Cellular morphology in outer medullary collecting duct: effect of 75% nephrectomy and K+ depletion

1992 ◽  
Vol 263 (6) ◽  
pp. F1119-F1127
Author(s):  
R. K. Zalups ◽  
D. A. Henderson
Keyword(s):  
Renal Mass ◽  
Morphological Changes ◽  
Collecting Duct ◽  
Fractional Excretion ◽  
Potassium Depletion ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Medullary Collecting Duct ◽  
Principal And Intercalated Cells ◽  
K Depletion

The present study was designed to determine, in rats, whether 75% nephrectomy and potassium depletion affect the principal and intercalated cells in the outer medullary collecting duct in the same manner as they affect the principal and intercalated cells in the cortical collecting duct. Ten days after a 75% reduction of renal mass, whole animal glomerular filtration rate decreased and the fractional excretion of potassium increased in rats. However, no morphological changes occurred in either the principal or intercalated cells of the outer medullary collecting duct after the reduction of renal mass. When 75% nephrectomized rats were placed on a diet deficient in potassium, the concentration of potassium in plasma and the absolute and fractional excretion of potassium decreased significantly. In addition, marked hypertrophy occurred in both the principal and intercalated cells in the outer medullary collecting duct. Previous findings from the same animals used in the present study show that 75% nephrectomy caused hypertrophic changes in principal cells of the cortical collecting duct, which could be inhibited by potassium depletion induced by the dietary restriction of potassium. The findings also show that the intercalated cells of the cortical collecting duct in 75% nephrectomized rats were unaffected by potassium depletion. On the basis of our findings, it appears there is an absence of hypertrophy in either the principal or intercalated cells in the outer medullary collecting duct of the rat after renal mass in the animal is reduced significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Minealocorticoid receptors and 11 beta-steroid dehydrogenase activity in renal principal and intercalated cells

1994 ◽  
Vol 266 (1) ◽  
pp. F76-F80 ◽  
Author(s):  
A. Naray-Fejes-Toth ◽  
E. Rusvai ◽  
G. Fejes-Toth
Keyword(s):  
Cell Sorting ◽  
Direct Action ◽  
Collecting Duct ◽  
Cell Types ◽  
Target Cells ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Specific Receptors ◽  
Principal And Intercalated Cells ◽  
Steroid Dehydrogenase

Aldosterone exerts complex effects on the cortical collecting duct (CCD): it increases Na+ and K+ transport, and it also influences H+ and HCO3 transport. Whether these latter effects represent direct action of aldosterone on intercalated cells (ICC) or are secondary to changes in the transport of other electrolytes is unclear. Because the presence of specific receptors is the prerequisite of a direct steroid action, and mineralocorticoid receptors (MR) have not yet been demonstrated in ICC, in this study we determined the density of MR directly in isolated principal cells (PC) and beta-ICC. Purified populations of these two cell types were obtained from rabbit renal cortex by immunodissection and fluorescence-activated cell sorting. We found that both PC and beta-ICC contained a significant number of MR, although receptor density was higher in PC than in beta-ICC (6,704 +/- 912 vs. 2,181 +/- 388 MR sites/cell; P < 0.001). 11 beta-Hydroxysteroid dehydrogenase (11 beta-OHSD), an enzyme that is present predominantly in mineralocorticoid target cells, exhibited a distribution similar to that of MR in the two cell types. 11 beta-OHSD activity, determined by measuring the rate of conversion of [3H]corticosterone to 11-dehydrocorticosterone, was 1.08 +/- 0.14 and 0.34 +/- 0.08 fmol.min-1 x 1,000 cells-1 (P < 0.001) in intact PC and beta-ICC, respectively. 11 beta-OHSD in both cell types utilized NAD as cofactor. These results suggest that beta-ICC are potential direct targets of aldosterone and that MR in both PC and beta-ICC are protected by 11 beta-OHSD.

