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.

Renal medullary plasma flow rate and reabsorption of salt and water from inner medullary collecting duct

1987 ◽  
Vol 65 (12) ◽  
pp. 2415-2421 ◽  
Author(s):  
W. A. Cupples ◽  
H. Sonnenberg
Keyword(s):  
Blood Flow ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Plasma Flow ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Renal Circulation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

It has been proposed that medullary washout secondary to increased blood flow will limit maximal urine osmolality and reabsorption of salt and water from the inner medullary collecting duct. We have tested this prediction. The function of the inner medullary collecting duct was examined by microcatheterization. Acetylcholine was infused directly into the renal circulation, captopril was infused intravenously, and angiotensin II was infused into the renal circulation in rats which also received captopril. Medullary plasma flow rate, measured by dye–dilution in parallel experiments, was not significantly increased by acetylcholine; it was increased 30% (p < 0.02) by systemic infusion of captopril, and was returned to control by angiotensin II. Acetylcholine increased both urine flow rate and sodium excretion (p < 0.01, p < 0.001, respectively), while captopril increased only sodium excretion (p < 0.025). Angiotensin II blocked the natriuresis due to captopril. None of the treatments altered urine osmolality (p > 0.4 in all cases). Acetylcholine increased the loads of water, sodium, chloride, and total solute delivered to the inner medullary collecting duct. Angiotensin II reduced delivery of water and solutes compared with captopril alone. None of the treatments affected load dependency of reabsorption of water, sodium, chloride, or total solute in the inner medullary collecting duct. We conclude that there is, at most, a weak interaction between medullary blood flow and reabsorption from the inner medullary collecting duct.

Effect of adrenal enucleation on inner medullary collecting duct function in the rat

1982 ◽  
Vol 242 (5) ◽  
pp. F453-F456
Author(s):  
H. H. Bengele ◽  
E. A. Alexander
Keyword(s):  
Sodium Chloride ◽  
Collecting Duct ◽  
Potassium Excretion ◽  
Collection Site ◽  
Salt Load ◽  
Inner Medullary Collecting Duct ◽  
Impaired Ability ◽  
Potassium Secretion ◽  
Medullary Collecting Duct ◽  
And Control

After adrenal enucleation rats have an impaired ability to excrete a salt load. From micropuncture studies comparing data obtained from the late distal collection site and the urine, it has been suggested that this antinatriuretic effect occurs along the collecting duct. These studies are indirect, however, and cannot evaluate the contribution of deep nephrons. We have performed studies directly measuring inner medullary collecting duct (IMCD) function in saline-loaded rats 6 days after adrenal enucleation (AE). The fraction of filtered fluid, sodium, chloride, and potassium was analyzed as a function of IMCD length. In six AE rats 35% of the fluid, 35% of the sodium, and 31% of the chloride delivered to the IMCD was reabsorbed. In six saline-loaded control rats, however, no statistically significant net reabsorption of fluid sodium, or chloride was detected. Net potassium secretion along the IMCD was found in both AE and control rats. No difference between groups was noted, and net addition accounted for 17% of the potassium excreted. We conclude that after AE, the excretion of fluid, sodium, and chloride is impaired during saline expansion because of enhanced reabsorption along the IMCD. AE does not affect potassium handling along the IMCD or potassium excretion.

Effect of volume expansion with NaCl or NaHCO3 on nephron fluid and Cl transport

1977 ◽  
Vol 233 (2) ◽  
pp. F118-F125
Author(s):  
J. H. Galla ◽  
J. E. Beaumont ◽  
R. G. Luke
Keyword(s):  
Proximal Tubule ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Loop Of Henle ◽  
Fluid Reabsorption ◽  
Micropuncture Technique ◽  
Chloride Excretion ◽  
Anion Composition

To assess the influence of plasma anions on nephron fluid and chloride transport following volume expansion (VE), rats were studied by micropuncture technique during hydropenia and after VE with NaCl (CVE) or NaHCO3 (BVE). VE with either solution produced increments in plasma volume, SNGFR, and fractional sodium excretion (FENa), and decrements in proximal and distal TF/P inulin ratio which were not different. The proximal transepithelial chloride ratio decreased similarly in CVE (from 1.34 to 1.16) and BVE (from 1.32 to 1.17). Following VE, proximal fractional Cl reabsorption decreased similarly in both CVE (-5.9%) and BVE (-7.4%). Early distal fractional Cl reabsorption also was decreased in CVE (-12%) but not in BVE (-1%). Fractional chloride excretion increased in CVE but not in BVE. Therefore, following VE plasma anion composition did not significantly modify either fluid reabsorption in proximal tubule or loop of Henle or urinary Na excretion. The fraction of sodium reabsorbed with chloride in the proximal tubule increased, and Cl conservation, primarily within the loop of Henle, can be maintained despite marked natriuresis.

scholarly journals Segmental chloride transport in the Dahl-S rat kidney during L-arginine administration.

