Mechanism of acidification along cortical distal tubule of the rat

1994 ◽  
Vol 266 (2) ◽  
pp. F218-F226 ◽  
Author(s):  
R. Fernandez ◽  
M. J. Lopes ◽  
R. F. de Lira ◽  
W. F. Dantas ◽  
E. J. Cragoe Junior ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Exchange Resin ◽  
Rat Kidney ◽  
Specific Inhibitor ◽  
Distal Tubule ◽  
Ringer Solution ◽  
Na Channel ◽  
Bafilomycin A1 ◽  
Bicarbonate Reabsorption ◽  
Distal Tubules

The cellular mechanism of luminal acidification (bicarbonate reabsorption) was studied in cortical distal tubules of rat kidney. The stopped-flow microperfusion technique was applied to early distal (ED) and late distal (LD) segments, perfused with bicarbonate Ringer solution to which specific inhibitors were added, to measure bicarbonate reabsorption [HCO3 flux (JHCO3)]. pH and transepithelial potential difference (Vt) were recorded by double-barreled H+ exchange resin/reference (1 M KCl) electrodes. Amiloride increased stationary pH and reduced Vt in both early and late segments. Hexamethylene-amiloride (HMA), a specific Na(+)-H+ exchange blocker, reduced JHCO3 in both segments (ED by 43.6 and LD by 40.3%) without affecting Vt. Benzamil, an Na(+)-channel blocker, reduced Vt by 75.9 in ED and 74.9% in LD but had no significant effect on acidification in both segments. The specific inhibitor of H(+)-ATPase, bafilomycin A1, inhibited LD JHCO3 at a concentration of 2 x 10(-7) M by 49%, but ED was inhibited by 24% only at 2 x 10(-6) M. Sch-28080, an inhibitor of gastric H(+)-K(+)-ATPase, reduced JHCO3 by 35% in LD of K(+)-depleted rats but not in control rats and had no effect on ED. These data indicate that, in ED, bicarbonate reabsorption is mediated mostly by Na(+)-H+ exchange. In LD, there is evidence for contribution of Na(+)-H+ exchange, vacuolar H(+)-ATPase, and H(+)-K(+)-ATPase (in K(+)-depleted rats) to bicarbonate reabsorption.

In vivo adaptation of bicarbonate reabsorption by rat distal tubules during acid loading

1994 ◽  
Vol 267 (5) ◽  
pp. F737-F747 ◽  
Author(s):  
D. Z. Levine ◽  
M. Iacovitti ◽  
S. Buckman ◽  
D. Vandorpe ◽  
V. Harrison ◽  
...  
Keyword(s):  
Water Flux ◽  
Distal Tubule ◽  
Bafilomycin A1 ◽  
Bicarbonate Reabsorption ◽  
Distal Tubules ◽  
Acid Loading ◽  
Fasted Rats ◽  
Predominant Effect ◽  
Stimulation Of

We carried out in vivo microperfusion experiments in acid-loaded rats to characterize the adaptive response of the unidirectional components secretory flux (Jsec) and reabsorptive flux (Jreab)] of distal tubule bicarbonate reabsorption and to test the hypothesis that Jreab is dependent on bafilomycin A1-sensitive H(+)-adenosinetriphosphatase activity. During 18 h of severe acidosis there was a significant decrease in Jsec (-15 +/- 3 vs. -38 +/- 5 pmol.min-1.mm-1, P < 0.05) and a significant increase in Jreab (37 +/- 6 vs. 0 +/- 5 pmol.min-1.mm-1, P < 0.05), which was insensitive to 10(-5) M bafilomycin A1, 10(-5) M Sch-28080, and 3 mM amiloride. After 3 days of acid loading, these same inhibitors reduced Jreab by approximately 60%. However, when water flux was completely inhibited by isosmotic perfusion, a significant Jreab (15 +/- 2 pmol.min-1.mm-1) resistant to 10(-5) M bafilomycin A1 persisted, as in severe acidosis. In reabsorbing distal tubules of overnight-fasted rats, Sch-28080 elicited no inhibition, whereas bafilomycin A1 and amiloride had significant effects (28 +/- 5, 24 +/- 4, respectively, vs. 50 +/- 4 pmol.min-1.mm-1 for fasted rats, P < 0.05). Thus, although Jsec is reduced in the transition from mild to severe metabolic acidosis of 18-h duration, the predominant effect is a stimulation of bafilomycin A1-resistant Jreab.

