scholarly journals Lumen-positive chloride transport potential in the early distal tubule of Triturus kidney: Its absolute dependence on the presence of Na+ and K+ in the luminal fluid.

1983 ◽  
Vol 33 (5) ◽  
pp. 855-861 ◽  
Author(s):  
Takeshi HOSHI ◽  
Gen KURAMOCHI ◽  
Koji YOSHITOMI
Keyword(s):  
Chloride Transport ◽  
Distal Tubule ◽  
Absolute Dependence ◽  
Transport Potential

Effects of Intraluminal sulfate on electrolyte transfers along the perfused rat nephron

1981 ◽  
Vol 59 (2) ◽  
pp. 122-130 ◽  
Author(s):  
Gary A. Quamme
Keyword(s):  
Proximal Tubule ◽  
Chloride Transport ◽  
Distal Tubule ◽  
Phosphate Transport ◽  
Loop Of Henle ◽  
Magnesium Transport ◽  
Calcium And Magnesium ◽  
A Site ◽  
Distal Delivery

Superficial nephrons were perfused in vivo to determine the effect of intraluminal sulfate (1–20 mM) on electrolyte reabsorption in the rat with special reference to calcium and magnesium transport. This technique allowed us the opportunity of investigating separate electrolyte transfers without alteration of extrarenal influences. The major amount of perfused sulfate was absorbed in the proximal tubule with little absorption distal to the late proximal collection site. Phosphate transport was not affected by high luminal sulfate concentrations indicating distinct reabsorptive mechanisms for these two anions. Intraluminal sulfate significantly inhibited calcium and magnesium reabsorption in the proximal tubule, loop of Henle, and superficial distal tubule, in distinction to modest effects on sodium transport in these nephron segments. Chloride transport was not altered. The inhibition of divalent cation transfer was not quantitively similar in the different tubule segments. Small amounts of sulfate completely inhibited proximal calcium and magnesium reabsorption with little effect on transport within the loop of Henle. Enhanced distal delivery of sulfate significantly inhibited calcium and magnesium reabsorption in the distal tubule, a site where the sulfate anion is not reabsorbed. These results demonstrate the importance of distal delivery of anionic ligands capable of forming nonreabsorbable complexes. Thus distal calcium and magnesium transport may be greatly modified by proximal control of anion reabsorption.

Effect of Intraluminal PGE2 and Systemic Indomethacin on Sodium Chloride Transport in the Rat Distal Tubule

1983 ◽  
Vol 6 (3) ◽  
pp. 105-111
Author(s):  
R.T. Kunau, Jr. ◽  
C. Geiger ◽  
J. Hull ◽  
R.M. Wong-Garcia
Keyword(s):  
Sodium Chloride ◽  
Chloride Transport ◽  
Distal Tubule

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.

Effect of acute potassium infusion on loop segment chloride reabsorption in the rat

1983 ◽  
Vol 244 (6) ◽  
pp. F599-F605 ◽  
Author(s):  
K. A. Kirchner
Keyword(s):  
Proximal Tubule ◽  
Plasma Volume ◽  
Filtration Rate ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Distal Tubule ◽  
Fluid Flow Rate ◽  
Single Nephron ◽  
Potassium Loading ◽  
Tubule Fluid

To assess the effect of acute potassium loading on proximal tubule and loop chloride handling, chloride transport was examined in superficial cortical nephrons in control rats and after infusion with either 0.3 M KNO3 (KVE) or 0.3 M NaNO3 (NaVE) using micropuncture techniques. Infusion with either salt increased plasma volume, single nephron glomerular filtration rate (SNGFR), and delivery of fluid and chloride out of the proximal tubule. Plasma volume, tubule fluid-to-plasma inulin ratio, proximal transepithelial chloride ratio, and absolute and fractional proximal chloride delivery, however, were not different in the NaVE and KVE groups. Early distal tubule fluid flow rate, SNGFR, and fluid reabsorption were greater than control values following either infusion but these were not different between KVE and NaVE. Early distal tubule chloride concentration and transepithelial chloride gradient were greater and fractional chloride reabsorption was less in KVE than in either control or NaVE groups. Calculated fractional loop segment chloride reabsorption was less in KVE animals. These data suggest that potassium loading reduces fractional chloride reabsorption in the loop segment of rat superficial cortical nephrons.

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.

Thiazide-sensitive sodium chloride cotransport in early distal tubule

1987 ◽  
Vol 253 (3) ◽  
pp. F546-F554 ◽  
Author(s):  
D. H. Ellison ◽  
H. Velazquez ◽  
F. S. Wright
Keyword(s):  
Sodium Transport ◽  
Chloride Transport ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Sodium Absorption ◽  
Transport Pathways ◽  
Luminal Membrane ◽  
Chloride Absorption ◽  
Distal Tubules

At least two pathways mediate sodium absorption across the luminal membrane of the renal distal tubule. One pathway is a conductive channel and the other appears to be a coupled Na-Cl cotransport pathway. The distal tubule comprises three segments: the distal convoluted tubule, the connecting tubule, and the initial collecting duct. To provide information about cellular locations of the proposed sodium transport pathways, we perfused early (14-38% of whole distal length) and late (61-83% of whole distal length) segments of whole distal tubules separately in vivo in anesthetized rats. When perfused with a solution that resembles fluid normally arriving at the distal tubule (75 mM Na, 68 mM Cl), rates of sodium absorption were similar in early and late segments (early 68 +/- 29.6, late 67 +/- 27.5 pmol X min-1 X mm-1). When perfused with a solution that resembles interstitial fluid (148 mM Na, 110 mM Cl), sodium transport was significantly higher in early than in late segments (276 +/- 28.4 vs. 113 +/- 29.7 pmol X min-1 X mm-1). Chlorothiazide (10(-3) M), which blocks sodium and chloride absorption in whole distal tubules, reduced sodium and chloride transport to zero in early distal tubules but had no significant effect in late distal tubules. Removing all chloride from perfusion solutions reduced sodium transport in early but not late distal segments.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of catecholamines on rat medullary thick ascending limb chloride transport: interaction with angiotensin II

