2 leaving the proximal tubule was 14 vs. 7% (P less than 0.001). Impaired acidification was also apparent beyond distal convoluted tubules, as judged by normal distal tCO2 reabsorption but increased HCO3(-) in the urine. During NaHCO3 loading, the proximal defect was ameliorated but not the distal. Turtle bladder studies showed that mucosal lithium inhibits H+ secretion secondary to reducing transepithelial electrical potential, presumably by hyperpolarization of the luminal membrane. A similar mechanism may be responsible for lithium's effect on the distal nephron. Inhibition of proximal tubular HCO3(-) reabsorption is probably not attributable to electrical potential changes but might be due to interference of luminal membrane Na+ entry by Li+ and reduced (Na+ + Li+)-H+ exchange.

Developmental maturation of Na(+)-H+ exchange in rat renal tubular brush-border membrane

1991 ◽  
Vol 261 (6) ◽  
pp. F1017-F1025 ◽  
Author(s):  
I. Zelikovic ◽  
E. Stejskal ◽  
P. Lohstroh ◽  
A. Budreau ◽  
R. W. Chesney
Keyword(s):  
Brush Border ◽  
Brush Border Membrane ◽  
Initial Rate ◽  
Neonatal Rat ◽  
Adult Rats ◽  
Luminal Membrane ◽  
Age Related ◽  
Proximal Tubular ◽  
Na Uptake ◽  
Developmental Maturation

The developmental maturation of the Na(+)-H+ exchanger present in the proximal tubular luminal membrane of the rat was investigated. An overshoot of 1 mM Na+ uptake was evident in brush-border membrane vesicles derived from the renal cortex of 7- and 21-day-old and adult rats in the presence of an outwardly directed H+ concentration ([H+]) gradient [intravesicular pH (pHi) = 5.5; extravesicular pH (pHo) = 7.5]. Na+ uptake was amiloride sensitive at all ages examined. Significantly higher initial rate (3 s) Na+ uptake and peak accumulation (60 s) in the presence of a [H+] gradient were found in vesicles from 7-day-old rats compared with adult animals. Significantly enhanced initial rate Na+ uptake by neonatal vesicles was also evident under pH-equilibrated conditions (pHi = pHo = 7.5). An age-related decrease in amiloride-sensitive Na+ accumulation by vesicles was found. Kinetic analysis of Na(+)-H+ exchange in voltage-clamped vesicles, in the presence of dimethylamiloride (DMA), and calculating 5-s Na+ uptake values showed a maturational decrease in capacity (decreasing Vmax) coupled with a maturational increase in affinity (decreasing Km) of Na(+)-H+ antiport. These data suggest that an enhanced amiloride-inhibitable Na(+)-H+ exchange activity due to increased capacity of exchange exists in the proximal tubular luminal membrane of the neonatal rat. This increased Na(+)-H+ exchange may potentially contribute to positive Na+ balance in the growing organism and may rapidly dissipate the electrochemical Na+ gradient across the luminal membrane necessary for Na(+)-solute contransport, thereby contributing to glycosuria and aminoaciduria of early life.

Determinants of proximal tubular reabsorption as mechanisms of glomerulotubular balance

1978 ◽  
Vol 235 (2) ◽  
pp. F142-F150 ◽  
Author(s):  
B. J. Tucker ◽  
R. C. Blantz
Keyword(s):  
Proximal Tubule ◽  
Filtration Rate ◽  
Oncotic Pressure ◽  
Peritubular Capillary ◽  
Nephron Filtration Rate ◽  
Vein Occlusion ◽  
Proximal Tubular ◽  
Range Of Values ◽  
Proximal Tubular Reabsorption ◽  
Glomerulotubular Balance

The determinants of absolute proximal reabsorption (APR) were studied in four groups of rats during hydropenia, partial renal vein occlusion (RVO), saline expansion, and RVO after saline expansion. Nephron filtration rate (SNGFR), nephron plasma flow (RPF), APR, and proximal tubule (Pt) peritubular capillary (HPc), and interstitial (HPi) hydrostatic pressures were measured by micropuncture techniques. Subcapsular space (pii) and star peritubular capillary (piE) oncotic pressures were also determined. The peritubular capillary permeability coefficiency (LpAR) and the corresponding effective reabsorptive pressure (ERP) were computed, where APR = LpAR . ERP, and ERP = net reabsorptive pressure across the peritubular capillary. The results indicate that APR correlates best with SNGFR (P less than 0.05), but not with (pii - HPi), RPF, or LpAR. There was a significant relationship between piE and LpAR, where LpAR fell with increases in piE (P less than 0.01). In conclusion, 1) changes in absolute proximal reabsorption correlate best with changes in nephron filtration rate but not with (pii - HPi) across this range of values, 2) changes in efferent oncotic pressure (piiE) correlated inversely with LpAR, and 3) glomerulotubular balance in the proximal tubule can be partially attributed to intraluminal factors.

