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.

Stimulation of chloride transport by HCO3-CO2 in rabbit cortical collecting tubule

1986 ◽  
Vol 251 (1) ◽  
pp. F49-F56 ◽  
Author(s):  
K. Tago ◽  
V. L. Schuster ◽  
J. B. Stokes
Keyword(s):  
Chloride Transport ◽  
Acid Base ◽  
Cl Transport ◽  
Collecting Tubule ◽  
Acid Base Status ◽  
Stimulation Of ◽  
Rabbit Cortical Collecting Tubule ◽  
Cortical Collecting Tubule

We examined both the role of HCO3-CO2 in Cl transport as well as the effect of in vivo acid-base status on Cl transport by the rabbit cortical collecting tubule. The lumen-to-bath 36Cl tracer flux, expressed as the rate coefficient KCl, was measured in either HEPES-buffered (CO2-free) or HCO3-CO2-containing solutions. Amiloride was added to the perfusate to minimize the transepithelial voltage and thus the electrical driving force for Cl diffusion. Because KCl fell spontaneously with time in HCO3-CO2 solutions in the absence but not the presence of cAMP, we used cAMP throughout to avoid time-dependent changes. Acute in vitro removal of bath HCO3-CO2 reduced KCl. Acetazolamide addition in HEPES-buffered solutions also lowered KCl; KCl could be restored to control values by adding exogenous HCO3-CO2 in the presence of acetazolamide. In vivo acid-base effects on Cl transport were determined by dissecting tubules from either NaHCO3-loaded or NH4Cl-loaded rabbits. Tubules from HCO3-loaded rabbits had higher rates of Cl self exchange. Acute in vitro addition of bath HCO3-CO2 increased KCl and did so to a greater degree in tubules from HCO3-loaded rabbits. Most of this effect of HCO3-CO2 addition on KCl could not be accounted for by Cl-HCO3 exchange; rather, it appeared due to stimulation of Cl self exchange. The data are consistent with 36Cl transport occurring via Cl-HCO3 exchange as well as Cl self exchange. Both processes are acutely stimulated by HCO3 and/or Co2, and both are chronically regulated by in vivo acid-base status.

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.

Effects of AVP and dDAVP on PGE2 synthesis in superfused cortical collecting tubules

1989 ◽  
Vol 256 (6) ◽  
pp. F1044-F1050 ◽  
Author(s):  
F. Jaisser ◽  
L. Bugeon ◽  
M. Blot-Chabaud ◽  
J. P. Bonvalet ◽  
N. Farman
Keyword(s):  
Arginine Vasopressin ◽  
Dose Range ◽  
Maximal Effect ◽  
Pge2 Synthesis ◽  
Collecting Tubule ◽  
V2 Receptor ◽  
Collecting Tubules ◽  
Dose Dependent ◽  
Stimulation Of ◽  
Cortical Collecting Tubule

Whereas interactions between antidiuretic hormone (ADH) and prostaglandins (PGs) have been reported in the cortical collecting tubule (CCD), the precise effects of arginine vasopressin (AVP) and its analogue, 1-desamino-8-D-arginine vasopressin (dDAVP) on PGE2 synthesis remain controversial. We examined the dynamic response of PGE2 synthesis to these two analogues in isolated rabbit CCD. Microdissected CCD were superfused, and basal and hormone-induced PGE2 synthesis were determined by enzyme immunoassay. Addition of arachidonic acid (AA) steeply increased basal PGE2 synthesis, in the 0-1 microM-dose range. The presence of AA was necessary to obtain a stimulatory effect of AVP on PGE2 synthesis. AVP induced an immediate, transitory, and dose-dependent stimulation of PGE2 synthesis. A maximal effect was obtained at 10(-8) M; PGE2 synthesis was increased by approximately 150-200% over the basal synthesis. With dDAVP, a very weak response was obtained only at 10(-7) M. From these results, we conclude that PGE2 synthesis in CCD is stimulated by ADH. This effect of ADH does not depend on the V2-receptor pathway and suggests the presence of V1-receptors in CCD.

