Single proximal tubules of Necturus kidney. VIII: Na and K determinations by glass electrodes

1963 ◽  
Vol 204 (5) ◽  
pp. 743-748 ◽  
Author(s):  
Raja N. Khuri ◽  
David A. Goldstein ◽  
David L. Maude ◽  
Charles Edmonds ◽  
A. K. Solomon
Keyword(s):  
Proximal Tubule ◽  
Distal Portion ◽  
Proximal Tubules ◽  
Living Animal ◽  
Flame Photometer ◽  
Proximal Tubular ◽  
Glass Electrodes ◽  
K Concentration

Cation-sensitive glass electrodes have been used to measure Na and K concentrations in Necturus serum and in glomerular and proximal tubular fluid from Necturus kidney. It has been found that the ratio [Na]glomerulus/[Na]serum is 1.00 ± 0.02 and the ratio [Na]tubule/[Na]glomerulus is 0.99 ± 0.01 thus confirming previous measurements with the flame photometer which indicated that tubular Na concentration did not change as fluid moved along the proximal tubule in Necturus kidney. These results were also confirmed with cation electrodes placed in situ in the living animal. The K concentration in fluid collected from the most distal portion of the proximal tubule was found to be 1.8 ± 0.1 times more concentrated than that in the glomerulus, in agreement with a ratio of 1.6 ± 0.1 previously obtained on the basis of flame photometer measurements by Oken and Solomon.

Effect of carbonic anhydrase inhibition on proximal tubular bicarbonate reabsorption

1963 ◽  
Vol 205 (4) ◽  
pp. 693-696 ◽  
Author(s):  
James R. Clapp ◽  
John F. Watson ◽  
Robert W. Berliner
Keyword(s):  
Carbonic Anhydrase ◽  
Proximal Tubule ◽  
Intravenous Administration ◽  
Distal Portion ◽  
Bicarbonate Concentration ◽  
Plasma Bicarbonate ◽  
Bicarbonate Reabsorption ◽  
Carbonic Anhydrase Inhibition ◽  
Before And After ◽  
Proximal Tubular

Samples of fluid from the proximal tubule were collected for the measurement of pH and bicarbonate concentration before and after the administration of acetazolamide (Diamox). Samples collected before acetazolamide were consistently more acid than plasma with the most acid samples coming from the more distal portion of the proximal tubule. After the intravenous administration of acetazolamide, the pH and bicarbonate concentration were consistently higher than in plasma. Bicarbonate concentrations as high as 2.8 times that in plasma were observed. The rise in proximal tubular fluid bicarbonate concentration after acetazolamide is presumably due to a reduction in the rate of bicarbonate reabsorption out of proportion to any impairment in proximal tubular fluid volume reduction.

Studies of the urinary acidification defect induced by lithium

1982 ◽  
Vol 242 (1) ◽  
pp. F23-F29 ◽  
Author(s):  
N. Bank ◽  
P. D. Lief ◽  
H. S. Aynedjian ◽  
B. F. Mutz
Keyword(s):  
Proximal Tubule ◽  
Renal Tubular Acidosis ◽  
Electrical Potential ◽  
Distal Renal Tubular Acidosis ◽  
Distal Nephron ◽  
Luminal Membrane ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Convoluted Tubules

Experiments were carried out in rats and isolated turtle bladders to study the defect in H+ transport induced by LiCl. After 3-4 days of intraperitoneal LiCl, rats developed urinary findings of "distal" renal tubular acidosis. Proximal tubular fluid pH measured in situ by glass microelectrodes was higher in lithium-treated rats than in acidotic controls. Proximal fluid total CO2 [tCO2] was also higher, and the fraction of tCO2 leaving the proximal tubule was 14 vs. 7% (P less than 0.001). Impaired acidification was also apparent beyond distal convoluted tubules, as judged by normal distal tCO2 reabsorption but increased HCO3(-) in the urine. During NaHCO3 loading, the proximal defect was ameliorated but not the distal. Turtle bladder studies showed that mucosal lithium inhibits H+ secretion secondary to reducing transepithelial electrical potential, presumably by hyperpolarization of the luminal membrane. A similar mechanism may be responsible for lithium's effect on the distal nephron. Inhibition of proximal tubular HCO3(-) reabsorption is probably not attributable to electrical potential changes but might be due to interference of luminal membrane Na+ entry by Li+ and reduced (Na+ + Li+)-H+ exchange.

