Induction of Na K ATPase in the proximal and distal convolution of the rat nephron after uninephrectomy

1974 ◽  
Vol 346 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Udo Schmidt ◽  
Ulrich C. Dubach ◽  
Barbara Funk ◽  
Kaija Paris
Keyword(s):  

2001 ◽  
Vol 281 (6) ◽  
pp. F1021-F1027 ◽  
Author(s):  
Johannes Loffing ◽  
Dominique Loffing-Cueni ◽  
Victor Valderrabano ◽  
Lea Kläusli ◽  
Steven C. Hebert ◽  
...  

First published August 15, 2001; 10.1152/ajprenal. 00085.2001.—The organization of Na+ and Ca2+ transport pathways along the mouse distal nephron is incompletely known. We revealed by immunohistochemistry a set of Ca2+ and Na+transport proteins along the mouse distal convolution. The thiazide-sensitive Na+-Cl− cotransporter (NCC) characterized the distal convoluted tubule (DCT). The amiloride-sensitive epithelial Na+ channel (ENaC) colocalized with NCC in late DCT (DCT2) and extended to the downstream connecting tubule (CNT) and collecting duct (CD). In early DCT (DCT1), the basolateral Ca2+-extruding proteins [Na+/Ca2+ exchanger (NCX), plasma membrane Ca2+-ATPase (PCMA)] and the cytoplasmic Ca2+-binding protein calbindin D28K (CB) were found at very low levels, whereas the cytoplasmic Ca2+/Mg2+-binding protein parvalbumin was highly abundant. NCX, PMCA, and CB prevailed in DCT2 and CNT, where we located the apical epithelial Ca2+ channel (ECaC1). Its subcellular localization changed from apical in DCT2 to exclusively cytoplasmic at the end of CNT. NCX and PMCA decreased in parallel with the fading of ECaC1 in the apical membrane. All three of them were undetectable in CD. These findings disclose DCT2 and CNT as major sites for transcellular Ca2+ transport in the mouse distal nephron. Cellular colocalization of Ca2+ and Na+ transport pathways suggests their mutual interactions in transport regulation.



1983 ◽  
Vol 245 (4) ◽  
pp. F419-F424
Author(s):  
R. G. Luke ◽  
J. H. Galla

Current concepts hold that volume expansion is essential to the correction of chloride-depletion alkalosis (CDA) with chloride repletion in a permissive role. In this scheme, intranephronal fluid reabsorption would be redistributed with increased delivery to the distal nephron where the provided chloride is readily reabsorbed and the limited capacity for bicarbonate reabsorption would promote bicarbonate excretion and correction of CDA. In a model of CDA produced by peritoneal dialysis against 0.15 M NaHCO3, we have shown complete correction of CDA within 24 h without volume expansion by either oral isotonic sodium or chloride salts with 70 mM chloride and despite an obligatory bicarbonate load and negative sodium and potassium balance. During correction of CDA without volume expansion in rats by intravenous isotonic fluids containing 80 mM chloride, fractional fluid and chloride reabsorptions in the proximal convoluted tubule and in the loop segment of superficial nephrons were not different from controls but chloride reabsorption was enhanced in the collecting duct segment and probably within the distal convolution. Despite no differences in serial hematocrits, blood pressure, and measured plasma volume, kidney and nephron glomerular filtration rate (GFR) were reduced in CDA and returned to normal upon recovery 24 h later.(ABSTRACT TRUNCATED AT 250 WORDS)



1963 ◽  
Vol 204 (5) ◽  
pp. 771-775 ◽  
Author(s):  
William E. Lassiter ◽  
Carl W. Gottschalk ◽  
Margaret Mylle

Anesthetized rats and hamsters were given Ca45 intravenously, and fluid was subsequently collected by micropuncture from glomeruli and surface tubules in the rats, and from loops of Henle in the hamsters. In nondiuretic animals, fluid:plasma calcium ratios averaged 0.71 in the glomerulus; 0.76 in the proximal tubule; 2.0 in the loop of Henle; 0.47 in the distal convolution; and 0.9 in ureteral urine. In mannitol diuresis, the calcium ratio of glomerular fluid was unchanged, but ratios as low as 0.21 were noted in the proximal tubule. In this circumstance, the average proximal ratio was 0.61, and the distal ratio 0.07. These results indicate active transport of calcium out of all major parts of the nephron, with the bulk of calcium reabsorption occurring in the convoluted portion of the proximal tubule. Furthermore, the pattern of tubular reabsorption of calcium is similar to that of sodium, suggesting that the two are related.



