scholarly journals Activation of Inwardly Rectifying K+ Channel in OK Proximal Tubule Cells Involves cGMP-Dependent Phosphorylation Process.

1998 ◽  
Vol 48 (6) ◽  
pp. 467-476 ◽  
Author(s):  
Manabu KUBOKAWA ◽  
Shigeyuki NAKAYA ◽  
Yoshichika YOSHIOKA ◽  
Kazuyoshi NAKAMURA ◽  
Fumio SATO ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
K Channel ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Inwardly Rectifying

Protein kinase G activates inwardly rectifying K+ channel in cultured human proximal tubule cells

2002 ◽  
Vol 283 (4) ◽  
pp. F784-F791 ◽  
Author(s):  
Kazuyoshi Nakamura ◽  
Junko Hirano ◽  
Shun-Ichi Itazawa ◽  
Manabu Kubokawa
Keyword(s):  
Proximal Tubule ◽  
Specific Inhibitor ◽  
K Channel ◽  
Channel Activity ◽  
Patch Clamp Technique ◽  
Proximal Tubule Cells ◽  
Bath Application ◽  
Tubule Cells ◽  
Inwardly Rectifying ◽  
Human Proximal Tubule

An ATP-regulated inwardly rectifying K+ channel, whose activity is enhanced by PKA, is present in the plasma membrane of cultured human proximal tubule cells. In this study, we investigated the effects of PKG on this K+ channel, using the patch-clamp technique. In cell-attached patches, bath application of a membrane-permeant cGMP analog, 8-bromoguanosine 3′,5′-monophosphate (8-BrcGMP; 100 μM), stimulated channel activity, whereas application of a PKG-specific inhibitor, KT-5823 (1 μM), reduced the activity. Channel activation induced by 8-BrcGMP was observed even in the presence of a PKA-specific inhibitor, KT-5720 (500 nM), which was abolished by KT-5823. Direct effects of cGMP and PKG were examined with inside-out patches in the presence of 1 mM MgATP. Although cytoplasmic cGMP (100 μM) alone had little effect on channel activity, subsequent addition of PKG (500 U/ml) enhanced it. Furthermore, bath application of atrial natriuretic peptide (ANP; 20 nM) in cell-attached patches stimulated channel activity, which was blocked by KT-5823. In conclusion, cGMP/PKG-dependent processes participate in activating the ATP-regulated K+ channel and producing the stimulatory effect of ANP on channel activity.

scholarly journals Involvement of Endogenous Nitric Oxide in the Regulation of K+ Channel Activity in Cultured Human Proximal Tubule Cells

2006 ◽  
Vol 56 (6) ◽  
pp. 407-413 ◽  
Author(s):  
Kazuyoshi Nakamura ◽  
Wataru Habano ◽  
Toshiyuki Kojo ◽  
You Komagiri ◽  
Takahiro Kubota ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Proximal Tubule ◽  
K Channel ◽  
Channel Activity ◽  
Proximal Tubule Cells ◽  
Endogenous Nitric Oxide ◽  
Tubule Cells ◽  
Human Proximal Tubule

Hypotonic shock activates a maxi K+ channel in primary cultured proximal tubule cells

1990 ◽  
Vol 259 (2) ◽  
pp. F348-F356 ◽  
Author(s):  
L. Dube ◽  
L. Parent ◽  
R. Sauve
Keyword(s):  
Proximal Tubule ◽  
Single Channel ◽  
Ionic Channels ◽  
K Channel ◽  
Activation Process ◽  
Proximal Tubule Cells ◽  
Hypotonic Shock ◽  
Calcium Dependent ◽  
Tubule Cells ◽  
And Function

The nature and function of the ionic channels at the apical membrane of primary cultured proximal tubule cells (PT) was investigated by use of the extracellular patch-clamp method. Several types of ionic channels were observed, including a calcium-dependent K+ channel of 206 pS in symmetrical 162 mM KCl activated at depolarizing potentials [maxi K+(Ca2+)]. Whole cell experiments were also carried out that clearly indicated that the PT cells respond to a hypotonic shock by activating electroconductive pathways. This response consisted of an initial hyperpolarization (from -47 to -58 mV, SD = 3, n = 4), followed by a strong depolarization (to -23 mV, SD = 4, n = 4). Furthermore, it was found in cell-attached experiments that the maxi K+(Ca2+) channel becomes activated during the hypotonic challenge. The activation process required external Ca2+, although some residual single-channel activity was measured in the absence of extracellular calcium (n = 3). On the basis of these results, it is concluded that the volume regulation process in PT cells in response to a hypotonic shock involves an influx of calcium from the external medium, which in turn triggers the opening of apical maxi K+(Ca2+) channels.

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