2010 ◽  
Vol 298 (4) ◽  
pp. R954-R958 ◽  
Author(s):  
Michel Baum
Keyword(s):  
Chloride Transport ◽  
Extracellular Fluid ◽  
Distal Tubule ◽  
Transport Rate ◽  
Thick Ascending Limb ◽  
Ang Ii ◽  
Adrenergic Agonists ◽  
Nephron Segments ◽  
Medullary Thick Ascending Limb ◽  
Stimulation Of

Previous studies have shown that in proximal and distal tubule nephron segments, peritubular ANG II stimulates sodium chloride transport. However, ANG II inhibits chloride transport in the medullary thick ascending limb (mTAL). Because ANG II and catecholamines are both stimulated by a decrease in extracellular fluid volume, the purpose of this study was to examine whether there was an interaction between ANG II and catecholamines to mitigate the inhibition in chloride transport by ANG II. In isolated perfused rat mTAL, 10−8 M bath ANG II inhibited transport (from a basal transport rate of 165.6 ± 58.8 to 58.8 ± 29.4 pmol·mm−1·min−1; P < 0.01). Bath norepinephrine stimulated chloride transport (from a basal transport rate of 298.1 ± 31.7 to 425.2 ± 45.8 pmol·mm−1·min−1; P < 0.05) and completely prevented the inhibition in chloride transport by ANG II. The stimulation of chloride transport by norepinephrine was mediated entirely by its β-adrenergic effect; however, both the β- and α-adrenergic agonists isoproterenol and phenylephrine prevent the ANG II-mediated inhibition in chloride transport. In the presence of 10−5 M propranolol, the effect of norepinephrine to prevent the inhibition of chloride transport by ANG II was still present. These data are consistent with an interaction of both α- and β-catecholamines and ANG II on net chloride transport in the mTAL.

Effect of Na and Cl infusion on loop function and plasma renin activity in rats

1990 ◽  
Vol 258 (5) ◽  
pp. F1328-F1335 ◽  
Author(s):  
J. N. Lorenz ◽  
T. A. Kotchen ◽  
C. E. Ott
Keyword(s):  
Plasma Renin Activity ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Specific Effect ◽  
Distal Tubule ◽  
Plasma Renin ◽  
Renin Activity ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Before And After

Inhibition of plasma renin activity (PRA) by saline has been shown to be related to a specific effect of chloride. The purpose of this study was to test the hypothesis that inhibition of renin release by selective chloride infusion in the rat is related to increased chloride transport in the thick ascending limb of the loop of Henle (TALH). Measurements of loop of Henle function were obtained by micropuncture before and after a 5% body wt infusion of solutions containing either 0.15 mol/l NaCl, 0.15 mol/l lysine monohydrochloride (LysCl), or 0.15 mol/l Na-assorted anions (NaAA). Both NaCl and LysCl infusion lowered PRA (60.8 +/- 11.9 to 22.6 +/- 3.7 ng angiotensin I (ANG I).ml-1.h-1 and 53.3 +/- 6.8 to 34.5 +/- 4.6 ng ANG I.ml-1.h-1; P less than 0.05), whereas NaAA infusion had no effect on PRA (66.7 +/- 15.1 to 59.1 +/- 12.4 ng ANG I.ml-1.h-1). Analysis of late proximal and early distal fluid showed that chloride transport in the TALH was significantly elevated by infusion in all three groups, and there were no differences among the groups after infusion. Distal chloride concentration increased in the NaCl and LysCl groups (26 +/- 2 to 37 +/- 1 meq/l and 26 +/- 2 to 36 +/- 2 meq/l; P less than 0.05), but distal chloride concentration decreased in the NaAA group (28 +/- 2 to 22 +/- 1 meq/l; P less than 0.05). There was no correlation between PRA and fluid flow rate or chloride delivery to the distal tubule.(ABSTRACT TRUNCATED AT 250 WORDS)

A micropuncture study of the renal concentrating defect of potassium depletion

1964 ◽  
Vol 206 (6) ◽  
pp. 1347-1354 ◽  
Author(s):  
Norman Bank ◽  
Hagop S. Aynedjian
Keyword(s):  
Chloride Transport ◽  
Distal Tubule ◽  
Potassium Depletion ◽  
Water Reabsorption ◽  
Low Concentrations ◽  
Collecting Ducts ◽  
Micropuncture Study ◽  
Almost All ◽  
Normal Controls ◽  
Concentrating Defect

In order to study the renal concentrating defect of potassium depletion, tubular fluid osmolality and segmental water reabsorption were measured in surface nephrons of K-deficient rats and normal controls, using micropuncture methods. The osmolality of proximal and distal tubular fluid was found to follow the same pattern as in normal rats. Many of the proximal TF/PIn ratios and almost all of the distal TF/PIn ratios were higher in the K-deficient rats than in the normals. The data from the early distal tubule suggest that sodium chloride transport by the ascending limb of Henle's loop is not markedly impaired. Delivery of fluid to the collecting ducts was diminished, thus exlcuding the possibility that increased volume flow to this segment is responsible for the concentrating defect. The finding of elevated proximal TF/PIn ratios suggests that delivery of solute to the loops of Henle may be chronically decreased. This could account for low concentrations of sodium and urea in the medullary interstitium and thus play an important contributing role in the hyposthenuria of potassium depletion.

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