Evidence for electroneutral sodium chloride transport in rat proximal convoluted tubule

1986 ◽  
Vol 250 (4) ◽  
pp. F644-F648
Author(s):  
K. J. Howlin ◽  
R. J. Alpern ◽  
C. A. Berry ◽  
F. C. Rector
Keyword(s):  
Sodium Chloride ◽  
Active Transport ◽  
Sodium Transport ◽  
Chloride Transport ◽  
Proximal Convoluted Tubule ◽  
Organic Solutes ◽  
Nacl Transport ◽  
Proximal Tubular ◽  
High Chloride

One- to two-thirds of NaCl absorption in the late proximal convoluted tubule (no luminal organic solutes present) is inhibited by cyanide and thus is dependent on active transport. To examine whether this active transport-dependent NaCl transport is electrogenic or electroneutral, the effect of cyanide on transepithelial potential difference (PD) was measured in the rat proximal convoluted tubule microperfused in vivo. In the presence of an ultrafiltrate-like luminal perfusate containing glucose and alanine, cyanide addition caused the transepithelial PD to change from -0.44 +/- 0.04 to -0.05 +/- 0.03 mV (P less than 0.001). In the presence of a late proximal tubular fluid (high chloride, low bicarbonate, no organics), the transepithelial PD was 1.23 +/- 0.06 mV and was unchanged at 1.19 +/- 0.05 mV after cyanide addition (NS). To eliminate the possibility that an effect of cyanide on a putative acidification-dependent lumen-positive PD was concealing an effect on an electrogenic sodium transport-dependent lumen-negative PD, the above studies were repeated in the presence of acetazolamide. Cyanide did not affect the transepithelial PD (1.17 +/- 0.05 vs. 1.07 +/- 0.06 mV, NS). We conclude that, although cyanide-inhibitable NaCl transport is electrogenic in the presence of luminal organic solutes, it does not generate a transepithelial PD in their absence and therefore is electroneutral.

Chloride transport in the rat S1 proximal tubule

1995 ◽  
Vol 268 (4) ◽  
pp. F723-F729 ◽  
Author(s):  
K. R. Wong ◽  
C. A. Berry ◽  
M. G. Cogan
Keyword(s):  
Angiotensin Ii ◽  
Active Transport ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Organic Solutes ◽  
Chloride Absorption ◽  
Sodium Isethionate ◽  
Organic Solute ◽  
High Chloride

In vivo microperfusion was used to elucidate the modes and regulation of the powerful chloride transport system resident in the rat early (S1) proximal convoluted tubule (PCT). From a complete, glomerular ultrafiltrate-like perfusate, omission of organic solutes reduced chloride absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001). From a high-chloride perfusate (a relatively pure NaCl solution devoid of bicarbonate and organic solutes), luminal addition of the active transport inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632 +/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium isethionate isosmotically replaced bicarbonate and organic solutes, preventing development of a chloride gradient. Intravenous angiotensin II caused a stimulation of chloride absorption from a high-chloride perfusate by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the components of the normal S1 PCT chloride reabsorption (approximately 300 peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following: active transport (40–50%), which can be regulated by angiotensin II; sodium-coupled organic solute transport (30%); and passive, chloride concentration gradient-driven transport (20–25%).

Flow dependence of chloride transport in rat S1 proximal tubules

1995 ◽  
Vol 269 (6) ◽  
pp. F870-F875 ◽  
Author(s):  
K. R. Wong ◽  
C. A. Berry ◽  
M. G. Cogan
Keyword(s):  
Proximal Tubule ◽  
Active Transport ◽  
Chloride Transport ◽  
Wistar Rat ◽  
Organic Solutes ◽  
Passive Transport ◽  
Total Chloride ◽  
Chloride Absorption ◽  
Glomerulotubular Balance

These studies examined whether the luminal flow dependency of chloride absorption in the S1 proximal tubule during glomerulotubular balance was due to change in active and/or passive transport of chloride. Using in vivo microperfusion in the Munich-Wistar rat and an essentially pure sodium chloride perfusate (devoid of bicarbonate and organic solutes), we found that an increase in luminal perfusion rate from 30 to 45 nl/min caused stimulation of total chloride absorption (active plus passive) by 87 peq.mm-1.min-1 (632 +/- 17 to 719 +/- 11, P < 0.001). When cyanide was added to this perfusate to eliminate active transport, the flow-induced change in passive transport was 58 peq.mm-1.min-1 (479 +/- 9 to 537 +/- 11, P < 0.001). The cyanide-inhibitable active transport component was therefore 29 peq.mm-1.min-1. With elimination of the transepithelial chloride gradient and, hence, passive transport by isethionate substitution, active transport increased by 63 peq.mm-1.min-1 (121 +/- 4 to 184 +/- 7, P < 0.001) as flow rate rose from 30 to 45nl/min. Removal of organic solutes from a glomerular ultrafiltrate-like perfusate had a minimal effect on flow-induced change in chloride transport (190 vs. 207 peq.mm-1.min-1). In conclusion, flow-dependent active and passive chloride transport in the S1 proximal tubule may both contribute to normal glomerulotubular balance.