Distal tubule unidirectional HCO3 reabsorption in vivo during acute and chronic metabolic alkalosis in the rat

1994 ◽  
Vol 266 (6) ◽  
pp. F919-F925 ◽  
Author(s):  
D. Z. Levine ◽  
M. Iacovitti ◽  
S. Buckman ◽  
D. Vandorpe ◽  
V. Harrison ◽  
...  
Keyword(s):  
Metabolic Alkalosis ◽  
Distal Tubule ◽  
Bicarbonate Secretion ◽  
Bafilomycin A1 ◽  
Secretory Phase ◽  
Plasma Bicarbonate ◽  
Bicarbonate Reabsorption ◽  
Chloride Depletion ◽  
Distal Tubules

During metabolic alkalosis (MA) associated with 2 days of dietary chloride restriction, there is net bicarbonate secretion by rat distal tubules in vivo, whereas after 5 wk of chloride depletion alkalosis there is net bicarbonate reabsorption. To examine unidirectional components of net bicarbonate reabsorption during chronic MA, we measured distal tubule unidirectional bicarbonate secretion (Jsec) and reabsorption (Jreab), as well as the inhibitor sensitivity of Jreab. In control, 2-day, and 7-day alkalosis, Jsec was similar. Jreab, however, was only present in 7-day MA (17 +/- 3 pmol.min-1.mm-1, P < 0.05). This Jreab was completely suppressed by perfusion with 10(-7) M bafilomycin A1, partially suppressed with 10(-5) M Schering (Sch)-28080 (4 +/- 2 pmol.min-1.mm-1, P < 0.1), and converted into a secretory flux by 3 mM amiloride. We conclude that adaptation to chloride depletion MA from the acute secretory phase to the chronic state, where plasma bicarbonate is sustained at elevated levels, does not involve suppression of distal tubule Jsec but rather enhanced Jreab, which is sensitive to bafilomycin, Sch-28080, and amiloride.

Electrical characteristics of snake distal tubules: studies of I-V relationships

1980 ◽  
Vol 239 (5) ◽  
pp. F402-F411 ◽  
Author(s):  
B. M. Koeppen ◽  
K. W. Beyenbach ◽  
W. H. Dantzler ◽  
S. I. Helman
Keyword(s):  
Chemical Potential ◽  
Distal Tubule ◽  
Ringer Solution ◽  
Open Circuit ◽  
Transepithelial Resistance ◽  
Constant Current ◽  
Toad Urinary Bladder ◽  
Current Voltage ◽  
Distal Tubules

Distal tubules of Thamnophis spp. were perfused in vitro with Ringer solution containing either 16 or 150 mM Na and bathed with 150 mM Na Ringer. Current-voltage relationships were obtained by injecting pulses of constant current, Io, into the tubule lumen and recording changes in voltage, delta Vo, at the proximal end of the perfused tubule segment. The Io-Vo plots showed a distinct break at a voltage E1 (approximately 85 mV) that was greater than the open-circuit voltage, VToc, and similar to values of ENa, the transepithelial driving force for Na transport estimated by other methods. The resistance of the shunt pathway, Rs, was estimated from the values of the transepithelial resistance after luminal addition of 10(-5) M amiloride, which caused a rapid fall of the VToc to 0 mV with concurrent increases of the transepithelial resistance. These estimates of Rs were the same as the values of E1/I1 obtained from the Io-Vo plots. The VToc, RT, and Rs were independent of the bath [Na] and were not influenced by the addition of amiloride to the bath. As in frog skin and toad urinary bladder, the ENa and Rs of the snake distal tubule can be estimated from studies of their Io-Vo plots, and the E1 appears to be independent of the transepithelial chemical potential for Na.

