Control of bicarbonate transport in collecting tubules from normal and remnant kidneys

1989 ◽  
Vol 256 (4) ◽  
pp. F680-F687 ◽  
Author(s):  
L. L. Hamm ◽  
K. S. Hering-Smith ◽  
V. M. Vehaskari
Keyword(s):  
Renal Mass ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Bicarbonate Secretion ◽  
Bicarbonate Reabsorption ◽  
Collecting Tubule ◽  
Collecting Tubules ◽  
Acid Loading

Bicarbonate transport in the rabbit cortical collecting tubule (CCT) and outer medullary collecting tubule (MCT) in vitro was studied under two types of conditions that were anticipated to alter distal tubule bicarbonate transport: 1) reduction of renal mass, and 2) acid and base loading in vivo. Bicarbonate secretion (both total and acetazolamide sensitive) and bicarbonate reabsorption (studied separately) in CCT and bicarbonate reabsorption in the MCT were not different between tubules from normal and remnant kidneys. The control or conditioning of the separate processes of bicarbonate secretion and bicarbonate reabsorption was also studied in CCT from normal and remnant kidneys. Bicarbonate secretion was not increased by base-loading animals with either normal or remnant kidneys. In contrast, bicarbonate secretion was consistently decreased by acid loading (studied in CCT from remnant kidneys). Bicarbonate reabsorption in the CCT was not altered by acid or base loads given to animals with normal kidneys. And bicarbonate reabsorption in MCT was not increased by acid loading of animals with remnant kidneys. These studies demonstrate that bicarbonate transport (and its conditioning by acid or base loads in vivo) in both CCT and MCT in vitro is not altered by reduction of renal mass in rabbits. The predominant conditioning effect of acid or base loads in vivo is for acid loads to inhibit CCT bicarbonate secretion.

Bicarbonate transport in cortical and outer medullary collecting tubules

1983 ◽  
Vol 244 (3) ◽  
pp. F289-F296 ◽  
Author(s):  
W. E. Lombard ◽  
J. P. Kokko ◽  
H. R. Jacobson
Keyword(s):  
Collecting Duct ◽  
Bicarbonate Transport ◽  
Duct System ◽  
Segmental Analysis ◽  
Bicarbonate Reabsorption ◽  
Positive Voltage ◽  
Collecting Ducts ◽  
Collecting Tubule ◽  
Collecting Tubules

The collecting ducts are thought to represent a low-capacity high-gradient acidification system. However, the inaccessibility of the various regions of the collecting duct system has prevented direct segmental analysis of its contribution to distal acidification. The present in vitro microperfusion studies compare bicarbonate transport (in pmol . mm-1 . min-1) in rabbit cortical (CCT) and outer medullary collecting tubules (MCT) perfused and bathed with symmetrical Ringer bicarbonate solution at pH 7.4. Cortical segments from normal animals exhibited no net bicarbonate transport (-2.15 +/- 1.93) whereas MCT from normal animals reabsorbed bicarbonate at a rate of 11.3 +/- 1.4. Both bicarbonate reabsorption and the lumen-positive voltage (+9.4 +/- 1.1 mV) in MCT were totally inhibited by 10(-4) M acetazolamide. CCT from NH4Cl-treated rabbits demonstrated significant bicarbonate reabsorption (1.8 +/- 0.7) when perfused at slow rates. CCT harvested from animals given a NaHCO3 load for 48 h prior to death secreted bicarbonate (-6.2 +/- 2.5). These studies confirm earlier observations of the ability of the CCT to reabsorb or secrete bicarbonate. In addition, they demonstrate significant axial heterogeneity in acidification in the collecting duct system and identify the outer medullary collecting tubule from inner stripe of outer medulla as a segment of major capacity.

Bicarbonate transport by amphibian nephron

1986 ◽  
Vol 251 (5) ◽  
pp. F865-F872 ◽  
Author(s):  
C. B. Yucha ◽  
L. C. Stoner
Keyword(s):  
Distal Tubule ◽  
The Other ◽  
Bicarbonate Transport ◽  
Free Solution ◽  
Diluting Segment ◽  
Chemical Gradients ◽  
Bicarbonate Reabsorption ◽  
Nephron Segment ◽  
Collecting Tubules

