Effect of benzolamide on pH in the proximal tubules and peritubular capillaries of the rat kidney

1980 ◽  
Vol 387 (1) ◽  
pp. 69-72
Author(s):  
F. John Gennari ◽  
Conrado Johns ◽  
Carlton R. Caflisch
1956 ◽  
Vol 185 (2) ◽  
pp. 430-439 ◽  
Author(s):  
Carl W. Gottschalk ◽  
Margaret Mylle

Methods are described for direct measurement of the hydrostatic pressure in the surface tubules and capillaries of the rat kidney. In fifty-six anesthetized rats intratubular pressure averaged 13.5 ± 2.4 mm Hg. Subsequent microdissection showed that all of the 112 puncture sites so localized were in the first two-thirds of the proximal convoluted tubule. Under all conditions studied, intratubular pressure and the pressure in the peritubular capillaries were approximately the same. Intravenous injection of hypertonic dextrose solution generally produced a brief rise in intratubular and peritubular capillary pressures, which returned to their preinjection levels while the diuresis so produced continued, although at less than the maximal rate. Obstruction of the ureter of kidneys undergoing diuresis resulted in a prompt rise in intratubular pressure, which agreed closely with the simultaneously determined ureteral pressure. Elevation of the ureteral pressure with a pressure bottle had no effect on intratubular or peritubular capillary pressures until it exceeded the pre-existing intratubular and peritubular capillary pressures, and then all rose together up to a maximum intratubular pressure above which elevation of ureteral pressure resulted in no further rise in intratubular or peritubular capillary pressure. Elevation of applied ureteral pressure in kidneys with collapsed tubules and in dead animals did not increase the intratubular pressure, demonstrating that the rise in intratubular pressure produced in this manner in functioning kidneys was not simply a direct back transmission of pressure. Elevation of renal venous pressure by compression of the renal vein also had no effect on intratubular and peritubular capillary pressures until their pre-existing values were exceeded, and then all three pressures rose together.


1989 ◽  
Vol 257 (4) ◽  
pp. F669-F675 ◽  
Author(s):  
R. Green ◽  
G. Giebisch

Simultaneous microperfusion of proximal tubules and peritubular capillaries in kidneys of rats anesthetized with Inactin was used to measure reabsorption of fluid in response to an imposed osmotic gradient. The tubular fluid was isotonic and the peritubular capillaries were made hypertonic with NaCl or NaHCO3. Mean gradients and ionic fluxes were measured. When no gradient was imposed tubular fluid became hypotonic and rate of fluid reabsorption was 0.700 nl.mm-1.min-1. Imposition of a 25 mM NaCl gradient increased fluid flux to 3.887 nl.mm-1.min-1, whereas 25 mM NaHCO3 stimulated 5.226 ml/mm fluid reabsorption. This gave a relative reflection coefficient of NaCl:NaHCO3 of 0.73. Apparent water permeability varied with highest values for the smallest gradients. This suggests the possibility of a compartment in the epithelium that is hypertonic to the peritubular capillaries. The hypertonicity required to account for fluid movement was 6-16 mosmol/kg.


1982 ◽  
Vol 242 (1) ◽  
pp. F78-F85 ◽  
Author(s):  
F. J. Gennari ◽  
C. R. Caflisch ◽  
C. Johns ◽  
D. A. Maddox ◽  
J. J. Cohen

PCO2 was measured in surface proximal tubules and peritubular capillaries in the rat under normal acid-base conditions and in three settings with decreased HCO3(-) reabsorption: benzolamide administration, respiratory alkalosis, and metabolic acidosis. Under normal conditions, PCO2 in the early proximal tubule (EP) was 10.5 mmHg higher than PaCO2 (P less than 0.001) and 3-4 mmHg higher than late proximal (LP) and peritubular capillary (PC) PCO2 (P less than 0.001). PCO2 in LP and PC was 7 mmHg higher than PaCO2 (P less than 0.001). Benzolamide (3 mg/kg) had no effect on the difference between PC and arterial PCO2 or between EP and PC PCO2. Increasing benzolamide to 8 mg/kg increased PCO2 in the surface structures relative to arterial PCO2 by 3-5 mmHg (P less than 0.01). Metabolic acidosis did not alter the relationships between cortical and arterial PCO2. By contrast, respiratory alkalosis decreased cortical PCO2 relative to PaCO2 by over 50%. Nonetheless, EP PCO2 was still higher than LP or PC PCO2 (P less than 0.01). Thus, reducing HCO3(-) reabsorption does not obliterate the difference between EP and LP or PC PCO2 nor does it invariably reduce PCO2 in the surface structures of the kidney relative to arterial PCO2.


1967 ◽  
Vol 15 (8) ◽  
pp. 456-469 ◽  
Author(s):  
N. O. JACOBSEN ◽  
F. JØRGENSEN ◽  
Å. C. THOMSEN

The distribution of several phosphatases in three segments of the proximal tubules was studied in frozen sections of glutaraldehyde-fixed rat kidneys. Two segments of the convoluted tubules were identified by in vivo injection of trypan blue. By increasing the concentration of adenosine triphosphate to 3 mM in the Wachstein and Meisel ATPase medium, a clear segmental differentiation in the reaction pattern of the brush border, cytoplasmic bodies and basal infoldings of the proximal tubules was obtained. The specificity of the reaction was investigated by substituting adenosine diphosphate, adenosine monophosphate or β-glycerophosphate for adenosine triphosphate in the incubation medium and by employing cyanide or fluoride as inhibitors. The reaction pattern was also compared with the localization of acid and alkaline phosphatase activities. In addition, the distribution of glucose 6-phosphatase activity was studied which showed differences in the three segments of the proximal tubules.