Cellular heterogeneity of uridine incorporation in collecting tubules: effect of DOCA

1985 ◽  
Vol 248 (4) ◽  
pp. F552-F564
Author(s):  
A. Vandewalle ◽  
F. Cluzeaud ◽  
M. Chavance ◽  
J. P. Bonvalet
Keyword(s):  
Rna Synthesis ◽  
Cellular Heterogeneity ◽  
Nuclear Surface ◽  
Intercalated Cells ◽  
Uridine Incorporation ◽  
Collecting Tubules ◽  
Silver Grains ◽  
Stimulation Of

In previous studies we showed that in vitro uridine incorporation along the renal tubule is heterogeneous and that DOCA induces a stimulation of RNA synthesis in distal cortical and medullary structures. The present work examines by autoradiography of isolated tubules and renal tissue sections the cellular heterogeneity of the connecting (CNT) and cortical collecting (CCT) tubules after in vivo injection of [3H]uridine in normal and DOCA-treated rabbits. Data confirmed the profile of uridine incorporation along the tubule, which was found in in vitro experiments, and the DOCA-induced stimulation of RNA synthesis. In microdissected CNT and CCT of control kidneys, statistical analysis of the distribution of labeling revealed the presence of two distinct cell populations: one with low labeling (2-3 silver grains per nucleus) and one with high labeling (10-13), which represent 64 and 36%, respectively (CNT), and 74 and 26%, respectively (CCT), of the whole population. Histological data showed that the respective proportions of intercalated cells (29% in CNT; 21% in CCT) and connecting tubule cells (65%) or principal cells (79%) are close to those of the populations with high or low labeling. In addition, autoradiographs on renal sections directly demonstrated that the labeling of intercalated cells (19.3 silver grains/100 micron2 nuclear surface in CNT; 14.7 in CCT) was three times higher than that of connecting (6.6) or principal (5.8) cells. In isolated CNT and CCT, DOCA induced similar absolute increases in the labeling of the two populations. However, the relative increase was more than two times higher in the population with low labeling (+131% in CNT, +210% in CCT) than in the one with high labeling (+71% and +98%). We conclude that cell population of the collecting cortical tubule (CNT and CCT) is heterogeneous with regard to uridine incorporation, reflecting RNA synthesis.

ADH-PGE2 interactions in cortical collecting tubule. II. inhibition of Ca and P reabsorption

1981 ◽  
Vol 241 (4) ◽  
pp. F461-F467 ◽  
Author(s):  
W. F. Holt ◽  
C. Lechene
Keyword(s):  
Prostaglandin E2 ◽  
Arginine Vasopressin ◽  
Inhibitory Action ◽  
Prolonged Incubation ◽  
Collecting Tubule ◽  
Calcium And Phosphorus ◽  
Collecting Tubules ◽  
Endogenous Synthesis ◽  
Cortical Collecting Tubule

In the absence of ADH, microperfused cortical collecting tubules of rabbits reabsorb calcium and phosphorus. Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) inhibits the reabsorption and may promote the secretion of calcium and phosphorus. At 5 min after incubation with ADH, there was a transitory increase in the potential difference and the reabsorption of sodium. The fluxes of calcium and phosphorus, however, showed no significant change from the control values. At 30-50 min after treatment with ADH, the reabsorption of calcium and phosphorus was inhibited and in some tubules calcium and phosphorus were secreted. The removal of vasopressin from the bath or the addition of 10(-5) M meclofenamate in vitro prevented ADH from inhibiting the reabsorption of calcium and phosphorus. Treatment of tubules with 10(-5) M prostaglandin E2 (PGE2) subsequent to incubation in a medium containing ADH and meclofenamate inhibited the reabsorption or even promoted the secretin of calcium and phosphorus, as did the prolonged incubation with ADH alone. We conclude that cortical collecting tubules reabsorb calcium and phosphorus in the absence of vasopressin and that ADH inhibits calcium and phosphorus reabsorption. Endogenous synthesis of PGE2 may mediate the inhibitory action of ADH, since meclofenamate (an inhibitor of the synthesis of prostaglandins) opposes and exogenous PGE2 mimics ADH.

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.