Endothelin inhibits thick ascending limb chloride flux via ETB receptor-mediated NO release

2000 ◽  
Vol 279 (2) ◽  
pp. F326-F333 ◽  
Author(s):  
Craig F. Plato ◽  
David M. Pollock ◽  
Jeffrey L. Garvin
Keyword(s):  
Intracellular Calcium ◽  
Chloride Transport ◽  
Inhibitory Effect ◽  
Thick Ascending Limb ◽  
Inhibitory Effects ◽  
Chloride Flux ◽  
Nacl Transport ◽  
No Release ◽  
Bq 610

Endothelin-1 (ET-1) inhibits transport in various nephron segments, and the thick ascending limb of the loop of Henle (TALH) expresses ET-1 receptors. In many tissues, activation of ETB receptors stimulates release of NO, and we recently reported that endogenous NO inhibits TALH chloride flux ( J Cl). However, the relationship between ET-1 and NO in the control of nephron transport has not been extensively studied. We hypothesized that ET-1 decreases NaCl transport by cortical TALHs through activation of ETBreceptors and release of NO. Exogenous ET-1 (1 nM) decreased J Cl from 118.3 ± 15.0 to 62.7 ± 13.6 pmol · mm−1 · min−1 (48.3 ± 8.2% reduction), whereas removal of ET-1 increased J Cl in a separate group of tubules from 87.6 ± 10.7 to 115.2 ± 10.3 pmol · mm−1 · min−1 (34.5 ± 6.2% increase). To determine whether NO mediates the inhibitory effects of ET-1 on J Cl, we examined the effect of inhibiting of NO synthase (NOS) with N G-nitro-l-arginine methyl ester (l-NAME) on ET-1-induced changes in J Cl. l-NAME (5 mM) completely prevented the ET-1-induced reduction in J Cl, whereas d-NAME did not. l-NAME alone had no effect on J Cl. These data suggest that the effects of ET-1 are mediated by NO. Blockade of ETBreceptors with BQ-788 prevented the inhibitory effects of 1 nM ET-1. Activation of ETB receptors with sarafotoxin S6c mimicked the inhibitory effect of ET-1 on J Cl (from 120.7 ± 12.6 to 75.4 ± 13.3 pmol · mm−1 · min−1). In contrast, ETA receptor antagonism with BQ-610 did not prevent ET-1-mediated inhibition of TALH J Cl (from 96.5 ± 10.4 to 69.5 ± 8.6 pmol · mm−1 · min−1). Endothelin increased intracellular calcium from 96.9 ± 14.0 to 191.4 ± 11.9 nM, an increase of 110.8 ± 26.1%. We conclude that exogenous endothelin indirectly decreases TALH J Cl by activating ETB receptors, increasing intracellular calcium concentration, and stimulating NO release. These data suggest that endothelin acts as a physiological regulator of TALH NO synthesis, thus inhibiting chloride transport and contributing to the natriuretic effects of ET-1 observed in vivo.

Sodium and chloride transport along the inner medullary collecting duct: effect of saline expansion

1980 ◽  
Vol 238 (6) ◽  
pp. F504-F508 ◽  
Author(s):  
H. H. Bengele ◽  
C. Lechene ◽  
E. A. Alexander
Keyword(s):  
Sodium Chloride ◽  
Sodium Transport ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Collecting Duct ◽  
Urine Flow ◽  
Fluid Reabsorption ◽  
Inner Medullary Collecting Duct ◽  
Chloride Excretion ◽  
Medullary Collecting Duct

The effect of volume expansion on inner medullary collecting duct (IMCD) sodium transport remains controversial. Studies employing micropuncture of the IMCD base and tip were interpreted to demonstrate enhanced sodium and chloride reabsorption. Data obtained by microcatheterization evaluating only sodium transport revealed either no reabsorption or net addition. We have examined both sodium and chloride transport by microcatheterization. Volume expansion was comparable to the micropuncture studies: 0.9% saline equal to 10% body wt and then matched to urine flow. The fraction of filtered fluid, sodium, and chloride was analyzed as a function of IMCD length. In eight hydropenic rats 60% of the fluid, 71% of the sodium, and 48% of the chloride delivered to the IMCD was reabsorbed. In six volume-expanded rats no significant net reabsorption of fluid, sodium, or chloride was found. Accordingly, in contrast to the micropuncture results, we have demonstrated that net sodium chloride and fluid reabsorption are absent during volume expansion. We conclude that during volume expansion, fluid, sodium, and chloride excretion increase, in part, because of a reduction in net reabsorption along the IMCD. The degree of volume expansion does not account for the discrepancy between the two techniques.