Single proximal tubules of Necturus kidney. VI: Nature of potassium transport

1963 ◽  
Vol 204 (3) ◽  
pp. 377-380 ◽  
Author(s):  
Donald E. Oken ◽  
A. K. Solomon
Keyword(s):  
Proximal Tubule ◽  
Concentration Ratio ◽  
Distal Segment ◽  
Potassium Transport ◽  
Proximal Tubules ◽  
Stopped Flow ◽  
Perfusion Fluid ◽  
Kidney Proximal Tubule ◽  
K Concentration

K concentration and apparent unidirectional K fluxes have been measured in Necturus kidney proximal tubule. Mean tubular K in 12 collections from the most distal segment of the tubule is 5.4 ± 0.3 mm, and the tubular K to serum K ratio in these experiments is 1.6 ± 0.1, not significantly different from the inulin concentration ratio, 1.4 ± 0.2. The glomerular fluid to serum K concentration ratio is 1.01 ± 0.03. Apparent unidirectional K fluxes were measured using stopped-flow microperfusion technique in 11 experiments with perfusion fluid containing about 7 mm K. The apparent mean K influx was 52 ± 6 pmoles/cm2 sec and the apparent efflux was 49 ± 3 pmoles/ cm2 sec.

Effects of formate and oxalate on volume absorption in rat proximal tubule

1992 ◽  
Vol 263 (1) ◽  
pp. F37-F42 ◽  
Author(s):  
T. Wang ◽  
G. Giebisch ◽  
P. S. Aronson
Keyword(s):  
Proximal Tubule ◽  
Channel Blocker ◽  
Ringer Solution ◽  
Proximal Tubules ◽  
Solution Ph ◽  
Physiological Range ◽  
Volume Absorption ◽  
Peritubular Capillaries ◽  
Rat Proximal Tubule

We examined the effects of formate and oxalate on the rate of fluid absorption (Jv) in the rat proximal convoluted tubule in situ. Proximal tubules were microperfused with a high-Cl-, low-HCO3- Ringer solution (pH 6.7), and the peritubular capillaries were perfused with a standard Ringer solution (pH 7.4), simulating conditions in the late proximal tubule. Jv, a measure of transtubular NaCl absorption under these conditions, was calculated from the change in luminal [3H]inulin. Addition of formate in the physiological range (500 microM) to the luminal perfusate increased Jv by 45%; addition of 500 microM formate to both luminal and capillary perfusates increased Jv by 57%. Similarly, addition of oxalate in the physiological range (5 microM) to the luminal perfusate increased Jv by 37%; addition of 5 microM oxalate to both luminal and capillary perfusates increased Jv by 57%. The stimulatory effects of formate and oxalate perfused in the lumen and capillaries were not additive. Addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS, 0.1 mM) to the luminal perfusate had no effect on baseline Jv measured in the absence of added formate and oxalate but completely abolished the increment in Jv induced by formate and oxalate. Addition of the Cl(-)-channel blocker diphenylamine-2-carboxylate (DPC, 0.2 mM) to the capillary perfusate had no effect on baseline Jv but completely abolished the increment in Jv induced by formate and oxalate.(ABSTRACT TRUNCATED AT 250 WORDS)