To determine the site of bicarbonate reabsorption, tubular fragments from five different segments of the salamander nephron (Ambystoma) were perfused in vitro. Bicarbonate contents (total CO2) of tubular fluid were determined by microcalorimetry. Bicarbonate was not transported by the diluting segment or the mid-distal tubule. Although proximal tubule fragments did appear to reabsorb bicarbonate (10.8 +/- 3.7 pmol X mm-1 X min-1, P less than 0.01, n = 14), the chemical gradients observed were small with respect to the sensitivity of our methods. In the late distal tubule (LDT), bicarbonate reabsorption averaged 28.9 +/- 8.2 pmol X mm-1 X min-1 (P less than 0.01, n = 16). Transport in this segment was inhibited by ethoxzolamide or by perfusing with a sodium-free solution. Ethoxzolamide had no effect on the trans-epithelial voltage. Thus bicarbonate is reabsorbed by the LDT of amphibia via a mechanism that is dependent on carbonic anhydrase and the presence of luminal sodium. The 13 initial collecting tubules (ICT) studied did not appear to reabsorb bicarbonate. On the other hand, some ICT developed substantial bicarbonate gradients. Therefore this nephron segment has the capacity to reabsorb bicarbonate.

Collecting tubule adaptation to respiratory acidosis induced in vivo

1990 ◽  
Vol 258 (1) ◽  
pp. F15-F20 ◽  
Author(s):  
M. E. Laski ◽  
N. A. Kurtzman
Keyword(s):  
Respiratory Acidosis ◽  
In Vitro Study ◽  
Co2 Flux ◽  
Urine Ph ◽  
Collecting Tubule ◽  
Bicarbonate Solutions ◽  
Animal Exposure ◽  
Collecting Tubules

To examine the effects of respiratory acidosis in vivo on the adaptation of acidification in the collecting tubule, New Zealand White rabbits were exposed to a 6.7% CO2-93.3% O2 gas mixture in an environmental chamber for 0, 6, 24, or 48 h before obtaining collecting tubules for in vitro study. These collecting tubules were then perfused and bathed in vitro in identical Krebs-Ringer bicarbonate solutions. After 1 h equilibration total CO2 flux (JtCO2) was measured. The urine pH of the rabbits fell, whereas the blood bicarbonate rose as CO2 exposure time increased. In cortical collecting tubules, JtCO2 in vitro correlated with length of animal exposure to hypercarbia (y = 1.14174 + 0.1437x, r = 0.57, P = 0.002), and with the blood bicarbonate of the animal (y = 26.8471 + 0.0858x, r = 0.59, P less than 0.05). In vitro JtCO2 in medullary collecting tubules from rabbits that had been in hypercarbic atmosphere for 48 h (23.2 +/- 4.9 pmol.mm-1.min-1) did not differ from JtCO2 in control tubules (25.0 +/- 3.2 pmol.mm-1.min-1, not significant). Thus the cortical collecting tubule exhibits an adaptive increase in JtCO2 in response to hypercarbia, whereas the medullary collecting tubule does not.

Short-term effect of aldosterone on NEM-sensitive ATPase in rat collecting tubule

1989 ◽  
Vol 257 (2) ◽  
pp. F177-F181 ◽  
Author(s):  
C. Khadouri ◽  
S. Marsy ◽  
C. Barlet-Bas ◽  
A. Doucet
Keyword(s):  
Atpase Activity ◽  
Affinity Constant ◽  
Short Term ◽  
Collecting Tubule ◽  
Lag Period ◽  
In Vitro Effects ◽  
Collecting Tubules

Because previous studies indicated that in the collecting tubule, N-ethylmaleimide (NEM)-sensitive ATPase, the biochemical equivalent of the proton pump, is controlled by mineralocorticoids in the long term, the present study was designed to investigate whether such control also exists in the short term. Therefore we investigated the in vivo and in vitro effects of aldosterone on the enzyme activity in cortical and outer medullary collecting tubules (CCT and MCT, respectively) from adrenalectomized rats. Administration of aldosterone (10 micrograms/kg body wt) markedly stimulated NEM-sensitive ATPase activity in the CCT and MCT within 3 h. Similarly, incubating CCT or MCT for 3 h in the presence of 10(-8) M aldosterone enhanced NEM-sensitive ATPase activity up to values similar to those previously measured in the corresponding nephron segments of normal rats. In vitro stimulation of NEM-sensitive ATPase was dose dependent in regard to aldosterone (apparent affinity constant approximately 10(-9) M), appeared after a 30-min lag period, and reached its maximum after 2-2.5 h. Finally, actinomycin D and cycloheximide totally abolished the in vitro action of aldosterone, demonstrating the involvement of protein synthesis in this process.

