Potassium Transport in the Cortical Collecting Duct

Schlatter, Eberhard

doi:10.1159/000187470

Cited by 9 publications

(3 citation statements)

References 36 publications

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“…Na + ions enter the cell through luminal Na + channels, and Na + ions are then pumped out of the cell via an Na+/K+-ATPase. For K + secretion, K + ions are taken up by the Na+/K+-ATPase and are subsequently secreted into the lumen via ATP-sensitive low-conductance K + channels (Wang, Schwab, and Giebisch, 1990;Frindt and Palmer, 1989;Ling, Hinton, and Eaton, 1991;Schlatter, 1993). A significant K + conductance is present in the basolateral membrane of the CCD.…”

Section: Introductionmentioning

confidence: 99%

Regulation of the hyperpolarization-activated K+ channel in the lateral membrane of the cortical collecting duct.

Wang

1995

The Journal of General Physiology

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An intermediate-conductance K + channel (I.K.), the activity of which is increased by hyperpolarization, was previously identified in the lateral membrane of the cortical collecting duct (CCD) of the rat kidney (Wang, W. H., C. M. McNicholas, A. S. Segal, and G. Giebisch. 1994. American Journal of Physiology. 266:F813-F822). The biophysical properties and regulatory mechanisms of this K + channel have been further investigated with patch clamp techniques in the present study. The slope conductance of the channel in inside-out patches was 50 pS with 140 mM KCI in the pipette and 5 mM KC1, 140 mM NaCI (NaCI Ringer's solution) in the bath. Replacement of the bath solution with symmetrical 140 mM KC1 solution changed the slope conductance of the channel to 85 pS and shifted the reversal potential by 55 mV, indicating that the selectivity ratio of K+/ Na + was at least 10:1. Channel open probability (Po) in inside-out patches was 0.12 at 0 mV and was increased by hyperpolarization. The voltage-dependent Po was fitted with the Boltzmann's equation: Po = 1/[1 + exp(V-V1/i)zF/R~, with z = 1.2 and V1/2 = -40 mV. Addition of 2 mM tetraethylammonium or 500 mM quinidine to the bath blocked the activity of the K + channel in inside-out patches. In addition, decrease in the bath pH from 7.40 to 6.70 reduced Po by 30%. Addition of the catalytic subunit of protein kinase A (PKA~; 20 U/ml) and 100 mM MgATP to the bath increased Po from 0.12 to 0.49 at 0 mV and shifted the voltage dependence curve of channel activity toward more positive potentials by 40 mV. Two exponentials were required to fit both the open-time and the closed-time histograms. Addition of PKA, increased the long open-time constant and shortened the long closed-time constant. In conclusion, PKA-mediated phosphorylation plays an important role in the regulation of the voltage dependence of the hyperpolarization-activated K + channel in the basolateral membrane of CCD.

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Section: Introductionmentioning

confidence: 99%

Regulation of the hyperpolarization-activated K+ channel in the lateral membrane of the cortical collecting duct.

Wang

1995

The Journal of General Physiology

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“…Na enters the cell via amiloride-sensitive apical Na channels due to the electrochemical gradient and is pumped from the cell by basolateral Na/K-ATPase (71). Luminal and basolateral membranes contain K channels involved in K secretion and recycling across the basolateral membrane, respectively (70).…”

Section: Principal Cellsmentioning

confidence: 99%

Role of nitric oxide in the regulation of nephron transport

Ortíz

Garvin

2002

American Journal of Physiology-Renal Physiology

234

195

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Nitric oxide (NO) plays an important role in various physiological processes in the kidney. In vivo experiments first suggested that the natriuretic and diuretic effects caused by NO may be due to decreased NaCl and fluid absorption by the nephron. In the last 10 years, several reports have directly demonstrated a role for NO in modulating transport in different tubule segments. The effects of NO on proximal tubule transport are still controversial. Both stimulation and inhibition of net fluid and bicarbonate have been reported in this segment, whereas only inhibitory effects of NO have been found in Na/H exchanger and Na/K-ATPase activity. The effects of NO in the thick ascending limb are more homogeneous than in the proximal tubule. In this segment, NO decreases net Cl and bicarbonate absorption. A direct inhibitory effect of NO on the Na-K-2Cl cotransporter and the Na/H exchanger has been reported, while NO was found to stimulate apical K channels in this segment. In the collecting duct, NO inhibits Na absorption and vasopressin-stimulated osmotic water permeability. An inhibitory effect of NO on H-ATPase has also been reported in intercalated cells of the collecting duct. Overall, the reported effects of NO in the different nephron segments mostly agree with the natriuretic and diuretic effects observed in vivo. However, the net effect of NO on transport is still controversial in some segments, and in cases like the distal tubule, it has not been studied.

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“…In particular, adenosine-5'-triphosphate-sensitive potassium (K-ATP) channels have been intensely investigated because of their wide distribution, key role in linking cellular metabolism to membrane potential, and therapeutic potential of K-ATP modulators (4,14,36,95). Many other reports have further described how K-ATP channels help to control insulin secretion (3,24,96), vascular smooth muscle tone (31,94,109), myocardial contractility and preconditioning (5,32,37,64), and renal tubular function (46,93,104,118). Common to these many in depth investigations has been an armamentarium of specific channel modulators, such as the K-ATP openers pinacidil, minoxidil sulfate, and cromakalim, and the K-ATP channel blockers glyburide (glibenclamide) and sodium 5-hydroxydecanoate (Fig.…”

Section: Introductionmentioning

confidence: 99%

Pharmacology of the K‐ATP Channel Blocking Morpholinoguanidine PNU‐37883A

Humphrey

1999

Cardiovascular Drug Reviews

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Potassium Transport in the Cortical Collecting Duct

Cited by 9 publications

References 36 publications

Regulation of the hyperpolarization-activated K+ channel in the lateral membrane of the cortical collecting duct.

Regulation of the hyperpolarization-activated K+ channel in the lateral membrane of the cortical collecting duct.

Role of nitric oxide in the regulation of nephron transport

Pharmacology of the K‐ATP Channel Blocking Morpholinoguanidine PNU‐37883A

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