H(+)-K(+)-ATPase activity in rat collecting duct segments

1992 ◽  
Vol 262 (4) ◽  
pp. F692-F695 ◽  
Author(s):  
J. D. Gifford ◽  
L. Rome ◽  
J. H. Galla
Keyword(s):  
Atpase Activity ◽  
Marked Decrease ◽  
Collecting Duct ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Medullary Collecting Duct ◽  
Gastric Proton Pump

Previous studies have suggested the presence of an H(+)-K(+)-ATPase in rat cortical and medullary intercalated cells with similar properties to the gastric proton pump. The purpose of this study was to determine the functional contribution of an H(+)-K(+)-adenosinetriphosphatase(ATPase) to total CO2 (tCO2) transport along the rat collecting duct. After baseline determination of tCO2 transport in isolated perfused collecting duct segments, Sch 28080 (10 microM) was added to either the perfusate or bath. When Sch 28080 was added to the perfusate, there was no effect in the cortical collecting duct (CCD, 20.8 +/- 6.7 vs. 25.3 + 3.0 pmol.mm-1.min-1), but a marked decrease in tCO2 absorption was effected in both the outer medullary (OMCD, 37.6 + 6.2 vs. 10.7 +/- 4.1 pmol.mm-1.min-1) and initial inner medullary collecting duct (IMCD1, 34.4 +/- 8.1 vs. 16.2 +/- 5.6 pmol.mm-1.min-1). In the CCD from rats with acute alkalosis in vivo, Sch 28080 added to the bath inhibited tCO2 secretion in the CCD (-17.1 +/- 4.4 vs 3.5 + 3.3 pmol.mm-1.min-1). These findings suggest that 1) H(+)-K(+)-ATPase is important in tCO2 absorption in the OMCD and IMCD1 and in tCO2 secretion in the CCD, 2) HCO3(-)-absorbing intercalated cells differ functionally in the cortex and medulla, 3) HCO3- secretion is not the reverse process of HCO3- absorption in the CCD, and 4) H(+)-K(+)-ATPase is important in distal acidification under normal and altered acid-base conditions.

Vasopressin resistance in potassium depletion: role of Na-K pump

1992 ◽  
Vol 263 (4) ◽  
pp. F705-F710 ◽  
Author(s):  
S. K. Mujais ◽  
Y. Chen ◽  
N. A. Nora
Keyword(s):  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pump Activity ◽  
Before And After ◽  
Directional Change ◽  
Medullary Collecting Duct ◽  
Low K ◽  
K Depletion

Resistance to the hydrosmotic effects of vasopressin has been described in K depletion. It is not clear whether other effects of vasopressin, notably its effects on the Na-K pump in the collecting duct, are similarly affected. Adrenalectomized male Sprague-Dawley rats were allocated to either a normal K (NK) or low-K (LK) diet. Na-K pump activity (pmol.mm-1.h-1) in cortical collecting duct (CCD) and medullary collecting duct (MCD) was determined at 21 days after allocation to the dietary groups before and after exogenous vasopressin (0.1 U twice daily for 3 days). In animals on NK diet, vasopressin (AVP) led to a doubling of Na-K pump activity in the CCD from 502 +/- 47 to 1,144 +/- 41 pmol.mm-1.h-1 (P < 0.01). In K-depleted animals, which had a higher baseline Na-K pump activity, an increase was also observed from 1,056 +/- 97 to 1,239 +/- 65 pmol.mm-1.h-1 (P < 0.05), but this increase was quantitatively less, with the change being 183 vs. 642 pmol.mm-1.h-1 in K-replete rats. The findings in the MCD were similar; in rats on a NK diet, AVP led to a significant increase in Na-K pump activity from 498 +/- 29 to 830 +/- 28 pmol.mm-1.h-1 (P < 0.01). With K depletion, this directional change was preserved, increasing from 1,380 +/- 49 to 1,556 +/- 45 pmol.mm-1.h-1 (P < 0.05), but was quantitatively less than in K-replete rats, the change being 176 vs. 332 pmol.mm-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Cellular remodeling of HCO3(-)-secreting cells in rabbit renal collecting duct in response to an acidic environment.