Direct Na+-K+ pump stimulation by K+ in cortical collecting tubules: a mechanism for early renal K+ adaptation

1989 ◽  
Vol 257 (4) ◽  
pp. F595-F601 ◽  
Author(s):  
Y. Fujii ◽  
A. I. Katz
Keyword(s):  
Turnover Rate ◽  
Rapid Rise ◽  
Hormonal Factors ◽  
Collecting Tubule ◽  
Collecting Tubules ◽  
Stimulation Of ◽  
External K ◽  
Cortical Collecting Tubule

To evaluate the mechanism of increased Na+-K+ pump turnover rate that characterizes the early cortical collecting tubule (CCT) response to K+ loading [Y. Fujii, S. K. Mujais, and A. I. Katz. Am. J. Physiol. 256 (Renal Fluid Electrolyte Physiol. 25): F279-F284, 1989.], we measured ouabain-sensitive 86Rb+ uptake in microdissected rat CCT exposed acutely to elevated ambient K+ in vivo and in vitro. Tubules preincubated in 10 mM K+ had higher 86Rb+ uptake than when preincubated in 5 mM K+ (25.9 +/- 1.2 vs. 18.9 +/- 0.7 pmol.mm-1.min-1, P less than 0.001). KCl infusion (5 mumol.100 g-1.min-1 x 60 min) increased 86Rb+ uptake from 19.2 +/- 1.0 to 31.2 +/- 1.4 pmol.mm-1.min-1, P less than 0.001; the increment was preserved in tubules subsequently treated with monensin or nystatin in vitro, suggesting that pump stimulation was not mediated by increased cell Na+. This conclusion was confirmed in separate experiments in which the effect of K+ on 86Rb+ uptake was not altered by concurrent preincubation with amiloride. Studies with CCT from isolated perfused kidneys and from adrenalectomized animals revealed that stimulation of 86Rb+ uptake by a K+ load occurs rapidly (less than or equal to 5 min) and is independent of hormonal factors. Increased external K+ produces a rapid rise in K+-transporting capacity (turnover rate) of the Na+-K+ pump in CCT. This phenomenon probably represents a direct effect on K+ on the pump and is an important component of the early renal response to increased K+ secretory load.

scholarly journals Uroguanylin inhibits H-ATPase activity and surface expression in renal distal tubules by a PKG-dependent pathway

2014 ◽  
Vol 307 (6) ◽  
pp. C532-C541 ◽  
Author(s):  
Vanessa da Silva Lima ◽  
Renato O. Crajoinas ◽  
Luciene R. Carraro-Lacroix ◽  
Alana N. Godinho ◽  
João L. G. Dias ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Distal Tubule ◽  
Surface Expression ◽  
Inhibitory Effect ◽  
Camp Content ◽  
Bicarbonate Reabsorption ◽  
Guanylate Cyclase C ◽  
Dependent Pathway

Cumulative evidence suggests that guanylin peptides play an important role on electrolyte homeostasis. We have previously reported that uroguanylin (UGN) inhibits bicarbonate reabsorption in a renal distal tubule. In the present study, we tested the hypothesis that the bicarbonaturic effect of UGN is at least in part attributable to inhibition of H+-ATPase-mediated hydrogen secretion in the distal nephron. By in vivo stationary microperfusion experiments, we were able to show that UGN inhibits H+-ATPase activity by a PKG-dependent pathway because KT5823 (PKG inhibitor) abolished the UGN effect on distal bicarbonate reabsorption and H89 (PKA inhibitor) was unable to prevent it. The in vivo results were confirmed by the in vitro experiments, where we used fluorescence microscopy to measure intracellular pH (pHi) recovery after an acid pulse with NH4Cl. By this technique, we observed that UGN and 8 bromoguanosine-cGMP (8Br-cGMP) inhibited H+-ATPase-dependent pHi recovery and that the UGN inhibitory effect was abolished in the presence of the PKG inhibitor. In addition, by using RT-PCR technique, we verified that Madin-Darby canine kidney (MDCK)-C11 cells express guanylate cyclase-C. Besides, UGN stimulated an increase of both cGMP content and PKG activity but was unable to increase the production of cellular cAMP content and PKA activity. Furthermore, we found that UGN reduced cell surface abundance of H+-ATPase B1 subunit in MDCK-C11 and that this effect was abolished by the PKG inhibitor. Taken together, our data suggest that UGN inhibits H+-ATPase activity and surface expression in renal distal cells by a cGMP/PKG-dependent pathway.