Developmental expression of sodium entry pathways in rat nephron

1999 ◽  
Vol 276 (3) ◽  
pp. F367-F381 ◽  
Author(s):  
Roland Schmitt ◽  
David H. Ellison ◽  
Nicolette Farman ◽  
Bernard C. Rossier ◽  
Robert F. Reilly ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Proximal Part ◽  
Distal Portion ◽  
Transport Proteins ◽  
Developmental Expression ◽  
Loop Of Henle ◽  
Transport Pathways ◽  
Proximal Tubular

During the past several years, sites of expression of ion transport proteins in tubules from adult kidneys have been described and correlated with functional properties. Less information is available concerning sites of expression during tubule morphogenesis, although such expression patterns may be crucial to renal development. In the current studies, patterns of renal axial differentiation were defined by mapping the expression of sodium transport pathways during nephrogenesis in the rat. Combined in situ hybridization and immunohistochemistry were used to localize the Na-Pi cotransporter type 2 (NaPi2), the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the thiazide-sensitive Na-Cl cotransporter (NCC), the Na/Ca exchanger (NaCa), the epithelial sodium channel (rENaC), and 11β-hydroxysteroid dehydrogenase (11HSD). The onset of expression of these proteins began in post-S-shape stages. NKCC2 was initially expressed at the macula densa region and later extended into the nascent ascending limb of the loop of Henle (TAL), whereas differentiation of the proximal tubular part of the loop of Henle showed a comparatively retarded onset when probed for NaPi2. The NCC was initially found at the distal end of the nascent distal convoluted tubule (DCT) and later extended toward the junction with the TAL. After a period of changing proportions, subsegmentation of the DCT into a proximal part expressing NCC alone and a distal part expressing NCC together with NaCa was evident. Strong coexpression of rENaC and 11HSD was observed in early nascent connecting tubule (CNT) and collecting ducts and later also in the distal portion of the DCT. Ontogeny of the expression of NCC, NaCa, 11HSD, and rENaC in the late distal convolutions indicates a heterogenous origin of the CNT. These data present a detailed analysis of the relations between the anatomic differentiation of the developing renal tubule and the expression of tubular transport proteins.

The effect of sodium taurocholate on proximal tubular reabsorption in the rat kidney

1987 ◽  
Vol 72 (1) ◽  
pp. 139-141 ◽  
Author(s):  
O. S. Better ◽  
V. Guckian ◽  
G. Giebisch ◽  
R. Green
Keyword(s):  
Proximal Tubule ◽  
Bile Salts ◽  
Rat Kidney ◽  
Sodium Taurocholate ◽  
Tubular Reabsorption ◽  
Major Site ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption ◽  
Proximal Tubular Reabsorption

1. Microperfusion of tubules in situ was used to study the direct effect of sodium taurocholate on reabsorption of fluid by the proximal tubule of the rat. 2. Sodium taurocholate (0.1 mmol/l) in the tubular perfusate reduced proximal tubular fluid reabsorption by approximately 30%. 3. Thus, the proximal tubule appears to be a major site at which bile salts cause a natriuresis in the rat, and possibly in obstructive jaundice in man.

scholarly journals Aquaporin-1 water channel expression in human kidney.

1997 ◽  
Vol 8 (1) ◽  
pp. 1-14
Author(s):  
A B Maunsbach ◽  
D Marples ◽  
E Chin ◽  
G Ning ◽  
C Bondy ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Water Channel ◽  
Neck Region ◽  
Human Kidney ◽  
Proximal Tubules ◽  
Mrna Levels ◽  
Outer Medulla ◽  
Aquaporin 1 ◽  
Peritubular Capillaries