Evidence that parallel Na+-H+ and Cl(-)-HCO3-(OH-) antiporters transport NaCl in the proximal tubule

1987 ◽  
Vol 252 (2) ◽  
pp. F338-F345 ◽  
Author(s):  
M. Baum
Keyword(s):  
Carbonic Anhydrase ◽  
Proximal Tubule ◽  
Driving Forces ◽  
Disulfonic Acid ◽  
Albumin Solution ◽  
Nacl Transport ◽  
Volume Absorption ◽  
Proximal Tubular ◽  
High Chloride

The present in vitro microperfusion study examined whether active NaCl transport in the proximal convoluted tubule (PCT) occurs via parallel Na+-H+ and Cl(-)-HCO3-(OH-) exchangers. PCT were perfused with a high-chloride, low-bicarbonate solution simulating late proximal tubular fluid, and were bathed in a similar solution containing 6 g/dl albumin. In this setting the driving forces responsible for passive NaCl transport are eliminated. Addition of 0.1 or 0.5 mM luminal 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), 0.5 mM luminal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), or 0.1 mM bath ethoxyzolamide, a lipophilic carbonic anhydrase inhibitor, resulted in an approximately 50% reduction in volume absorption. Inhibition of the Na+-H+ antiporter with 1.0 mM luminal amiloride inhibited volume absorption by 50%. The transepithelial potential difference (PD) was not significantly different from zero, consistent with an electroneutral mechanism for active NaCl transport. The effect of a Cl(-)-HCO3-(OH-) exchanger on acidification was examined in PCT perfused with an ultrafiltrate-like solution and bathed in a serumlike albumin solution. Addition of 0.5 mM DIDS did not significantly decrease volume absorption, demonstrating that luminal DIDS did not result in a nonspecific decrease in solute transport. Luminal DIDS significantly stimulated bicarbonate absorption, consistent with a Na+-H+ antiporter running in parallel with a Cl(-)-HCO3-(OH-) antiporter, which exchanges luminal Cl- for cellular HCO3- (or OH-). In conclusion, these data are consistent with parallel Na+-H+ and Cl(-)-HCO3-(OH-) antiporters mediating neutral active NaCl transport in the PCT.

Evidence for PAH extraction from superficial cortical efferent vessel plasma

1983 ◽  
Vol 245 (5) ◽  
pp. F577-F583
Author(s):  
S. W. Weinstein ◽  
R. Klose ◽  
A. M. Kumar
Keyword(s):  
Proximal Tubule ◽  
Tubular Secretion ◽  
Proximal Convoluted Tubule ◽  
Peritubular Capillary ◽  
Blood Samples ◽  
Rapid Extraction ◽  
Peritubular Capillaries ◽  
Pars Recta ◽  
Proximal Tubular

Consistent with its anatomical association with the proximal tubule we have previously shown that superficial cortical efferent vessel blood contains an admixture of early and late proximal tubular reabsorbate. Since tubular secretion of p-aminohippurate (PAH) occurs predominantly in the late proximal tubule, extraction of this compound should occur preferentially from efferent vessel blood. As a result, the midportion of the proximal convoluted tubule supplied by the more downstream peritubular capillaries would receive blood containing a disproportionately reduced concentration of PAH. To study this, proximal and distal tubular fluid and efferent vessel blood samples were collected from rats. The data confirm that preferential secretion of PAH occurs in the pars recta and demonstrate that PAH is extracted from efferent vessel plasma by the pars recta. This in turn preferentially reduces PAH concentration in early postglomerular blood before it reaches the peritubular capillary network. We speculate that PAH and similar substances secreted by the pars recta are short-circuited by rapid extraction from early postglomerular blood, reducing their delivery to the mid-proximal convoluted tubule. Such circumstances must be considered in any analysis of organic compound secretion by the in vivo proximal tubule.