Flow dependence of bicarbonate transport in the early (S1) proximal convoluted tubule

1988 ◽  
Vol 254 (6) ◽  
pp. F851-F855 ◽  
Author(s):  
F. Y. Liu ◽  
M. G. Cogan
Keyword(s):  
Wistar Rat ◽  
Proximal Convoluted Tubule ◽  
Bicarbonate Transport ◽  
Bicarbonate Concentration ◽  
Perfusion Rate ◽  
Proton Secretion ◽  
Pump Rate ◽  
Luminal Perfusion ◽  
Luminal Flow

We previously found, using an in vivo microperfusion pump rate of 30 nl/min, that proton secretion in the early (S1) proximal convoluted tubule (PCT) of the Munich-Wistar rat exhibited saturation kinetics. The maximal transport capacity was very high, approximately 500–600 peq.mm-1.min-1. The present studies assessed the change in early PCT acidification kinetics in response to an increase in microperfusion rate to 45 nl/min. First, bicarbonate permeability in the early PCT was measured and was found to be flow dependent. Proton secretion was then calculated using perfusate bicarbonate concentrations from 8 to 100 mM. Saturation of early proximal acidification (Vmax) still occurred at approximately 500–600 peq.mm-1.min-1, but the bicarbonate concentration effecting half-maximal acidification (apparent Km) decreased (from approximately 11 mM at 30 nl/min perfusion rate to less than 6 mM at 45 nl/min). By increasing luminal perfusion rate further to 60 nl/min at constant luminal bicarbonate concentration (25 mM), we confirmed that luminal flow rate did not affect the maximal level of acidification. Similar flow-dependent changes in acidification kinetics in the late PCT were also found, as has been previously shown. In conclusion, although an increase in luminal flow increased bicarbonate permeability and apparent affinity for substrate transport, there was no effect on maximal acidification rate in the early PCT.

scholarly journals Models for coupling of salt and water transport; Proximal tubular reabsorption in Necturus kidney.

1975 ◽  
Vol 66 (6) ◽  
pp. 671-733 ◽  
Author(s):  
H Sackin ◽  
E L Boulpaep
Keyword(s):  
Water Transport ◽  
Epithelial Transport ◽  
Driving Forces ◽  
Water Fluxes ◽  
Transport Parameters ◽  
Na Transport ◽  
Continuous Version ◽  
Leaky Epithelia ◽  
Proximal Tubular ◽  
Proximal Tubular Reabsorption

Models for coupling of salt and water transport are developed with two important assumptions appropriate for leaky epithelia. (a) The tight junction is permeable to both sale and water. (b) Active Na transport into the lateral speces is assumed to occur uniformly along the length of the channel. The proposed models deal specifically with the intraepithelial mechanism of proximal tubular resbsorption in the Necturus kidney although they have implications for epithelial transport in the gallbladder and small intestine as well. The first model (continuous version) is similar to the standing gradient model devised by Diamond and Bossert but used different boundary conditions. In contrast to Diamond and Bossert's model, the predicted concentration profiles are relatively flat with no sizable gradients along the interspace. The second model (compartment version) expands Curran's model of epithelial salt and water transport by including additional compartments and considering both electrical and chemical driving forces for individual Na and Cl ions as well as hydraulic and osmotic driving forces for water. In both models, ion and water fluxes are investigated as a function of the transport parameters. The behavior of the models is consistent with previously suggested mechanisms for the control of net transport, particularly during saline diuresis. Under all conditions the predicted ratio of net solute to solvent flux, or emergent concentration, deviates from exact isotonicity (except when the basement membrane has an appreciable salt reflection coefficient). However, the degree of hypertonicity may be small enough to be experimentally indistinguishable from isotonic transport.

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