1995 ◽  
Vol 5 (8) ◽  
pp. 1567-1572
Author(s):  
K A Kirchner ◽  
B A Crosby ◽  
A R Patel ◽  
J P Granger
Keyword(s):  
Sodium Chloride ◽  
Perfusion Pressure ◽  
Chloride Transport ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Fluid Reabsorption ◽  
Nephron Segments ◽  
Single Nephron ◽  
Chloride Excretion ◽  
Pressure Natriuresis

L-Arginine normalizes pressure natriuresis in Dahl salt-sensitive (DS) rats. The nephron segments responsible for improvement in sodium chloride handling during L-arginine administration are unknown. Micropuncture techniques were used to examine fluid and chloride transport along superficial nephron segments in DS rats maintained on an 8% sodium diet and given L-arginine or vehicle ip for 3 wk. Renal perfusion pressure in vehicle-treated DS rats was reduced to that of L-arginine-treated DS rats with an aortic snare. Dahl salt-resistant (DR) rats receiving vehicle were examined for comparison. In agreement with previous studies, urinary sodium chloride excretion was greater (P < 0.05) in L-arginine DS rats than in vehicle DS rats and not different from DR rats at equivalent renal perfusion pressures. Whole-kidney and single-nephron GFR were not different (P = not significant) among groups. Fractional proximal tubule chloride and fluid reabsorption was not different among groups. Fractional loop chloride reabsorption was greater in vehicle-treated DS rats than in DR rats (58.5 +/- 1.5 versus 46.6 +/- 1.7%; P < 0.05), confirming the enhanced chloride reabsorption at this location in DS rats previously reported. Fractional loop chloride reabsorption was identical in vehicle- and L-arginine-treated DS rats (58.4 +/- 1.4 versus 58.9 +/- 3.9%; P = not significant). Fractional loop fluid reabsorption was not different among groups. Fractional distal fluid and chloride reabsorption was not different between DS rat groups.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Activation of P2Y1 and P2Y2 receptors induces chloride secretion via calcium-activated chloride channels in kidney inner medullary collecting duct cells

2011 ◽  
Vol 301 (3) ◽  
pp. F544-F553 ◽  
Author(s):  
Madhumitha Rajagopal ◽  
Paru P. Kathpalia ◽  
Sheela V. Thomas ◽  
Alan C. Pao
Keyword(s):  
Volume Expansion ◽  
Salt Intake ◽  
Collecting Duct ◽  
Short Circuit ◽  
Extracellular Fluid ◽  
Extracellular Nucleotides ◽  
Inner Medullary Collecting Duct ◽  
Apical Side ◽  
Medullary Collecting Duct ◽  
Nacl Excretion

Dysregulation of urinary sodium chloride (NaCl) excretion can result in extracellular fluid (ECF) volume expansion and hypertension. Recent studies demonstrated that urinary nucleotide excretion increases in mice ingesting a high-salt diet and that these increases in extracellular nucleotides can signal through P2Y2 receptors in the kidney collecting duct to inhibit epithelial Na+ channels (ENaC). However, under conditions of ECF volume expansion brought about by high-dietary salt intake, ENaC activity should already be suppressed. We hypothesized that alternative pathways exist by which extracellular nucleotides control renal NaCl excretion. We used an inner medullary collecting duct (mIMCD-K2) cell line in an Ussing chamber system as a model to study additional ion transport pathways that are regulated by extracellular nucleotides. When ENaC was inhibited, the addition of adenosine triphosphate (ATP) to the basal side of cell sheets activated both P2Y1 and P2Y2 receptors, inducing a transient increase in short-circuit current ( Isc); addition of ATP to the apical side activated only P2Y2 receptors, inducing first a transient and then a sustained increase in Isc. The ATP-induced increases in Isc were blocked by pretreatment with a phospholipase C (PLC) inhibitor, a calcium (Ca2+) chelator, or Ca2+-activated Cl− channel (CACC) inhibitors, suggesting that ATP signals through both PLC and intracellular Ca2+ to activate CACC. We propose that P2Y1 and P2Y2 receptors operate in tandem in IMCD cells to provide an adaptive mechanism for enhancing urinary NaCl excretion in the setting of high-dietary NaCl intake.

Water permeability of apical and basolateral cell membranes of rat inner medullary collecting duct

1990 ◽  
Vol 259 (6) ◽  
pp. F986-F999 ◽  
Author(s):  
B. Flamion ◽  
K. R. Spring
Keyword(s):  
Water Flow ◽  
Water Permeability ◽  
Cell Membranes ◽  
Apical Membrane ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Volume Regulatory Decrease ◽  
Water Permeation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

To quantify the pathways for water permeation through the kidney medulla, knowledge of the water permeability (Posmol) of individual cell membranes in inner medullary collecting duct (IMCD) is required. Therefore IMCD segments from the inner two thirds of inner medulla of Sprague-Dawley rats were perfused in vitro using a setup devised for rapid bath and luminal fluid exchanges (half time, t1/2, of 55 and 41 ms). Differential interference contrast microscopy, coupled to video recording, was used to measure volume and approximate surface areas of single cells. Volume and volume-to-surface area ratio of IMCD cells were strongly correlated with their position along the inner medullary axis. Transmembrane water flow (Jv) was measured in response to a variety of osmotic gradients (delta II) presented on either basolateral or luminal side of the cells. The linear relation between Jv and delta II yielded the cell membrane Posmol, which was then corrected for membrane infoldings. Basolateral membrane Posmol was 126 +/- 3 microns/s. Apical membrane Posmol rose from a basal value of 26 +/- 3 microns/s to 99 +/- 5 microns/s in presence of antidiuretic hormone (ADH). Because of amplification of basolateral membrane, the ADH-stimulated apical membrane remained rate-limiting for transcellular osmotic water flow, and the IMCD cell did not swell significantly. Calculated transcellular Posmol, expressed in terms of smooth luminal surface, was 64 microns/s without ADH and 207 microns/s with ADH. IMCD cells in anisosmotic media displayed almost complete volume regulatory decrease but only partial volume regulatory increase.

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