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 bicarbonate reabsorption during rebound metabolic alkalosis

1991 ◽  
Vol 69 (11) ◽  
pp. 1784-1788 ◽  
Author(s):  
David H. Vandorpe ◽  
Steven P. Nadler ◽  
David Z. Levine
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Bicarbonate Concentration ◽  
Plasma Bicarbonate ◽  
Bicarbonate Reabsorption ◽  
Collecting Ducts ◽  
Persistent Elevation

Rebound metabolic alkalosis is a transient alkalemia that is seen during recovery from NH4Cl-induced metabolic acidosis. The persistent elevation of plasma bicarbonate concentration is the result of continuing excretion of net acid by the kidney. Bicarbonate transport by inner medullary collecting ducts has been reported by others to proceed normally (i.e., bicarbonate reabsorption continues in this segment) during rebound metabolic alkalosis. No other segmental responses have been evaluated. Since the surface distal tubule of the rat is known to both reabsorb and secrete bicarbonate in vivo, it was of interest to determine the response of this segment. Our results show that the distal tubule microperfused in vivo during rebound metabolic alkalosis continues to reabsorb significant amounts of bicarbonate, despite the presence of systemic alkalemia that we have previously shown to be associated with distal tubule bicarbonate secretion.Key words: rebound metabolic alkalosis, distal tubule, micropuncture, bicarbonate reabsorption.

Biochemical and functional characterization of H(+)-K(+)-ATPase in distal amphibian nephron

1991 ◽  
Vol 260 (6) ◽  
pp. F806-F812
Author(s):  
G. Planelles ◽  
T. Anagnostopoulos ◽  
L. Cheval ◽  
A. Doucet
Keyword(s):  
Functional Characterization ◽  
Distal Tubule ◽  
Significant Rise ◽  
Proton Secretion ◽  
High Affinity ◽  
Collecting Tubule ◽  
Collecting Tubules ◽  
In Vivo Administration

Because proton secretion and K+ reabsorption in the late distal tubule of amphibians are active, we evaluated whether these processes could be mediated by an H(+)-K(+)-ATPase similar to the gastric H(+)-K+ pump and to the K(+)-ATPase previously described in the terminal segments of the mammalian nephron. K(+)-stimulated ATPase activity was detected in microdissected segments of frog and Necturus nephron: its activity was high in the late distal and collecting tubules, whereas it was undetectable in the proximal convoluted tubule and early distal tubule. In frog collecting tubule, K(+)-ATPase had a high affinity for K+ (Km approximately 0.30 mM), was inhibited by vanadate, omeprazole, and the imidazopyridine Sch 28080, and was insensitive to ouabain. Furthermore, in vivo administration of Sch 28080 to anesthetized Necturus induced a significant rise of the steadystate intratubular pH in the late distal tubule, demonstrating that this drug inhibited tubular fluid acidification. It is suggested that K(+)-ATPase present in the terminal segments of amphibian nephron is similar to the gastric H(+)-K+ pump and is involved in urinary acidification.

Short-term effect of aldosterone on vasopressin-sensitive adenylate cyclase in rat collecting tubule

1993 ◽  
Vol 264 (5) ◽  
pp. F821-F826 ◽  
Author(s):  
G. el Mernissi ◽  
C. Barlet-Bas ◽  
C. Khadouri ◽  
L. Cheval ◽  
S. Marsy ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Affinity Constant ◽  
Short Term ◽  
Collecting Tubule ◽  
Lag Period ◽  
In Vitro Effects ◽  
Collecting Tubules ◽  
Adrenalectomized Rats

Because previous studies indicated that, in the rat collecting tubule, vasopressin (AVP)-sensitive adenylate cyclase (AC) is controlled by mineralocorticoids in the long term, the present study was designed to investigate whether such a control also exists in the short term. Therefore, we investigated the in vivo and in vitro effects of aldosterone on AC activity in cortical and outer medullary collecting tubules (CCD and OMCD, respectively) from adrenalectomized rats. Injection of aldosterone (10 micrograms/kg body wt) to adrenalectomized rats restored within 3 h AVP-sensitive AC activity in the CCD and OMCD up to the levels observed in the corresponding segments of adrenal intact rats. Similarly, incubating CCD or OMCD from adrenalectomized rats for 2.5 h in the presence of 10(-8) M aldosterone enhanced AVP-sensitive AC activity up to values similar to those found in normal rats. In vitro stimulation of AVP-sensitive AC activity was dose dependent with regard to aldosterone [apparent affinity constant (K0.5) approximately 10(-9) M], appeared after a 30-min lag period, and reached its maximum after 2-2.5 h. In addition, it was totally abolished by the antimineralocorticoid spironolactone, whereas the specific glucocorticoid antagonist RU 38486 had no effect. Finally, actinomycin D and cycloheximide totally abolished the in vitro action of aldosterone, demonstrating the involvement of protein synthesis in that process.

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