1957 ◽  
Vol 105 (6) ◽  
pp. 615-622 ◽  
Author(s):  
Joseph F. Smith ◽  
Yin Chen Lee

Experimental uric acid lesions in the kidney of the rabbit have been reinvestigated using the technique of miscrodissection for location of lesions. The maximal initial lesion was found to occur in the first part of the collecting, and not in the ascending Henle and the distal convoluted tubule. Such lesions were only produced by very high dosage (approximately 0.5–1 gm. per kg.). It was concluded that the argument by analogy with the uric acid lesion cannot be used to support a hypothetical toxic damage to the segments of ascending Henle and the distal convolution in the crush syndrome.



1960 ◽  
Vol 198 (3) ◽  
pp. 581-585 ◽  
Author(s):  
Carl W. Gottschalk ◽  
William E. Lassiter ◽  
Margaret Mylle

Fluid was collected by micropuncture from individual renal tubules of anesthetized rats and its pH determined with the quinhydrone microelectrode. The single glomerular sample and early proximal fluid were isohydric with arterial blood, but later proximal fluid usually showed progressive acidification. The maximum proximal fall in pH was 0.43 u in nondiuretic rats, 0.56 u during profuse glucose or mannitol diuresis, and 0.78 u in rats previously loaded with ammonium chloride and undergoing glucose diuresis. Fluid from the early distal convolution was usually acidified relative to arterial blood but was not significantly different from late proximal fluid. Progressive acidification probably also occurred in the distal convolution. The pH decreased further in the collecting ducts, much more so in the nondiuretic state than during diuresis. The quantitative importance of proximal reabsorption of HCO3– and, by inference, H+ secretion is emphasized. It is suggested that the pH of tubular fluid may increase in the thin descending limb of the loop of Henle, especially in a kidney elaborating a concentrated urine, because of increased concentration of HCO3–.



1989 ◽  
Vol 257 (1) ◽  
pp. F107-F113
Author(s):  
J. H. Galla ◽  
D. N. Bonduris ◽  
R. G. Luke

Chloride is necessary and sufficient to correct alkalosis induced by dialysis vs. 0.15 M NaHCO3. To determine the contribution of the cortical (SC) distal convolution (DCT) and juxtamedullary (JM) nephrons to correction, we examined Cl and total CO2 (tCO2) transport in alkalotic Sprague-Dawley rats infused with 5% dextrose (group DM) or with 5% dextrose and 80 mM Cl (group CC); in papillary studies in alkalotic Munich-Wistar rats, 6% albumin was added to the infusate. In cortical studies, changes in plasma Cl and tCO2 were 4.9 +/- 0.7 vs. 0.7 +/- 0.9 and -6.0 +/- 0.8 vs. 0.4 +/- 0.9 meq/l and in tCO2 excretion (133 +/- 28 vs. -8 +/- 10 mueq/min) in groups CC and DM, respectively; results in papillary studies were similar. Delivery of tCO2 out of late SC DCT (CC 146 +/- 20 and DM 146 +/- 23 pmol/min) and Henle's loop (CC 145 +/- 18 and DM 202 +/- 56 pmol/min) and reabsorption within DCT (CC 15 +/- 24 and DM 45 +/- 19 pmol/min) did not differ. During correction of chloride-depletion alkalosis, the increment in bicarbonate excretion does not emanate from DCT of SC nephrons or JM nephrons but rather from the collecting duct.



2002 ◽  
Vol 13 (4) ◽  
pp. 836-847 ◽  
Author(s):  
Helena Lagger Biner ◽  
Marie-Pierre Arpin-Bott ◽  
Johannes Loffing ◽  
Xiaoyan Wang ◽  
Mark Knepper ◽  
...  