Effect of luminal angiotensin II and ANP on early and late cortical distal tubule HCO3- reabsorption

1996 ◽  
Vol 271 (5) ◽  
pp. F977-F984 ◽  
Author(s):  
M. L. Barreto-Chaves ◽  
M. Mello-Aires
Keyword(s):  
Angiotensin Ii ◽  
Exchange Resin ◽  
Distal Tubule ◽  
Ang Ii ◽  
Bafilomycin A1 ◽  
Capillary Perfusion ◽  
At1 Receptors ◽  
Luminal Perfusion

Bicarbonate reabsorption was evaluated by stationary microperfusion “in vivo“ early distal (ED) and late distal (LD) segments of at kidney. Intratubular pH was recorded by double-barreled of H+ exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO3- reabsorption. In the presence of angiotensin II (ANG II) (10(-12) M), a significant increase in HCO3- reabsorption was observed both in ED (from 0.930 +/- 0.060 to 2.64 +/- 0.210 nmol.cm-2.s-1 in luminally perfused tubules and from 0.850 +/- 0.040 to 2.03 +/- 0.210 nmol.cm-2.s-1 during capillary perfusion) and LD segments from 0.310 +/- 0.130 to 2.16 +/- 0.151 nmol.cm-2.s-1 during luminal perfusion and from 0.530 +/- 0.031 to 2.16 +/- 0.211 nmol.cm-2.s-1 with capillary perfusion). The addition of the AT1-receptor antagonist losartan (10(-6) M) to luminal perfusion blocked luminal ANG II-mediated stimulation in ED and LD segments. 5-(N,N-hexamethylene)amiloride (10(-4) M) added to luminal perfusion inhibited luminal ANG II-mediated stimulation in ED (by 81%) and LD (by 54%) segments. The addition of bafilomycin A1 (2 x 10(-7) M) to luminal perfusion does not affect luminal ANG II-mediated stimulation in ED segments but reduces it in LD segments (by 33%). During the addition of atrial natriuretic peptide (ANP) (10(-6) M) or ANG II plus ANP in both segments, no significant differences in HCO3- reabsorption were observed. Our results indicate that luminal ANG II acts to stimulate Na+/H+ exchange in ED and LD segments via activation of AT1 receptors, as well as the vacuolar H(+)-adenosinetriphosphatase in LD segments. ANP does not affect HCO3- reabsorption in either ED or LD segments and does not impair the stimulation caused by ANG II.

Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V1 and V2receptors

2002 ◽  
Vol 282 (2) ◽  
pp. F256-F264 ◽  
Author(s):  
Raif Musa-Aziz ◽  
Maria Luisa Morais Barreto-Chaves ◽  
Margarida De Mello-Aires
Keyword(s):  
Receptor Antagonist ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Distal Tubule ◽  
Ion Exchange Resin ◽  
Capillary Perfusion ◽  
Bicarbonate Reabsorption ◽  
Peritubular Capillaries ◽  
Dose Dependent

