Hormone effects on NaCl permeability of rat inner medullary collecting duct

1988 ◽  
Vol 255 (3) ◽  
pp. F421-F428 ◽  
Author(s):  
J. M. Sands ◽  
H. Nonoguchi ◽  
M. A. Knepper
Keyword(s):  
Atrial Natriuretic Factor ◽  
Collecting Duct ◽  
Transepithelial Resistance ◽  
Ion Fluxes ◽  
Chloride Permeability ◽  
Hormonal Effects ◽  
Inner Medullary Collecting Duct ◽  
Hormone Effects ◽  
Medullary Collecting Duct ◽  
Nacl Excretion

It has been proposed that regulation of NaCl excretion occurs in part by hormonal effects on NaCl permeability in the inner medullary collecting duct (IMCD). We carried out experiments in isolated perfused terminal IMCDs to determine whether atrial natriuretic factor (ANF), vasopressin, or deoxycorticosterone (DOC) affects NaCl permeability. Apparent Cl- or Na+ permeabilities (PCl and PNa) were determined by measuring ion fluxes resulting from imposed electrochemical gradients. Transepithelial resistance (RT) was calculated from voltage deflections at the perfusion and collection ends of the tubule, which resulted from perfusion end current injection (cable analysis). ANF [rat ANF-(1–28), 100 nM in the peritubular bath] significantly decreased PCl from 2.20 to 1.84 x 10(-5) cm/s and did not alter PNa (1.11 to 1.18 x 10(-5) cm/s). ANF also decreased PCl in IMCDs from DOC-treated rats (1.14 to 0.98 x 10(-5) cm/s). Vasopressin (10 nM in the peritubular bath) did not affect PCl. RT averaged 39.3 omega.cm2 in IMCDs from control rats and was significantly increased to 62.3 omega.cm2 in tubules from DOC-treated rats. Neither ANF nor vasopressin significantly affected RT in either group. We conclude the following: 1) the results do not support the hypothesis that ANF causes natriuresis by increasing the NaCl permeability of the terminal IMCD. Instead, ANF significantly decreases the chloride permeability. 2) Vasopressin does not affect NaCl permeability. 3) Mineralocorticoid-induced antinatriuresis may be due in part to reduced NaCl permeability in the terminal IMCD.

Effects of ANF on cGMP synthesis in inner medullary collecting duct subsegments of rats

1990 ◽  
Vol 259 (3) ◽  
pp. F535-F538
Author(s):  
K. Ujiie ◽  
H. Nonoguchi ◽  
K. Tomita ◽  
F. Marumo
Keyword(s):  
Atrial Natriuretic Factor ◽  
Collecting Duct ◽  
Target Site ◽  
Cyclic Monophosphate ◽  
Inner Medullary Collecting Duct ◽  
Camp Synthesis ◽  
Target Sites ◽  
Medullary Collecting Duct ◽  
Cgmp Synthesis ◽  
Major Target

The inner medullary collecting duct (IMCD) is thought to be a major target site for atrial natriuretic factor (ANF) action. The IMCD is divided into two subsegments (IMCD1, outer third; and IMCD2,3, inner two-thirds) based on differences in urea and water permeability. IMCD1 has similar characteristics to the outer medullary collecting duct (OMCD). To elucidate whether there are any differences among these segments in ANF actions, we investigated the effects of ANF on guanosine 3',5'-cyclic monophosphate (cGMP) synthesis in IMCD subsegments and the OMCD. We also examined the effects of arginine vasopressin (AVP) on adenosine 3',5'-cyclic monophosphate (cAMP) synthesis. IMCD subsegments (IMCD1,2,3) and OMCD were microdissected; and ANF-stimulated cGMP synthesis and AVP-stimulated cAMP synthesis were measured. cGMP synthesis stimulated by 10(-6) M ANF in IMCD1,2,3 (0.78 +/- 0.15, 0.81 +/- 0.19, 0.62 +/- 0.10 fmol.mm-1 x 3 min-1, mean +/- SE respectively, n = 10-11) was significantly (greater than 20-fold) higher than that in OMCD (0.03 +/- 0.02 fmol.mm-1 x 3 min-1, n = 7), and there was no difference among IMCD subsegments. On the other hand, cAMP synthesis stimulated by 10(-7) M AVP in IMCD subsegments was similar to that in OMCD. We conclude that IMCD is homogenous as a target site of ANF and is clearly distinguished from OMCD. In addition, more than half of ANF-stimulated cGMP synthesis in IMCD are considered to occur in IMCD1, simply because IMCD1 is dominant in population among IMCD subsegments. As target sites of AVP, IMCD subsegments are similar to OMCD.