The pattern of aquaporin-1 water channel protein (AQP1) expression in the human kidney was analyzed by immunocytochemistry using semi-thin and optimized high-resolution immunoelectron microscopy based on freeze-substituted and Lowicryl HM20 embedded tissue. In addition, in situ hybridization was used to determine AQP1 mRNA distribution. Immunoblots revealed a 28-kd band and a 35- to 45-kd band corresponding to unglycosylated and glycosylated AQP1. Glomerular capillary endothelium exhibited extensive AQP1 labeling, whereas glomerular podocytes and Bowman's capsule epithelium were unlabeled. AQP1 was localized in the proximal tubule, including the neck region directly connected to the glomerulus. However, there was a marked difference in the level of expression between cross-sections of the convoluted part and the proximal straight tubules, the latter displaying the most intense labeling. AQP1 labeling continued uninterrupted from the proximal straight tubule into descending thin limbs in outer medulla. Abrupt transitions from heavily labeled to unlabeled segments of thin limbs were observed, primarily in the inner medulla. This may represent the transition from the water-permeable thin descending limb to the water-impermeable thin ascending limb. In addition, heavy labeling of fenestrated endothelium was also observed in peritubular capillaries in cortex, outer medulla, and inner medulla. Immunolabeling controls were negative. In situ hybridization documented a marked difference in AQP1 mRNA levels within the proximal tubule, with the greatest AQP1 mRNA expression in straight proximal tubules. Glomeruli also showed marked signals, and descending thin limbs exhibited extensive expression in exact concordance with the immunocytochemical results. It was concluded that: (1) AQP1 is present in all proximal tubule segments, including segment 1 and the neck region, but there is a pronounced difference in expression levels with respect to both protein and mRNA levels; (2) AQP1 labeling is observed in the endothelium of fenestrated peritubular capillaries, as well as fenestrated glomerular capillaries; (3) AQP1 labeling continues directly from proximal tubules to descending thin limbs; and (4) abrupt transitions from labeled to unlabeled thin limb epithelium are noted.

scholarly journals Antiproteinuric Therapy while Preventing the Abnormal Protein Traffic in Proximal Tubule Abrogates Protein- and Complement-Dependent Interstitial Inflammation in Experimental Renal Disease

1999 ◽  
Vol 10 (4) ◽  
pp. 804-813
Author(s):  
MAURO ABBATE ◽  
CARLA ZOJA ◽  
DANIELA ROTTOLI ◽  
DANIELA CORNA ◽  
NORBERTO PERICO ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Proximal Tubules ◽  
Complement C3 ◽  
Abnormal Protein ◽  
Protein Traffic ◽  
Tubular Cells ◽  
Mhc Ii ◽  
Interstitial Inflammation ◽  
Proximal Tubular ◽  
Protein Reabsorption

Abstract. In proteinuric glomerulopathies, the excess traffic of proteins into the renal tubule is a candidate trigger of interstitial inflammatory and immune events leading to progressive injury, and a key target for the renoprotective action of antiproteinuric drugs. Among proteins trafficked to the proximal tubule, the third component of complement (C3) can be activated locally and contribute to inflammation at sites of protein reabsorption. Experiments were performed in rats with renal mass reduction (RMR, 5/6 nephrectomy) with the following aims: (1) to study Ig (IgG) and complement deposition in proximal tubules, and interstitial macrophage infiltration and MHC class II expression at intervals after surgery by double immunofluorescence analysis; (2) to assess whether lisinopril (angiotensin-converting enzyme inhibitor [ACEi], 25 mg/L in the drinking water, from either day 1 or day 7) limited IgG and C3 accumulation and interstitial inflammation at day 30. In 7-d remnant kidneys, intracellular staining for both IgG and C3 was detectable in proximal tubules in focal areas; C3 was restricted to IgG-positive tubular cells, and there were no interstitial ED-1 macrophage and MHC II-positive cellular infiltrates. In 14-d and 30-d remnant kidneys, proximal tubular IgG and C3 staining was associated with the appearance of interstitial infiltrates that preferentially localized to areas of tubules positive for both proteins. RMR rats given ACEi had no or limited increases in levels of urinary protein excretion, tubular IgG, and C3 reactivity, and interstitial cellular infiltrates in kidneys at 30 d, even when ACEi was started from day 7 after surgery. These findings document that (1) in RMR, IgG and C3 accumulation in proximal tubular cells is followed by leukocyte infiltration and MHC II overexpression in the adjacent interstitium; (2) ACEi while preventing proteinuria limits both tubular accumulation of IgG and C3 and interstitial inflammation. The data suggest that ACE inhibition can be renoprotective by limiting the early abnormal protein traffic in proximal tubule and consequent deleterious effects of excess protein reabsorption, including the accumulation and local activation of complement as well as the induction of chemokines and endothelin genes known to promote interstitial inflammation and fibrosis.