10.1152/ajprenal.00056.2001. Peritubular arginine vasopressin (AVP) regulates bicarbonate reabsorption in the cortical distal tubule via V1 and V2 receptors. The dose-dependent effects of peritubular AVP on net bicarbonate reabsorption ( J HCO[Formula: see text] ) were evaluated by stationary microperfusion of in vivo early (ED; distal convoluted tubule) and late distal (LD; connecting tubule and initial collecting duct) segments of rat kidney, using double-barreled H+-sensitive, ion-exchange resin/reference (1 M KCl) microelectrodes. AVP (10−11 M) perfused into peritubular capillaries increased J HCO[Formula: see text] , compared with basal levels during intact capillary perfusion with blood, in ED and LD segments. AVP (10−9 M) also increased J HCO[Formula: see text] in both segments, but the effect of AVP (10−11 M) was significantly higher. A specificV1-receptor antagonist alone or with AVP (10−11 or 10−9 M) reduced J HCO[Formula: see text] below basal levels. A specific V2-receptor antagonist alone or plus AVP (10−11 M) did not affect J HCO[Formula: see text] but increased AVP (10−9 M)-mediated stimulation. 8-Bromoadenosine 3′,5′-cyclic monophosphate alone reduced J HCO[Formula: see text] below basal levels and also reduced AVP (10−11 M)-mediated stimulation. (Deamino-Cys1, d-Arg8) vasopressin (a V2-selective agonist) also reduced J HCO[Formula: see text] below basal levels. These results show that peritubular AVP stimulates J HCO[Formula: see text] in ED and LD segments via basolateral V1 receptors and that basolateral V2 receptors have a dose-dependent inhibitory effect mediated by cAMP. The data also indicate that endogenous AVP stimulates distal J HCO[Formula: see text] via basolateral V1 receptors.

Determination of disequilibrium pH in the rat kidney in vivo: evidence of hydrogen secretion

1981 ◽  
Vol 240 (2) ◽  
pp. F138-F146 ◽  
Author(s):  
T. D. DuBose ◽  
L. R. Pucacco ◽  
N. W. Carter
Keyword(s):  
Carbonic Anhydrase ◽  
Metabolic Alkalosis ◽  
Rat Kidney ◽  
Respiratory Acidosis ◽  
Distal Tubule ◽  
Distal Nephron ◽  
Bicarbonate Reabsorption ◽  
Disequilibrium Ph ◽  
Tubule Fluid

The recent demonstration of elevated PCO2 in structures of the rat renal cortex indicated that previous determinations of disequilibrium pH (pHDq), and thus the differentiation of H+ secretion from bicarbonate reabsorption per se, required further evaluation. A new aspiration pH electrode was developed to allow tubule fluid to achieve chemical equilibrium at the PCO2 prevailing in vivo. In control and bicarbonate-loaded rats a pHDq was not observed in either proximal or distal tubules. After intravenous benzolamide a significant acid pHDq was observed in the proximal (but not the distal) nephron, and increased further during metabolic alkalosis. During combined metabolic alkalosis and respiratory acidosis a significant pHDq was present in the distal but not in the proximal tubule. Aldosterone administration to bicarbonate-loaded, hypercapnic rats did not alter the distal pHDq further. When present, the pHDq in the distal tubule was obliterated by carbonic anhydrase infusion. We conclude that proximal but not distal tubule fluid is in functional contact with carbonic anhydrase; the enzyme is in excess in the proximal lumen and H2CO3 did not accumulate even during conditions associated with increased H+ secretion; the basal rate of H+ secretion in the distal nephron accessible to cortical micropuncture is less than previously assumed. The data support the view that H+ secretion is the major mechanism of renal bicarbonate reabsorption.

scholarly journals Renal potassium transport: the pioneering studies of Gerhard Giebisch

2010 ◽  
Vol 298 (2) ◽  
pp. F233-F234 ◽  
Author(s):  
Bruce A. Stanton
Keyword(s):  
Rat Kidney ◽  
Distal Tubule ◽  
Potassium Transport ◽  
Historical Significance ◽  
Potassium Adaptation ◽  
Micropuncture Study ◽  
On Line ◽  
Potassium Secretion ◽  
Distal Tubules ◽  
Renal Potassium Excretion