Evidence suggesting that cadmium induces a non-thyroidal illness syndrome in the rat

1997 ◽  
Vol 154 (1) ◽  
pp. 113-117 ◽  
Author(s):  
M A Pavia ◽  
B Paier ◽  
M I Noli ◽  
K Hagmüller ◽  
A A Zaninovich
Keyword(s):  
Body Weight ◽  
Wistar Rats ◽  
Turnover Rate ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Normal Response ◽  
Stimulation Of ◽  
Fractional Turnover

Abstract The effect of in vivo administration of cadmium chloride on the pituitary-thyroidal axis was assessed in 200 g body weight Wistar rats. A dose of 2·5 mg/kg body weight was injected i.v. 24 h before the experiments were initiated. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations in cadmium-treated rats were significantly (P<0·01) decreased, whereas plasma TSH failed to increase in response to low T4 and T3. However, the TSH response to TRH and the pituitary content of TSH in these rats were both normal. Cadmium induced a significant (P<0·01) decrease in 4-h thyroidal 131I uptake and in thyroid/plasma radioactivity ratio. The in vitro conversion of T4 to T3 in the pituitary was significantly (P<0·01) blocked by cadmium whereas there was no in vivo effect. Parameters of peripheral T4 kinetics in cadmium-treated rats, such as metabolic clearance rate (P<0·01), fractional turnover rate (P<0·01), absolute disposal rate (P<0·05), urinary clearance (P<0·05) and faecal clearance (P<0·05), were all decreased by cadmium. The lack of response of TSH to low plasma T4 and T3 and the normal response to exogenous TRH in this and in other non-thyroidal illness syndromes produced by other pathologies suggest a decreased stimulation of pituitary thyrotrophs by endogenous TRH. Journal of Endocrinology (1997) 154, 113–117

NH4Cl inhibition of transport in the rabbit cortical collecting tubule

1985 ◽  
Vol 248 (5) ◽  
pp. F631-F637 ◽  
Author(s):  
L. L. Hamm ◽  
C. Gillespie ◽  
S. Klahr
Keyword(s):  
Cation Transport ◽  
Sodium Reabsorption ◽  
Bathing Solution ◽  
Collecting Tubule ◽  
Potassium Secretion ◽  
Transepithelial Voltage ◽  
Rabbit Cortical Collecting Tubule ◽  
Cortical Collecting Tubule

Ammonium has previously been found to inhibit transport in a number of tissues. The present experiments were designed to evaluate the effect of ammonium chloride on transepithelial voltage (VTE) and cation transport in the isolated rabbit cortical collecting tubule perfused in vitro. Peritubular NH4Cl (2-10 mM) inhibited VTE in these tubules independent of bath or lumen pH. Luminal NH4Cl had a similar effect. However, VTE did not change with bath NH4Cl in tubules treated with amiloride or ouabain. Furthermore, when bath PCO2 was lowered simultaneously with the addition of NH4Cl to the bath, little change in VTE occurred, raising the possibility that intracellular pH falls after addition of NH4Cl to the bath. Consistent with the voltage effects, 5 mM NH4Cl in the bathing solution inhibited net sodium reabsorption by 36% and potassium secretion by 44%. Unidirectional lumen-to-bath tracer fluxes were consistent with predominant inhibition of the sodium reabsorptive flux and the potassium secretory flux. These findings may have relevance to metabolic acidosis in vivo because ionic ammonium concentrations attain the levels used in this study.

Na+ transport properties of the peritubular membrane of cortical collecting tubule

1982 ◽  
Vol 242 (6) ◽  
pp. F664-F671 ◽  
Author(s):  
E. Natke ◽  
L. C. Stoner
Keyword(s):  
Efflux Rate ◽  
Bathing Medium ◽  
Sodium Efflux ◽  
Collecting Tubule ◽  
Potassium Influx ◽  
Collecting Tubules ◽  
Low K ◽  
Sodium And Potassium ◽  
Cortical Collecting Tubule

The effects of varying endogenous aldosterone levels on the passive and active properties of the peritubular membrane were studied. Rabbits that were fed either a low Na+ (normal K+) diet or a high Na+, low K+ diet increased or decreased plasma aldosterone, respectively. Tubules were dissected, filled with oil, and incubated in 0 K+ medium to increase intracellular sodium. Cellular sodium and potassium content was measured by helium-glow photometry. The degree to which cells accumulate sodium and lose potassium is a function not only of time of exposure but also of diet. Tubules from animals on a low Na+ diet are about 6 times more permeable to sodium than those from animals fed a high Na+ diet. When tubules were loaded with sodium and returned to a normal (5 mM K+) bathing medium, net sodium efflux and potassium influx occurred. The rate of sodium efflux by cortical collecting tubules dissected from animals on the low Na+ diet was 2.3 times greater than the efflux rate of tubules from animals on the high Na+ diet. These data suggest that high levels of endogenous aldosterone enhance sodium transport measured in vitro across the peritubular membrane of cortical collecting tubule.

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