ABSTRACT. The exact distributions of the different salt transport systems along the human cortical distal nephron are unknown. Immunohistochemistry was performed on serial cryostat sections of healthy parts of tumor nephrectomized human kidneys to study the distributions in the distal convolution of the thiazide-sensitive Na-Cl cotransporter (NCC), the β subunit of the amiloride-sensitive epithelial Na channel (ENaC), the vasopressin-sensitive water channel aquaporin 2 (AQP2), and aquaporin 3 (AQP3), the H+ ATPase, the Na-Ca exchanger (NCX), plasma membrane calcium-ATPase, and calbindin-D28k (CaBP). The entire human distal convolution and the cortical collecting duct (CCD) display calbindin-D28k, although in variable amounts. Approximately 30% of the distal convolution profiles reveal NCC, characterizing the distal convoluted tubule. NCC overlaps with ENaC in a short portion at the end of the distal convoluted tubule. ENaC is displayed all along the connecting tubule (70% of the distal convolution) and the CCD. The major part of the connecting tubule and the CCD coexpress aquaporin 2 with ENaC. Intercalated cells, undetected in the first 20% of the distal convolution, were interspersed among the segment-specific cells of the remainder of the distal convolution, and of the CCD. The basolateral calcium extruding proteins, Na-Ca exchanger (NCX), and the plasma membrane Ca2+-ATPase were found all along the distal convolution, and, in contrast to other species, along the CCD, although in varying amounts. The knowledge regarding the precise distribution patterns of transport proteins in the human distal nephron and the knowledge regarding the differences from that in laboratory animals may be helpful for diagnostic purposes and may also help refine the therapeutic management of electrolyte disorders.



1983 ◽  
Vol 244 (2) ◽  
pp. F140-F149 ◽  
Author(s):  
E. Pastoriza-Munoz ◽  
D. R. Mishler ◽  
C. Lechene

The sites of enhanced phosphate (PO4) reabsorption after PO4 deprivation were investigated before and after infusion of parathyroid hormone (PTH) in acutely thyroparathyroidectomized rats. Animals were fed either a control PO4 diet (1.6% P) or a low PO4 diet (0.025% P) for 2 days or 7-10 days. In control rats, PTH decreased PO4 reabsorption in the proximal tubule, loop of Henle, and distal convolution. PO4 reabsorption in the proximal tubule was enhanced after 2 days of PO4 deprivation. In this group, proximal PO4 reabsorption was decreased by PTH but remained greater than in control rats (70 +/- 6 vs. 45 +/- 6 pmol/min; P less than 0.025). After PTH, PO4 reabsorption increased in the loop of Henle from 3 +/- 0.5 to 13 +/- 2 pmol/min (P less than 0.005), whereas it was unaltered in the distal convolution in PO4-deprived rats. PTH markedly increased fractional excretion of PO4 in control rats but not in PO4-deprived rats. After prolonged PO4 deprivation, PO4 reabsorption along the nephron was unaltered by PTH. These results demonstrate that acute PO4 deprivation enhances PO4 reabsorption in the proximal tubule, although the phosphaturic effect of PTH in this segment is not abolished. Resistance to the inhibitory effect of PTH on PO4 reabsorption in some portion of the loop of Henle and possibly also in the distal convolution accounts for the absence of a significant phosphaturic effect of the hormone in acutely PO4-deprived rats. Prolongation of PO4 deprivation results in unresponsiveness to PTH extending to the proximal tubule.



1964 ◽  
Vol 206 (4) ◽  
pp. 669-673 ◽  
Author(s):  
William E. Lassiter ◽  
Margaret Mylle ◽  
Carl W. Gottschalk

Anesthetized rats were given urea-C14 intravenously and infused with 5% NaCl solution containing inulin-methoxy-H3. Fluid was collected by micropuncture from surface tubules for simultaneous determination of H3 and C14 activities and osmolality. Inulin clearances, plasma and urine sodium, urine volume, and urea excretion were all greatly increased, but fractional water and urea reabsorption in the proximal convolution was similar to that in nondiuretic rats. Inulin fluid/plasma ratios in hypotonic early distal samples were slightly lower than those observed in nondiuretic rats. Urea/inulin ratios in distal samples and in ureteral urine were similar to the late proximal convolution, indicating little or no addition of urea in the loop of Henle or loss from distal convolution or collecting ducts, in contrast to nondiuretic rats. These results suggest that in the proximal convolution sodium (and therefore water) reabsorption is proportional to the rate of delivery of sodium to the tubule. Furthermore, the absence of demonstrable net transtubular movement of urea beyond the proximal convolution under conditions in which concentration gradients are reduced is consistent with the hypothesis that urea movement is largely passive.



1978 ◽  
Vol 235 (4) ◽  
pp. F321-F330 ◽  
Author(s):  
E. Pastoriza-Munoz ◽  
R. E. Colindres ◽  
W. E. Lassiter ◽  
C. Lechene


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