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%).

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.

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.

Mutual dependence of sodium and chloride absorption by renal distal tubule

1984 ◽  
Vol 247 (6) ◽  
pp. F904-F911 ◽  
Author(s):  
H. Velazquez ◽  
D. W. Good ◽  
F. S. Wright
Keyword(s):  
Chloride Transport ◽  
Chloride Concentration ◽  
Distal Tubule ◽  
Sodium Concentration ◽  
Sodium Absorption ◽  
Similar Extent ◽  
Luminal Membrane ◽  
Chloride Absorption ◽  
Transepithelial Voltage

Sodium transport and chloride transport by the renal distal tubule of rats were studied by in vivo continuous microperfusion to determine the effects of separately altering luminal sodium and chloride concentrations. Results showed that sodium absorption depends on luminal sodium concentration and chloride absorption depends on luminal chloride concentration; both relations are linear between approximately 10 and 100 mM and have slopes of approximately 2.5 pmol X min-1 X mM-1. Sodium absorption is also a saturable function of luminal chloride concentration, and chloride absorption is a saturable function of luminal sodium concentration; the half-maximal chloride and sodium concentrations are approximately 10 mM. Furosemide, 10(-4) M, when added to the fluid used to perfuse this segment inhibited sodium absorption and chloride absorption to a similar extent. Removal of chloride from luminal fluid (replaced with sulfate) and addition of furosemide to the perfusion fluid had little or no effect on the measured transepithelial voltage. The results are consistent with the presence of a mechanism in the luminal membrane of distal tubule cells that couples the absorptive transport of sodium and chloride.

α2-Adrenergic-mediated tubular NO production inhibits thick ascending limb chloride absorption

2001 ◽  
Vol 281 (4) ◽  
pp. F679-F686 ◽  
Author(s):  
Craig F. Plato ◽  
Jeffrey L. Garvin
Keyword(s):  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Chloride Transport ◽  
Receptor Activation ◽  
Inhibitory Effect ◽  
No Production ◽  
Thick Ascending Limb ◽  
Chloride Absorption ◽  
Ly 83583

Stimulation of α2-adrenergic receptors inhibits transport in various nephron segments, and the thick ascending limb of the loop of Henle (THAL) expresses α2-receptors. We hypothesized that selective α2-receptor activation decreases NaCl absorption by cortical THALs through activation of NOS and increased production of NO. We found that the α2-receptor agonist clonidine (10 nM) decreased chloride flux ( J Cl) from 119.5 ± 15.9 to 67.4 ± 13.8 pmol · mm−1 · min−1 (43% reduction; P < 0.02), whereas removal of clonidine from the bath increased J Cl by 20%. When NOS activity was inhibited by pretreatment with 5 mM N G-nitro-l-arginine methyl ester, the inhibitory effects of clonidine on THAL J Clwere prevented (81.7 ± 10.8 vs. 71.6 ± 6.9 pmol · mm−1 · min−1). Similarly, when the NOS substrate l-arginine was deleted from the bath, addition of clonidine did not decrease THAL J Cl from control (106.9 ± 11.6 vs. 132.2 ± 21.3 pmol · mm−1 · min−1). When we blocked the α2-receptors with rauwolscine (1 μM), we found that the inhibitory effect of 10 nM clonidine on THAL J Cl was abolished, verifying that α2, rather than I1, receptors mediate the effects of clonidine in the THAL. We investigated the mechanism of NOS activation and found that intracellular calcium concentration did not increase in response to clonidine, whereas pretreatment with 150 nM wortmannin abolished the clonidine-mediated inhibition of THAL J Cl, indicating activation of phosphatidylinositol 3-kinase and the Akt pathway. We found that pretreatment of THALs with 10 μM LY-83583, an inhibitor of soluble guanylate cyclase, blocked clonidine-mediated inhibition of THAL J Cl. In conclusion, α2-receptor stimulation decreases THAL J Cl by increasing NO release and stimulating guanylate cyclase. These data suggest that α2-receptors act as physiological regulators of THAL NO synthesis, thus inhibiting chloride transport and participating in the natriuretic and diuretic effects of clonidine in vivo.

scholarly journals Effects of halides and bicarbonate on chloride transport in human red blood cells.

1976 ◽  
Vol 67 (2) ◽  
pp. 223-234 ◽  
Author(s):  
M Dalmark
Keyword(s):  
Red Blood Cells ◽  
Binding Sites ◽  
Blood Cells ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Human Red Blood Cells ◽  
Half Saturation Constant ◽  
Saturation Kinetics ◽  
Transport Site ◽  
High Chloride

Chloride self-exchange was determined by measuring the rate of 36Cl efflux from human red blood cells at pH 7.2 (0 degrees C) in the presence of fluoride, bromide, iodide, and bicarbonate. The chloride concentration was varied between 10--400 mM and the concentration of other halides and bicarbonate between 10--300 mM. Chloride equilibrium flux showed saturation kinetics. The half-saturation constant increased and the maximum flux decreased in the presence of halides and bicarbonate: the inhibition kinetics were both competitive and noncompetitive. The competitive and the noncompetitive effects increased proportionately in the sequence: fluoride less than bromide less than iodide. The inhibitory action of bicarbonate was predominantly competitive. The noncompetitive effect of chloride (chloride self-inhibition) on chloride transport was less dominant at high inhibitor concentrations. Similarly, the noncompetitive action of the inhibitors was less dominant at high chloride concentrations. The results can be described by a carrier model with two anion binding sites: a transport site, and a second site which modifies the maximum transport rate. Binding to both types of sites increases proportionately in the sequence: fluoride less than chloride less than bromide less than iodide.