This essay looks at the historical significance of six APS Classic Papers that are freely available on line: Malnic G, Klose RM, Giebisch G. Micropuncture study of renal potassium excretion in the rat. Am J Physiol 206: 674–686, 1964 ( http://ajplegacy.physiology.org/cgi/reprint/206/4/674 ). Malnic G, Klose RM, Giebisch G. Micropuncture study of distal tubular potassium and sodium transport in rat nephron. Am J Physiol 211: 529–547, 1966 ( http://ajplegacy.physiology.org/cgi/reprint/211/3/529 ). Malnic G, Klose RM, Giebisch G. Microperfusion study of distal tubular potassium and sodium transfer in rat kidney. Am J Physiol 211: 548–559, 1966 ( http://ajplegacy.physiology.org/cgi/reprint/211/3/548 ). Duarte CG, Chomety F, Giebisch G. Effect of amiloride, ouabain, and furosemide on distal tubular function in the rat. Am J Physiol 221: 632–640, 1971 ( http://ajplegacy.physiology.org/cgi/reprint/221/2/632 ). Malnic G, De Mello Aires M, Giebisch G. Potassium transport across renal distal tubules during acid-base disturbances. Am J Physiol 221: 1192–1208, 1971 ( http://ajplegacy.physiology.org/cgi/reprint/221/4/1192 ). Wright FS, Strieder N, Fowler NB, Giebisch G. Potassium secretion by distal tubule after potassium adaptation. Am J Physiol 221: 437–448, 1971 ( http://ajplegacy.physiology.org/cgi/reprint/221/2/437 ).

Effect of uroguanylin on potassium and bicarbonate transport in rat renal tubules

2006 ◽  
Vol 84 (10) ◽  
pp. 1003-1010 ◽  
Author(s):  
José Benedito Oliveira Amorim ◽  
Raif Musa-Aziz ◽  
Lucilia M.A. Lessa ◽  
Gerhard Malnic ◽  
Manassés Claudino Fonteles
Keyword(s):  
Rat Kidney ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Control Group ◽  
Renal Tubules ◽  
Stationary Concentration ◽  
K Channels ◽  
Series Of Experiments ◽  
Distal Tubules

The effect of uroguanylin (UGN) on K+ and H+ secretion in the renal tubules of the rat kidney was studied using in vivo stationary microperfusion. For the study of K+ secretion, a tubule was punctured to inject a column of FDC-green-colored Ringer's solution with 0.5 mmol KCl/L ± 10−6 mol UGN/L, and oil was used to block fluid flow. K+ activity and transepithelial potential differences (PD) were measured with double microelectrodes (K+ ion-selective resin vs. reference) in the distal tubules of the same nephron. During perfusion, K+ activity rose exponentially, from 0.5 mmol/L to stationary concentration, allowing for the calculation of K+ secretion (JK). JK increased from 0.63 ± 0.06 nmol·cm–2·s–1 in the control group to 0.85 ± 0.06 in the UGN group (p < 0.01). PD was –51.0 ± 5.3 mV in the control group and –50.3 ± 4.98 mV in the UGN group. In the presence of 10−7 mol iberiotoxin/L, the UGN effect was abolished: JK was 0.37 ± 0.038 nmol·cm–2·s–1 in the absence of, and 0.38 ± 0.025 in the presence of, UGN, indicating its action on maxi-K channels. In another series of experiments, renal tubule acidification was studied, using a similar method: proximal and distal tubules were perfused with solutions containing 25 mmol NaHCO3/L. Acidification half-time was increased both in proximal and distal segments and, as a consequence, bicarbonate reabsorption decreased in the presence of UGN (in proximal tubules, from 2.40 ± 0.26 to 1.56 ± 0.21 nmol·cm–2·s–1). When the Na+/H+ exchanger was inhibited by 10−4 mol hexamethylene amiloride (HMA)/L, the control and UGN groups were not significantly different. In the late distal tubule, after HMA, UGN significantly reduced JHCO3–, indicating an effect of UGN on H+-ATPase. These data show that UGN stimulated JK+ by acting on maxi-K channels, and decreased JHCO3– by acting on NHE3 in proximal and H+-ATPase in distal tubules.