scholarly journals Prostaglandin E2 induces chloride secretion through crosstalk between cAMP and calcium signaling in mouse inner medullary collecting duct cells

2014 ◽  
Vol 306 (3) ◽  
pp. C263-C278 ◽  
Author(s):  
Madhumitha Rajagopal ◽  
Sheela V. Thomas ◽  
Paru P. Kathpalia ◽  
Yu Chen ◽  
Alan C. Pao
Keyword(s):  
Prostaglandin E2 ◽  
Molecular Mechanisms ◽  
Salt Intake ◽  
Collecting Duct ◽  
Short Circuit ◽  
Flufenamic Acid ◽  
Dietary Salt ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Nacl Excretion

Under conditions of high dietary salt intake, prostaglandin E2 (PGE2) production is increased in the collecting duct and promotes urinary sodium chloride (NaCl) excretion; however, the molecular mechanisms by which PGE2 increases NaCl excretion in this context have not been clearly defined. We used the mouse inner medullary collecting duct (mIMCD)-K2 cell line to characterize mechanisms underlying PGE2-regulated NaCl transport. When epithelial Na+ channels were inhibited, PGE2 exclusively stimulated basolateral EP4 receptors to increase short-circuit current ( IscPGE2). We found that IscPGE2 was sensitive to inhibition by H-89 and CFTR-172, indicating that EP4 receptors signal through protein kinase A to induce Cl− secretion via cystic fibrosis transmembrane conductance regulator (CFTR). Unexpectedly, we also found that IscPGE2 was sensitive to inhibition by BAPTA-AM (Ca2+ chelator), 2-aminoethoxydiphenyl borate (2-APB) (inositol triphosphate receptor blocker), and flufenamic acid (FFA) [Ca2+-activated Cl− channel (CACC) inhibitor], suggesting that EP4 receptors also signal through Ca2+ to induce Cl− secretion via CACC. Additionally, we observed that PGE2 stimulated an increase in Isc through crosstalk between cAMP and Ca2+ signaling; BAPTA-AM or 2-APB inhibited a component of IscPGE2 that was sensitive to CFTR-172 inhibition; H-89 inhibited a component of IscPGE2 that was sensitive to FFA inhibition. Together, our findings indicate that PGE2 activates basolateral EP4 receptors and signals through both cAMP and Ca2+ to stimulate Cl− secretion in IMCD-K2 cells. We propose that these signaling pathways, and the crosstalk between them, may provide a concerted mechanism for enhancing urinary NaCl excretion under conditions of high dietary NaCl intake.

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.

scholarly journals Claudin-19 Is Regulated by Extracellular Osmolality in Rat Kidney Inner Medullary Collecting Duct Cells

2019 ◽  
Vol 20 (18) ◽  
pp. 4401 ◽  
Author(s):  
Annalisa Ziemens ◽  
Svenja Sonntag ◽  
Vera Wulfmeyer ◽  
Bayram Edemir ◽  
Markus Bleich ◽  
...  
Keyword(s):  
Tight Junction ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Transepithelial Resistance ◽  
Transepithelial Transport ◽  
Ussing Chambers ◽  
Inner Medullary Collecting Duct ◽  
Cation Selectivity ◽  
Junction Protein ◽  
Medullary Collecting Duct

The inner medullary collecting duct (IMCD) is subject to severe changes in ambient osmolality and must either allow water transport or be able to seal the lumen against a very high osmotic pressure. We postulate that the tight junction protein claudin-19 is expressed in IMCD and that it takes part in epithelial adaptation to changing osmolality at different functional states. Presence of claudin-19 in rat IMCD was investigated by Western blotting and immunofluorescence. Primary cell culture of rat IMCD cells on permeable filter supports was performed under different osmotic culture conditions and after stimulation by antidiuretic hormone (AVP). Electrogenic transepithelial transport properties were measured in Ussing chambers. IMCD cells cultivated at 300 mosm/kg showed high transepithelial resistance, a cation selective paracellular pathway and claudin-19 was mainly located in the tight junction. Treatment by AVP increased cation selectivity but did not alter transepithelial resistance or claudin-19 subcellular localization. In contrast, IMCD cells cultivated at 900 mosm/kg had low transepithelial resistance, anion selectivity, and claudin-19 was relocated from the tight junctions to intracellular vesicles. The data shows osmolality-dependent transformation of IMCD epithelium from tight and sodium-transporting to leaky, with claudin-19 expression in the tight junction associated to tightness and cation selectivity under low osmolality.

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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