1989 ◽  
Vol 109 (3) ◽  
pp. 1279-1288 ◽  
Author(s):  
L M Satlin ◽  
G J Schwartz
Keyword(s):  
Apical Membrane ◽  
Collecting Duct ◽  
Low Ph ◽  
Membrane Receptors ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Similar Reduction ◽  
Fourfold Increase ◽  
Principal And Intercalated Cells

The renal cortical collecting duct (CCD) consists of principal and intercalated cells. Two forms of intercalated cells, those cells involved in H+/HCO3- transport, have recently been described. H+-secreting cells are capable of apical endocytosis and have H+ATPase on the apical membrane and a basolateral Cl-/HCO3- exchanger. HCO3(-)-secreting cells bind peanut agglutinin (PNA) to apical membrane receptors and have diffuse or basolateral distribution of H+ATPase; their Cl-/HCO3- exchanger is on the apical membrane. We found that 20 h after acid feeding of rabbits, there was a fourfold increase in number of cells showing apical endocytosis and a numerically similar reduction of cells binding PNA. Incubation of CCDs at pH 7.1 for 3-5 h in vitro led to similar, albeit less pronounced, changes. Evidence to suggest internalization and degradation of the PNA binding sites included a reduction in apical binding of PNA, decrease in pH in the environment of PNA binding, and incorporation of electron-dense PNA into cytoplasmic vesicles. Such remodeling was dependent on protein synthesis. There was also functional evidence for loss of apical Cl-/HCO3- exchange on PNA-labeled cells. Finally, net HCO3- flux converted from secretion to absorption after incubation at low pH. Thus, exposure of CCDs to low pH stimulates the removal/inactivation of apical Cl-/HCO3- exchangers and the internalization of other apical membrane components. Remodeling of PNA-labeled cells may mediate the change in polarity of HCO3- flux observed in response to acid treatment.

Localization of the ammonium transporter proteins RhBG and RhCG in mouse kidney

2003 ◽  
Vol 284 (2) ◽  
pp. F323-F337 ◽  
Author(s):  
Jill W. Verlander ◽  
R. Tyler Miller ◽  
Amy E. Frank ◽  
Ines E. Royaux ◽  
Young-Hee Kim ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Immunoblot Analysis ◽  
Mouse Kidney ◽  
Ammonium Transporter ◽  
Ammonium Transport ◽  
Apical Region ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Principal Cells ◽  
Medullary Collecting Duct

Ammonia is both produced and transported by renal epithelial cells, and it regulates renal ion transport. Recent studies have identified a family of putative ammonium transporters; mRNA for two members of this family, Rh B-glycoprotein (RhBG) and Rh C-glycoprotein (RhCG), is expressed in the kidney. The purpose of this study was to determine the cellular location of RhBG and RhCG protein in the mouse kidney. We generated RhBG- and RhCG-specific anti-peptide antibodies. Immunoblot analysis confirmed that both proteins were expressed in the mouse kidney. RhBG localization with immunohistochemistry revealed discrete basolateral labeling in the connecting segment (CNT) and in the majority of initial collecting tubule (ICT) and cortical collecting duct (CCD) cells. In the outer medullary collecting duct (OMCD) and inner medullary collecting duct (IMCD) only a subpopulation of cells exhibited basolateral immunoreactivity. Colocalization of RhBG with carbonic anhydrase II, the thiazide-sensitive transporter, and the anion exchangers AE1 and pendrin demonstrated RhBG immunoreactivity in all CNT cells and all CCD and ICT principal cells. In the ICT and CCD, basolateral RhBG immunoreactivity is also present in A-type intercalated cells but not in pendrin-positive CCD intercalated cells. In the OMCD and IMCD, only intercalated cells exhibit RhBG immunoreactivity. Immunoreactivity for a second putative ammonium transporter, RhCG, was present in the apical region of cells with almost the same distribution as RhBG. However, RhCG immunoreactivity was present in all CCD cells, and it was present in outer stripe OMCD principal cells, in addition to OMCD and IMCD intercalated cells. Thus the majority of RhBG and RhCG protein expression is present in the same epithelial cell types in the CNT and collecting duct but with opposite polarity. These findings suggest that RhBG and RhCG may play important and cell-specific roles in ammonium transport and signaling in these regions of the kidney.