scholarly journals Review: Evidence for a functional intracellular angiotensin system in the proximal tubule of the kidney

2012 ◽  
Vol 302 (5) ◽  
pp. R494-R509 ◽  
Author(s):  
Brianne Ellis ◽  
Xiao C. Li ◽  
Elisa Miguel-Qin ◽  
Victor Gu ◽  
Jia L. Zhuo
Keyword(s):  
Blood Pressure ◽  
Proximal Tubule ◽  
Renin Angiotensin System ◽  
Proximal Tubules ◽  
Renal Physiology ◽  
The Novel ◽  
Ang Ii ◽  
Angiotensin System ◽  
Proximal Tubular

ANG II is the most potent and important member of the classical renin-angiotensin system (RAS). ANG II, once considered to be an endocrine hormone, is now increasingly recognized to also play novel and important paracrine (cell-to-cell) and intracrine (intracellular) roles in cardiovascular and renal physiology and blood pressure regulation. Although an intracrine role of ANG II remains an issue of continuous debates and requires further confirmation, a great deal of research has recently been devoted to uncover the novel actions and elucidate underlying signaling mechanisms of the so-called intracellular ANG II in cardiovascular, neural, and renal systems. The purpose of this article is to provide a comprehensive review of the intracellular actions of ANG II, either administered directly into the cells or expressed as an intracellularly functional fusion protein, and its effects throughout a variety of target tissues susceptible to the impacts of an overactive ANG II, with a particular focus on the proximal tubules of the kidney. While continuously reaffirming the roles of extracellular or circulating ANG II in the proximal tubules, our review will focus on recent evidence obtained for the novel biological roles of intracellular ANG II in cultured proximal tubule cells in vitro and the potential physiological roles of intracellular ANG II in the regulation of proximal tubular reabsorption and blood pressure in rats and mice. It is our hope that the new knowledge on the roles of intracellular ANG II in proximal tubules will serve as a catalyst to stimulate further studies and debates in the field and to help us better understand how extracellular and intracellular ANG II acts independently or interacts with each other, to regulate proximal tubular transport and blood pressure in both physiological and diseased states.

scholarly journals Metabolic substrates alter attachment and differentiated functions of proximal tubule cell culture.

1994 ◽  
Vol 4 (11) ◽  
pp. 1908-1911
Author(s):  
M J Tang ◽  
R L Tannen
Keyword(s):  
Proximal Tubule ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Culture Media ◽  
Proximal Tubules ◽  
Proximal Tubule Cell ◽  
Metabolic Substrates ◽  
Standard Culture ◽  
Leucine Amino Peptidase ◽  
Proximal Tubular

Proximal tubules cultured in vitro gradually lose their differentiated functions. Because standard culture media lacks several substrates important for renal proximal tubule oxidative metabolism, whether a mixture of substrates including butyrate, alanine, and lactate (BAL) would modify growth and/or differentiated function of proximal tubular cells in culture was examined. Tubules cultured in media supplemented with 2 mM butyrate, alanine, and lactate exhibited enhanced attachment but did not exhibit an altered growth rate. Higher levels of phosphoenolpyruvate carboxykinase and leucine-amino peptidase were sustained, although these activities were still diminished in comparison with that in fresh tubules. Sodium-dependent glucose uptake and dome formation--other reflections of epithelial cell differentiated function--also were enhanced. These studies demonstrate that the substrates used to culture proximal tubules can modify both their attachment and their manifestation of differentiated function in culture.

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