ADH-PGE2 interactions in cortical collecting tubule. I. Depression of sodium transport

1981 ◽  
Vol 241 (4) ◽  
pp. F452-F460 ◽  
Author(s):  
W. F. Holt ◽  
C. Lechene
Keyword(s):  
Prostaglandin E2 ◽  
Inhibitory Action ◽  
Inhibitory Effect ◽  
Bathing Medium ◽  
Ionic Fluxes ◽  
Collecting Tubule ◽  
Collecting Tubules ◽  
Net Fluxes ◽  
Cortical Collecting Tubule

Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) causes a transitory increase followed by a sustained decrease in the potential difference (PD) and in the net fluxes of sodium and chloride across rabbit cortical collecting tubules perfused in vitro. The inhibitory action of vasopressin is reversible; removal of the hormone from the bath promotes recovery in the PD and in the transport of sodium and chloride to the level of the controls. After 70 min of incubation with ADH, 10(-5) M meclofenamate, an inhibitor of the synthesis of prostaglandins, was added to the bath of some tubules. Despite the presence of ADH, the PD and ionic fluxes increased to control levels. The introduction of exogenous prostaglandin E2 (10(-5) M PGE2) to the bathing medium containing ADH and meclofenamate mimicked the inhibitory action of ADH, decreasing the PD and the reabsorption of sodium and chloride. Pretreatment of collecting tubules with meclofenamate prevented the inhibitory effect of ADH. These findings show that vasopressin exerts a prolonged inhibitory action on PD and on net reabsorption of Na and Cl and that this action may be exerted through stimulating the biosynthesis of prostaglandin E2 by the cortical collecting tubule.

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.

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.

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.

Phosphate transport by isolated rabbit cortical collecting tubule

1980 ◽  
Vol 238 (5) ◽  
pp. F358-F362
Author(s):  
R. A. Peraino ◽  
W. N. Suki
Keyword(s):  
Specific Activity ◽  
Collecting Duct ◽  
Phosphate Transport ◽  
Cortical Collecting Duct ◽  
Renal Handling ◽  
Bathing Medium ◽  
Collecting Tubule ◽  
Absorptive Flux ◽  
Cortical Collecting Tubule

Renal handling of phosphate occurs in the proximal convoluted tubule. Absorption of this anion also occurs in the pars recta and distal convoluted tubule, the latter a structurally and functionally diverse segment. The purpose of the present investigation was to examine phosphate transport by the cortical collecting duct of the rabbit. Segments of cortical collecting tubule, beyond the last cortical branch, were isolated and perfused in vitro with an artificial solution simulating plasma as the perfusing and bathing medium. The perfusion solution contained either 3 or 25 mM bicarbonate. Net phosphate transport was measured using 32P as the radionuclide tracer, with identical specific activity in perfusing and bathing solutions. A net absorptive flux for phosphate was demonstrated, amounting to 2-3% of the delivered load. In addition, this absorptive flux was linearly related to perfusion rate and, thus, delivered load, but independent of the lumen bicarbonate concentration or pH.

Synthesis of prostaglandin E2 in different segments of isolated collecting tubules from adult and neonatal rabbits

1985 ◽  
Vol 248 (1) ◽  
pp. F134-F144 ◽  
Author(s):  
D. Schlondorff ◽  
J. A. Satriano ◽  
G. J. Schwartz
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Feedback Loop ◽  
Pge2 Production ◽  
Large Variability ◽  
Pge2 Synthesis ◽  
Collecting Tubule ◽  
Concentrate Urine ◽  
Collecting Tubules