Depressed distal tubule acidification corrects chloride-deplete alkalosis in rats

1990 ◽  
Vol 259 (4) ◽  
pp. F636-F644 ◽  
Author(s):  
D. E. Wesson
Keyword(s):  
Linear Regression ◽  
Proximal Tubule ◽  
Metabolic Alkalosis ◽  
Wistar Rats ◽  
Distal Tubule ◽  
Bicarbonate Reabsorption ◽  
Dependent Relationship ◽  
Distal Tubules ◽  
Lower Slope ◽  
Filtered Load

We investigated the relative contributions made by the proximal and distal tubule to the correction of Cl-deplete metabolic alkalosis induced by systemic administration of NaCl. Free-flow micropuncture was used to examine net bicarbonate reabsorption in superficial proximal and distal tubules of anesthetized Munich-Wistar rats during maintenance and correction of chronic furosemide-induced Cl-deplete metabolic alkalosis. The distal tubule of animals with correcting vs. maintained alkalosis had a lower fractional reabsorption of bicarbonate (38 vs. 75%, P less than 0.001) and a lower slope of the linear regression comparing absorption to delivered load (0.48 vs. 0.99, P less than 0.02). By contrast, proximal tubule of animals with correcting vs. maintained alkalosis had fractional reabsorption (85 vs. 90%, P = 0.07) and slopes of the regression comparing reabsorption to filtered load (1.09 vs. 0.98, P = 0.48) that were not different. The data indicate that correction of Cl-deplete metabolic alkalosis induced by NaCl administration involves a qualitative decreased in bicarbonate reabsorption in distal tubule with maintenance of the same load-dependent relationship for bicarbonate reabsorption in proximal tubule.

Urea handling by the distal tubule and collecting duct of the rat during urea–saline, isotonic saline, or urea diuresis

1982 ◽  
Vol 60 (2) ◽  
pp. 128-133 ◽  
Author(s):  
H. Sonnenberg ◽  
D. R. Wilson
Keyword(s):  
Collecting Duct ◽  
Rat Kidney ◽  
Isotonic Saline ◽  
Distal Tubule ◽  
Plasma Urea ◽  
Paired Samples ◽  
Corticomedullary Junction ◽  
Medullary Collecting Duct ◽  
Distal Tubules ◽  
High Concentrations

The aims of the present study were to examine the effects of urea and isotonic saline loads separately and together on urea handling in the medullary collecting duct and surface distal tubules of the rat kidney. Microcatheterization of the medullary collecting duct during isotonic saline diuresis (saline at 5% of body weight per hour, plasma urea 4.3 mM/L), showed an increase in the remaining fraction of filtered urea from 56.2% at the beginning (corticomedullary junction) to 68.5% at the end (papillary tip) of the medullary collecting duct (n = 17 paired samples in six rats, p < 0.05). There was no change in the fraction of filtered urea along the medullary collecting duct during urea diuresis (plasma urea 87 mM/L, n = 15 paired samples in six rats) or during urea–saline diuresis (plasma urea 103 mM/L, n = 32 paired samples in nine rats). Micropuncture of surface distal tubules in the same animals showed an increase in the fraction of filtered urea between end-distal samples and the beginning of the medullary collecting duct from 28.9 to 56.2% during isotonic saline diuresis (p < 0.001), and from 53.6 to 75.3% during urea–saline diuresis (p < 0.01), but no change during urea diuresis (63.6 to 60.0%, p = NS). Our conclusions are as follows. (1) Urea entry into the medullary collecting duct during steady-state diuresis occurs at low intratubular urea concentrations (isotonic saline diuresis) but not at high concentrations (urea–saline diuresis and urea diuresis). (2) Urea entry between the surface distal tubule and the beginning of the medullary collecting duct occurs during saline diuresis (isotonic saline diuresis and urea–saline diuresis) but not urea diuresis. The latter finding suggests that isotonic saline loads affect urea transport differently in juxtamedullary nephrons compared to superficial nephrons.

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