Effect of flow and stretch on the [Ca2+]i response of principal and intercalated cells in cortical collecting duct

2003 ◽  
Vol 285 (5) ◽  
pp. F998-F1012 ◽  
Author(s):  
Wen Liu ◽  
Shiyun Xu ◽  
Craig Woda ◽  
Paul Kim ◽  
Sheldon Weinbaum ◽  
...  
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Cell Types ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Duration Magnitude ◽  
Luminal Flow ◽  
Principal And Intercalated Cells ◽  
Circumferential Stretch

An acute increase in tubular fluid flow rate in the microperfused cortical collecting duct (CCD), associated with a ∼20% increase in tubular diameter, leads to an increase in intracellular Ca2+ concentration ([Ca2+]i)in both principal and intercalated cells (Woda CB, Leite M Jr, Rohatgi R, and Satlin LM. Am J Physiol Renal Physiol 283: F437-F446, 2002). The apical cilium present in principal but not intercalated cells has been proposed to be a flow sensor. To determine whether flow across the cilium and/or epithelial stretch mediates the [Ca2+]i response, CCDs from New Zealand White rabbits were microperfused in vitro, split-open (to isolate the effect of flow across cilia), or occluded (to examine the effect of stretch and duration/magnitude of the flow impulse), and [Ca2+]i was measured using fura 2. In perfused and occluded CCDs, a rapid (<1 s) but not slow (>3 min) increase in luminal flow rate and/or circumferential stretch led to an approximately threefold increase in [Ca2+]i in both principal and intercalated cells within ∼10 s. This response was mediated by external Ca2+ entry and inositol 1,4,5-trisphosphate-mediated release of cell Ca2+ stores. In split-open CCDs, an increase in superfusate flow led to an approximately twofold increase in [Ca2+]i in both cell types within ∼30 s. These experimental findings are interpreted using mathematical models to predict the fluid stress on the apical membranes of the CCD and the forces and torques on and deformation of the cilia. We conclude that rapid increases in luminal flow rate and circumferential stretch, leading to shear or hydrodynamic impulses at the cilium or apical membrane, lead to increases in [Ca2+]i in both principal and intercalated cells.

K+ depletion increases HCO 3 − reabsorption in OMCD by activation of colonic H+-K+-ATPase

1998 ◽  
Vol 274 (4) ◽  
pp. F687-F692 ◽  
Author(s):  
Suguru Nakamura ◽  
Zhaohui Wang ◽  
John H. Galla ◽  
Manoocher Soleimani
Keyword(s):  
Collecting Duct ◽  
Potassium Depletion ◽  
Mrna Levels ◽  
Inhibitory Effects ◽  
Outer Medulla ◽  
Flux Formula ◽  
Medullary Collecting Duct ◽  
K Depletion

To probe the role of the isoforms of H+-K+-ATPase (HKA) in potassium depletion (KD), rats were placed on a KD diet for 2 wk. Colonic HKA (cHKA) mRNA levels increased ∼30-fold in outer medulla, and net [Formula: see text] flux ([Formula: see text]) in outer medullary collecting duct (OMCD) increased (13.1 pmol ⋅ min−1 ⋅ mm tubule length−1 in control to 17.7 pmol ⋅ min−1 ⋅ mm tubule length−1 in KD; P < 0.01). In normal rats, 1 mM ouabain in perfusate had no effect on[Formula: see text], whereas 10 μM Sch-28080 decreased[Formula: see text]to 5.1 pmol ⋅ min−1 ⋅ mm tubule length−1( P < 0.001). In KD rats, ouabain 1 mM decreased[Formula: see text]to 6.3 pmol ⋅ min−1 ⋅ mm tubule length−1( P < 0.001). Although 10 μM Sch-28080 also decreased[Formula: see text]to 4.6 pmol ⋅ min−1 ⋅ mm tubule length−1( P < 0.001), the inhibitory effects of Sch-28080 and ouabain were not additive. Removal of K+ from perfusate blocked Sch-28080-sensitive[Formula: see text]in both normal and KD tubules. The data suggest that, in KD, cHKA is induced and mediates increased [Formula: see text]reabsorption in OMCD, cHKA in vivo is sensitive to both Sch-28080 and ouabain, and cHKA activity is dominant.

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