Prostaglandin E2 (PGE2) inhibits the action of the antidiuretic hormone (ADH) in isolated collecting tubules. A negative feedback loop has been postulated whereby ADH stimulates PGE2 synthesis. Furthermore, lysyl-bradykinin (LBK) inhibits the antidiuretic effect of ADH, probably via PGE2. Enhanced PGE2 synthesis has also been implicated as contributing to the inability to maximally concentrate urine during the neonatal period. We investigated PGE2 synthesis in microdissected cortical (CCT), medullary (MCT), and branched cortical (BCT) collecting tubules from adult and in corticomedullary collecting tubules (CT) from newborn rabbits. Isolated BCT produced significantly less PGE2 (12 +/- 2 pg X mm-1 X 20 min-1) than CCT (65 +/- 9) or MCT (76 +/- 8) from kidneys of adult rabbits. CT from newborn rabbits produced only 19 +/- 3 pg/mm, significantly less than either CCT or MCT from adults. A large variability in basal PGE2 production and hormonal response was observed from tubule to tubule. Under either basal conditions or in the presence of 2 microM arachidonic acid, LBK enhanced PGE2 synthesis in CCT and MCT from adults. ADH enhanced PGE2 production in MCT under basal conditions and in CCT in the presence of arachidonic acid. Neither LBK nor ADH stimulated PGE2 synthesis in neonatal CT. A23187 consistently stimulated PGE2 synthesis in CCT and MCT from adults and, to a lesser extent, in CT from newborn rabbits. Our results support the hypothesis that ADH and LBK enhance PGE2 synthesis in the collecting tubule. This response is, however, subject to large variations from tubule to tubule and depends on the in vitro incubation conditions.

Cell volume regulation of rabbit cortical collecting tubule in anisotonic media

1990 ◽  
Vol 258 (6) ◽  
pp. F1657-F1665 ◽  
Author(s):  
E. Natke
Keyword(s):  
Volume Regulation ◽  
Control Volume ◽  
Cell Volume Regulation ◽  
Volume Regulatory Decrease ◽  
Collecting Tubule ◽  
Collecting Tubules ◽  
Volume Regulatory Increase ◽  
Rabbit Cortical Collecting Tubule ◽  
Cortical Collecting Tubule

Volume regulation of nonperfused rabbit cortical collecting tubules in anisotonic bathing media was examined in vitro. When media osmolality is abruptly increased by 150 mosmol/kgH2O with the addition of NaCl, tubules shrink by 20% but do not volume regulate. However, volume regulatory increase (VRI) is observed when 1 mM butyrate is present in the bathing media or when tubules are pretreated with hypotonic media. When media osmolality is increased, butyrate-treated tubules shrink to 74% of their isotonic control volume. As evidence of volume regulation, butyrate-treated tubules swell while still bathed in hypertonic media, recovering in 30 min 78% of the volume lost due to osmotic shrinkage. The butyrate effect requires external Na+ and is inhibited by amiloride. When media osmolality is lowered to 150 mosmol/kgH2O, nonbutyrate tubules swell before showing typical volume regulatory decrease. When these tubules are returned to isotonic media, they immediately shrink to 78% of control volume before showing evidence of VRI. These results suggest that, under the appropriate conditions, cortical collecting tubules are capable of VRI.

Mechanism of the Antiplatelet Action of Dipyridamole in Whole Blood: Modulation of Adenosine Concentration and Activity

1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Receptor ◽  
Whole Blood ◽  
Blood Cells ◽  
Inhibitory Action ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Adenosine Concentration ◽  
Pharmacological Studies

SummaryDipyridamole inhibits platelet aggregation in whole blood at lower concentrations than in plasma. The blood cells responsible for increased effectiveness in blood are the erythrocytes. Using the impedance aggregometer we have carried out a series of pharmacological studies in vitro to elucidate the mechanism of action of dipyridamole in whole blood. Adenosine deaminase, an enzyme breaking down adenosine, reverses the inhibitory action of dipyridamole. Two different adenosine receptor antagonists, 5’-deoxy-5’-methylthioadenosine and theophylline, also partially neutralize the activity of dipyridamole in blood. Enprofylline, a phosphodiesterase inhibitor with almost no adenosine receptor antagonistic properties, potentiates the inhibition of platelet aggregation by dipyridamole. An inhibitory effect similar to that of dipyridamole can be obtained combining a pure adenosine uptake inhibitor (RE 102 BS) with a pure phosphodiesterase inhibitor (MX-MB 82 or enprofylline). Mixing the blood during preincubation with dipyridamole increases the degree of inhibition. Lowering the haematocrit slightly reduces the effectiveness.Although we did not carry out direct measurements of adenosine levels, the results of our pharmacological studies clearly show that dipyridamole inhibits platelet aggregation in whole blood by blocking the reuptake of adenosine formed from precursors released by red blood cells following microtrauma. Its slight phosphodiesterase inhibitory action potentiates the effects of adenosine on platelets.