Sodium and chloride transport in the large intestine of potassium-loaded rats

1986 ◽  
Vol 251 (2) ◽  
pp. G249-G252 ◽  
Author(s):  
M. E. Budinger ◽  
E. S. Foster ◽  
J. P. Hayslett ◽  
H. J. Binder
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Sodium Absorption ◽  
Chloride Absorption ◽  
Dietary Potassium ◽  
Potassium Secretion ◽  
Potassium Loading

Increased dietary potassium ("potassium loading") induces several adaptive changes in colonic function, including increased potential-dependent potassium secretion, active potassium secretion, and Na-K-ATPase activity, but does not alter net sodium absorption in vivo. To establish whether potassium loading stimulates active sodium transport, unidirectional, net sodium, and chloride fluxes were determined under voltage-clamp conditions across isolated rat distal colonic mucosa. In normal animals net sodium flux (JNanet), net chloride flux (JClnet) and short-circuit current (Isc) were 6.1 +/- 1.1, 8.4 +/- 1.0, and 0.7 +/- 0.1 mu eq X h-1. cm-2, respectively; potassium loading significantly increased JNanet and Isc by 4.9 +/- 1.4 and 3.5 +/- 0.7 mu eq X h-1 X cm-2, respectively, without changing JClnet. Amiloride (0.1 mM) inhibited the increases in JNanet and Isc produced by potassium loading. In Cl-free Ringer solution in normal animals JNanet was reduced to 0.6 +/- 0.3 mu eq X h-1 X cm-2. Potassium loading produced identical increases in JNanet and Isc, which were also completely inhibited by 0.1 mM amiloride. These studies establish that potassium loading induces amiloride-sensitive electrogenic sodium absorption without affecting electroneutral sodium-chloride absorption.

The Role of the Colon in the Pathogenesis of Hyperchloraemic Acidosis in Ureterosigmoid Anastomosis

1979 ◽  
Vol 57 (4) ◽  
pp. 305-312 ◽  
Author(s):  
J. B. McConnell ◽  
J. Murison ◽  
W. K. Stewart
Keyword(s):  
Colonic Mucosa ◽  
Chloride Concentration ◽  
Direct Consequence ◽  
Normal Subjects ◽  
Ionic Diffusion ◽  
Chloride Absorption ◽  
Total Ammonia ◽  
Colonic Secretion

1. The composition of urine-faeces mixture in seven patients with ureterosigmoid anastomosis has been studied by a dialysis in vivo method using cellulose bags. Urine—faeces dialysate obtained from these patients contained much greater amounts of both bicarbonate and total ammonia than has been reported for faecal dialysate in normal subjects. 2. Total ammonia concentrations in urine– faeces specimens obtained by catheter suggest that urine excreted by the kidneys in these patients becomes increasingly acid with increasing systemic acidosis. The highly alkaline nature of urine-faeces mixtures, especially in acidotic patients, indicates rapid alkalinization of the mixture in the colon. It appears that colonic secretion of bicarbonate is a direct consequence of the acidity of urine excreted by the kidney and draining into the colon. 3. The study suggests that the development of hyperchloraemic acidosis in patients with ureterosigmoid anastomosis is due to bicarbonate secretion by the colonic mucosa, with concomitant chloride absorption. With the development of metabolic acidosis, rapid alkalinization of the urine still occurs in the colon, but during further retention of the urine-faeces in the colon some reabsorption of bicarbonate occurs, probably in part by ionic diffusion since chloride concentration in the lumen increases. 4. Evidence suggestive of non-ionic diffusion of ammonia was found in only one patient. It seems probable that higher rates of urea breakdown in other patients mask the expected relationship between total ammonia and bicarbonate.