2006 ◽  
Vol 290 (5) ◽  
pp. F1034-F1043 ◽  
Author(s):  
Tarek M. El-Achkar ◽  
Xiaoping Huang ◽  
Zoya Plotkin ◽  
Ruben M. Sandoval ◽  
Georges J. Rhodes ◽  
...  

Toll-like receptors (TLRs) are now recognized as the major receptors for microbial pathogens on cells of the innate immune system. Recently, TLRs were also identified in many organs including the kidney. However, the cellular distribution and role of these renal TLRs remain largely unknown. In this paper, we investigated the expression of TLR4 in a cecal ligation and puncture (CLP) model of sepsis in Sprague-Dawley rats utilizing fluorescence microscopy. In sham animals, TLR4 was expressed predominantly in Tamm-Horsfall protein (THP)-positive tubules. In CLP animals, TLR4 expression increased markedly in all tubules (proximal and distal), glomeruli, and the renal vasculature. The staining showed a strong apical distribution in all tubules. A moderately less intense cellular signal colocalized partially with the Golgi apparatus. In addition, kidneys from septic rats showed increased expression of CD14 and THP. They each colocalized strongly with TLR4, albeit in different tubular segments. We also imaged the kidneys of live septic animals with two-photon microscopy after fluorescent lipopolysaccharide (LPS) injection. Within 10 min, LPS was seen at the brush border of some proximal tubules. Within 60 min, LPS was fully cytoplasmic in proximal tubules. Conversely, distal tubules showed no LPS uptake. We conclude that TLR4, CD14, and THP have specific renal cellular and tubular expression patterns that are markedly affected by sepsis. Systemic endotoxin can freely access the tubular and cellular sites where these proteins are present. Therefore, locally expressed TLRs and other interacting proteins could potentially modulate the renal response to systemic sepsis.


2003 ◽  
Vol 285 (3) ◽  
pp. C608-C617 ◽  
Author(s):  
Snezana Petrovic ◽  
Liyun Ma ◽  
Zhaohui Wang ◽  
Manoocher Soleimani

SLC26A6 (or putative anion transporter 1, PAT1) is located on the apical membrane of mouse kidney proximal tubule and mediates [Formula: see text] exchange in in vitro expression systems. We hypothesized that PAT1 along with a [Formula: see text] exchange is present in apical membranes of rat kidney proximal tubules. Northern hybridizations indicated the exclusive expression of SLC26A6 (PAT1 or CFEX) in rat kidney cortex, and immunocytochemical staining localized SLC26A6 on the apical membrane of proximal tubules, with complete prevention of the labeling with the preadsorbed serum. To examine the functional presence of apical [Formula: see text] exchanger, proximal tubules were isolated, microperfused, loaded with the pH-sensitive dye BCPCF-AM, and examined by digital ratiometric imaging. The pH of the perfusate and bath was kept at 7.4. Buffering capacity was measured, and transport rates were calculated as equivalent base flux. The results showed that in the presence of basolateral DIDS (to inhibit [Formula: see text] cotransporter 1) and apical EIPA (to inhibit Na+/H+ exchanger 3), the magnitude of cell acidification in response to addition of luminal Cl– was ∼5.0-fold higher in the presence than in the absence of [Formula: see text]. The Cl–-dependent base transport was inhibited by ∼61% in the presence of 0.5 mM luminal DIDS. The presence of physiological concentrations of oxalate in the lumen (200 μM) did not affect the [Formula: see text] exchange activity. These results are consistent with the presence of SLC26A6 (PAT1) and [Formula: see text] exchanger activity in the apical membrane of rat kidney proximal tubule. We propose that SLC26A6 is likely responsible for the apical [Formula: see text] (and Cl–/OH–) exchanger activities in kidney proximal tubule.


2005 ◽  
Vol 288 (3) ◽  
pp. F530-F538 ◽  
Author(s):  
Sunita Goyal ◽  
SueAnn Mentone ◽  
Peter S. Aronson

In situ hybridization studies demonstrated that Na+/H+ exchanger NHE8 is expressed in kidney proximal tubules. Although membrane fractionation studies suggested apical brush-border localization, precise membrane localization could not be definitively established. The goal of the present study was to develop isoform-specific NHE8 antibodies as a tool to directly establish the localization of NHE8 protein in the kidney by immunocytochemistry. Toward this goal, two sets of antibodies that label different NHE8 epitopes were developed. Monoclonal antibody 7A11 and polyclonal antibody Rab65 both specifically labeled NHE8 by Western blotting as well as by immunofluorescence microscopy. The immunolocalization pattern in the kidney seen with both antibodies was the same, thereby validating NHE8 specificity. In particular, NHE8 expression was observed on the apical brush-border membrane of all proximal tubules from S1 to S3. The most intense staining was evident in proximal tubules in the deeper cortex and medulla with a significant but somewhat weaker staining in superficial proximal tubules. Colocalization studies with γ-glutamyltranspeptidase and megalin indicated expression of NHE8 on both the microvillar surface membrane and the coated-pit region of proximal tubule cells, suggesting that NHE8 may be subject to endocytic retrieval and recycling. Although colocalizing in the proximal tubule with NHE3, no significant alteration in NHE8 protein expression was evident in NHE3-null mice. We conclude that NHE8 is expressed on the apical brush-border membrane of proximal tubule cells, where it may play a role in mediating or regulating ion transport in this nephron segment.


FEBS Letters ◽  
1990 ◽  
Vol 269 (1) ◽  
pp. 77-78 ◽  
Author(s):  
Reinaldo Marín ◽  
Daniela C. Gómez ◽  
Gloria A. Rodríguez ◽  
Teresa Proverbio ◽  
Fulgencio Proverbio

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