Na+-K+-ATPase-dependent sodium flux in cortical collecting tubule

1988 ◽  
Vol 255 (4) ◽  
pp. F605-F613 ◽  
Author(s):  
M. Blot-Chabaud ◽  
F. Jaisser ◽  
M. Gingold ◽  
J. P. Bonvalet ◽  
N. Farman
Keyword(s):  
Special Device ◽  
Instantaneous Rate ◽  
Sodium Flux ◽  
Na Efflux ◽  
Collecting Tubule ◽  
Pump Activity ◽  
Total Capacity ◽  
Collecting Tubules ◽  
Kinetics Of ◽  
Cortical Collecting Tubule

The instantaneous rate of efflux of intracellular Na was studied in rabbit isolated cortical collecting tubules (CCT) as a function of temperature and intracellular Na concentration ([Na]i). [Na]i of microdissected CCT was increased by cold and K-free exposure in the presence of 22Na and the extracellular tracer [3H] sorbitol. [Na]i rose rapidly to 40 mM at 30 min, after which it rose more slowly, reaching 120-140 mM at 6 h. Kinetics of Na efflux were studied after rapid rewarming, using a special device allowing measurements at 20-s intervals. Under control conditions, the total Na load was extruded in less than 8 min, whereas, in the presence of 10(-4) M ouabain, only 50% of the load was extruded during this period of time. Ouabain-sensitive Na efflux was first evident at 13 degrees C and gradually increased between 13 and 35 degrees C. At 37 degrees C, Na+-K+-ATPase-dependent Na efflux was dependent on [Na]i. This efflux gradually increased, from 0.05 to 0.5 peq.nl tubular volume-1.s-1 as a function of [Na]i and reached a plateau at 70 mM [Na]i. It is concluded that [Na]i is a major modulator of the pump activity in CCT; at normal levels of [Na]i, the pump is operating at only a small fraction of its total capacity.

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.

Functional identification of H-K-ATPase in intercalated cells of cortical collecting tubule

1993 ◽  
Vol 264 (2) ◽  
pp. F259-F266 ◽  
Author(s):  
R. B. Silver ◽  
G. Frindt
Keyword(s):  
Cell Types ◽  
Intercalated Cells ◽  
Functional Identification ◽  
Proton Extrusion ◽  
Collecting Tubule ◽  
Initial Ph ◽  
Acid Load ◽  
Extrusion Mechanism ◽  
Collecting Tubules ◽  
Cortical Collecting Tubule

A K-dependent proton extrusion mechanism was investigated by means of fluorescence techniques in rabbit cortical collecting tubules. These experiments were performed in split opened tubules from normal animals exposed to the intracellular pH (pH(i)) indicator 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. This preparation permitted the separate study of the intercalated cells (IC) from the principal cells (PC). In IC pH(i) recovery in response to an acute acid load was observed under Na-free conditions on addition of 5 mM K. This K-dependent recovery of pH(i) in the IC was only partial, but was Sch 28080 inhibitable (10(-5) M) and ouabain insensitive. This suggests the process is mediated by an H-K-adenosinetriphosphatase similar to that of gastric cells. The PC were capable of recovering from the acid load, but this Na-independent response was not blocked by the Sch 28080, suggesting some other mechanism for this result. In both cell types reintroduction of Na into the superfusate resulted in full recovery back to the initial pH(i), presumably the result of Na/H exchange.

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