An electrophysiological study of the salt gland of the herring gull

1962 ◽  
Vol 202 (3) ◽  
pp. 597-600 ◽  
Author(s):  
S. Thesleff ◽  
K. Schmidt-Nielsen
Keyword(s):  
Sodium Chloride ◽  
Active Transport ◽  
Sodium Transport ◽  
Electrophysiological Study ◽  
Salt Gland ◽  
Gland Secretion ◽  
Herring Gull ◽  
Active Sodium ◽  
Positive Potential ◽  
Active Sodium Transport

When the salt gland of the herring gull excretes sodium chloride the duct of the gland becomes positive relative to the blood. Strophanthin, an inhibitor of active sodium transport, prevents the establishment of the positive potential and also blocks gland secretion. The findings suggest that an active transport of sodium from the blood to the gland lumen may be a primary secretory mechanism.

scholarly journals Maturation of proximal straight tubule NaCl transport: role of thyroid hormone

2000 ◽  
Vol 278 (4) ◽  
pp. F596-F602 ◽  
Author(s):  
Mehul Shah ◽  
Raymond Quigley ◽  
Michel Baum
Keyword(s):  
Thyroid Hormone ◽  
Apical Membrane ◽  
Organic Solutes ◽  
Nacl Transport ◽  
Straight Tubule ◽  
Proximal Straight Tubule ◽  
Tubule Fluid ◽  
High Chloride

We have recently demonstrated that the rates of both active and passive proximal straight tubule (PST) NaCl transport in neonatal rabbits were less than in adults. In this segment NaCl entry across the apical membrane is via parallel Na+/H+ and Cl−/OH− exchangers, which increases in activity with maturation. The present in vitro microperfusion study examined whether thyroid hormone plays a role in the maturational increase in PST NaCl transport. Neonatal and adult PST were perfused with a high-chloride-low bicarbonate solution without organic solutes, simulating late proximal tubule fluid. Thyroid hormone-treated neonates had a higher rate of PST total and passive NaCl transport. In 8-wk-old animals that were hypothyroid since birth, the maturational increase in total and passive NaCl transport was prevented. Thyroid treatment for 4 days in hypothyroid 8-wk-old rabbits increased the rate of both total and passive NaCl transport. The maturational increases in both Na+/H+ and Cl−/OH− exchange activities were blunted in 8-wk-old hypothyroid animals and increased to control levels with thyroid treatment. This study demonstrates that thyroid hormone is a factor responsible for the maturational increase in both active and passive PST NaCl transport.

Transport of sodium and chloride by the isolated rumen epithelium

1964 ◽  
Vol 206 (5) ◽  
pp. 1099-1105 ◽  
Author(s):  
Charles E. Stevens
Keyword(s):  
Sodium Chloride ◽  
Active Transport ◽  
Chloride Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Exchange Diffusion ◽  
Rumen Epithelium ◽  
Tissue Resistance ◽  
Affected Tissue

Transepithelial electrical potential, short-circuit current, and resistance measurements were made under different conditions of tissue collection and maintenance. The collection procedure greatly affected tissue resistance and, since the magnitude of the current was relatively independent of the procedure, potential was affected to about the same degree. The highest and least variable resistances were recorded when the tissue was removed from the anesthetized cow and the epithelium carefully dissected free. Short-circuit current and net ion flux decreased with time but the decrease was relatively linear and sufficiently slow to allow their comparison. Rumen epithelium of both species demonstrated active transport of Na and Cl in the direction of lumen to blood. Calculation of partial Na conductances indicated that part of the sodium was transported by exchange diffusion or a sodium chloride transport system.

Ionic requirements of proximal tubular sodium transport. III. Selective luminal anion substitution

1979 ◽  
Vol 236 (3) ◽  
pp. F268-F277 ◽  
Author(s):  
R. Green ◽  
J. H. Bishop ◽  
G. Giebisch
Keyword(s):  
Sodium Transport ◽  
Concentration Gradient ◽  
Fluid Transport ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Transport Systems ◽  
Sodium Reabsorption ◽  
Perfusion Fluid ◽  
Moderate Amount ◽  
Proximal Tubular

The effect of substitution of luminal anions on sodium and fluid absorption in rat renal proximal convoluted tubules was studied with continuous luminal microperfusion methods. Substitution of bicarbonate in the control Ringer perfusion fluid by 25 mM acetate reduced net sodium reabsorption by 40%; substitution by chloride reduced it by 25%; and substitution by cyclamate reduced it by 70%. Infusion of acetazolamide reduced net sodium and fluid transport in all cases except chloride-Ringer perfusion. Cyanide added to the perfusion fluid inhibited fluid and sodium movement completely when there was no imposed chloride concentration gradient, but only reduced fluid and solute movement by 68% when a nominal 36 mM transepithelial chloride concentration gradient existed. We conclude from these observations that passive forces for sodium reabsorption can account for a moderate amount of sodium transport, that the effects of acetazolamide in low concentrations are dependent on the presence of bicarbonate in the lumen, and that some anions alter net sodium transport either by reducing the availability of permeant anion for co-transport with sodium or by a direct effect on the sodium and/or chloride transport systems.

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