Angiotensin II increases chloride absorption in the cortical collecting duct in mice through a pendrin-dependent mechanism

2007 ◽  
Vol 292 (3) ◽  
pp. F914-F920 ◽  
Author(s):  
Vladimír Pech ◽  
Young Hee Kim ◽  
Alan M. Weinstein ◽  
Lorraine A. Everett ◽  
Truyen D. Pham ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Chloride Transport ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Wild Type ◽  
Atpase Inhibitor ◽  
Chloride Absorption ◽  
Transepithelial Voltage ◽  
Dependent Mechanism

Pendrin ( Slc26a4) localizes to type B and non-A, non-B intercalated cells in the distal convoluted tubule, the connecting tubule, and the cortical collecting duct (CCD), where it mediates apical Cl−/HCO3− exchange. The purpose of this study was to determine whether angiotensin II increases transepithelial net chloride transport, JCl, in mouse CCD through a pendrin-dependent mechanism. JCl and transepithelial voltage, VT, were measured in CCDs perfused in vitro from wild-type and Slc26a4 null mice ingesting a NaCl-replete diet or a NaCl-replete diet and furosemide. In CCDs from wild-type mice ingesting a NaCl-replete diet, VT and JCl were not different from zero either in the presence or absence of angiotensin II (10−8 M) in the bath. Thus further experiments employed mice given the high-NaCl diet and furosemide to upregulate renal pendrin expression. CCDs from furosemide-treated wild-type mice had a lumen-negative VT and absorbed Cl−. With angiotensin II in the bath, Cl− absorption doubled although VT did not become more lumen negative. In contrast, in CCDs from furosemide-treated Slc26a4 null mice, Cl− secretion and a VT of ∼0 were observed, neither of which changed with angiotensin II application. Inhibiting ENaC with benzamil abolished VT although JCl fell only ∼50%. Thus substantial Cl− absorption is observed in the absence of an electromotive force. Attenuating apical anion exchange with the peritubular application of the H+-ATPase inhibitor bafilomycin abolished benzamil-insensitive Cl− absorption. In conclusion, angiotensin II increases transcellular Cl− absorption in the CCD through a pendrin- and H+-ATPase-dependent process.

Effect of volume expansion and plasma chloride on function of the loop segment

1983 ◽  
Vol 245 (1) ◽  
pp. F41-F47 ◽  
Author(s):  
B. B. Booker ◽  
R. H. Williams ◽  
R. G. Luke
Keyword(s):  
Volume Expansion ◽  
Chloride Concentration ◽  
Ringer Solution ◽  
Thick Ascending Limb ◽  
Chloride Uptake ◽  
Gradient Effect ◽  
Time Control ◽  
Chloride Absorption ◽  
Plasma Chloride

To determine the effect of acute volume expansion and changes in plasma chloride on fluid and chloride uptake in superficial loop segments of rats, this segment was microperfused in vivo at 22 nl/min with a fluid containing Na 145, Cl and 36Cl 130, and HCO3 15 meq/liter during hydropenia and after acute volume expansion with 0.15 M NaCl, 0.15 M NaHCO3, or an isotonic bicarbonate Ringer (Cl 106 meq/liter) solution. Fractional fluid, chloride, and 36Cl reabsorption and early distal chloride concentration did not change during maintained hydropenia (time control) or during volume expansion with NaCl (plasma chloride 120 meq/liter) or bicarbonate Ringer solution (plasma chloride 104 meq/liter). Absolute and fractional reabsorption of chloride and 36Cl increased, without change in fluid reabsorption, and early distal chloride diminished after infusion of NaHCO3 (plasma chloride 90 meq/liter). It is concluded that acute volume expansion, per se, has no effect on either net fluid or net chloride absorption in the superficial loop segment at the load studied. Hypochloremia is associated with increased net reabsorption of chloride and an increased unidirectional efflux of chloride from the loop segment during acute volume expansion, most likely due to a gradient effect on the thick ascending limb of the loop of Henle.

Effect of potassium depletion on chloride transport in the loop of Henle in the rat

1985 ◽  
Vol 248 (5) ◽  
pp. F682-F687 ◽  
Author(s):  
R. G. Luke ◽  
B. B. Booker ◽  
J. H. Galla
Keyword(s):  
Chloride Transport ◽  
Chloride Concentration ◽  
Distal Tubule ◽  
Normal Diet ◽  
Potassium Depletion ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Chloride Absorption ◽  
Altered Response ◽  
And Control

Microperfusion of the superficial loop segment (latest proximal to earliest distal tubule) was performed in potassium-depleted and control rats. Potassium depletion was confirmed by analysis of muscle content (control 45 +/- 2, potassium depletion 33.5 +/- 0.9 meq/100 g dry solids). During perfusion at 20 nl/min net chloride absorption was decreased (66 +/- 3 vs. 77 +/- 2%, P less than 0.01) and early distal chloride concentration increased (70 +/- 5 vs. 50 +/- 4 meq/liter, P less than 0.01) in the potassium-depleted rats. In separate paired experiments in potassium-depleted rats, indomethacin infusion increased net chloride absorption (P less than 0.05) and lowered early distal chloride concentration (P less than 0.05) toward, but not to, normal. A similar effect of indomethacin to decrease early distal chloride concentration was seen in rats ingesting a normal diet and in control rats. We conclude that in potassium-depleted rats there is impaired net chloride absorption in the loop segment, most likely in the thick ascending limb, and that this effect is not produced by an altered response to prostaglandins. This defect in chloride transport may be responsible, at least in part, for the impaired concentrating capacity seen in potassium-depleted rats.

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