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Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells.

ABSTRACT: Using the perforated patch voltage clamp, we investigated swelling-activated ionic channels (SACs) in rat urinary bladder smooth muscle cells.?Hypo-osmotic (60%) bath solution increased a membrane current which was inhibited by the SAC inhibitor, gadolinium.?The reversal potential of the hypotonicity-induced current shifted in the positive direction by increasing external K(+) concentration.?The hypotonicity-induced current was inhibited by extracellular acidic pH, phorbol ester and forskolin.?These pharmacological properties are identical to those of arachidonic acid-induced current present in these cells, suggesting the presence of TREK-1, a four-transmembrane two pore domain K(+) channel.?Using RT-PCR we screened rat bladder smooth muscles and cerebellum for expression of TREK-1, TREK-2 and TRAAK mRNAs.?Only TREK-1 mRNA was expressed in the bladder, while all three were expressed in the cerebellum.?We conclude that a mechanosensitive K(+) channel is present in rat bladder myocytes, which is activated by arachidonic acid and most likely is TREK-1.?This K(+) channel may have an important role in the regulation of bladder smooth muscle tone during urine storage.

SUBMITTER: Fukasaku M

PROVIDER: S-EPMC5131577 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells.

Fukasaku Mitsuko M Kimura Junko J Yamaguchi Osamu O

Fukushima journal of medical science 20160225 1

Using the perforated patch voltage clamp, we investigated swelling-activated ionic channels (SACs) in rat urinary bladder smooth muscle cells.　Hypo-osmotic (60%) bath solution increased a membrane current which was inhibited by the SAC inhibitor, gadolinium.　The reversal potential of the hypotonicity-induced current shifted in the positive direction by increasing external K(+) concentration.　The hypotonicity-induced current was inhibited by extracellular acidic pH, phorbol ester and forskolin.　T ...[more]

PMID: 26911303

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Project description:Elevation of extracellular Ca(2+) concentration induces intracellular Ca(2+) signaling in parathyroid cells. The response is due to stimulation of the phospholipase C/Ca(2+) pathways, but the direct mechanism responsible for the rise of intracellular Ca(2+) concentration has remained elusive. Here, we describe the electrophysiological property associated with intracellular Ca(2+) signaling in frog parathyroid cells and show that Ca(2+)-activated Cl(-) channels are activated by intracellular Ca(2+) increase through an inositol 1,4,5-trisphophate (IP(3))-independent pathway. High extracellular Ca(2+) induced an outwardly-rectifying conductance in a dose-dependent manner (EC(50) ?6 mM). The conductance was composed of an instantaneous time-independent component and a slowly activating time-dependent component and displayed a deactivating inward tail current. Extracellular Ca(2+)-induced and Ca(2+) dialysis-induced currents reversed at the equilibrium potential of Cl(-) and were inhibited by niflumic acid (a specific blocker of Ca(2+)-activated Cl(-) channel). Gramicidin-perforated whole-cell recording displayed the shift of the reversal potential in extracellular Ca(2+)-induced current, suggesting the change of intracellular Cl(-) concentration in a few minutes. Extracellular Ca(2+)-induced currents displayed a moderate dependency on guanosine triphosphate (GTP). All blockers for phospholipase C, diacylglycerol (DAG) lipase, monoacylglycerol (MAG) lipase and lipoxygenase inhibited extracellular Ca(2+)-induced current. IP(3) dialysis failed to induce conductance increase, but 2-arachidonoylglycerol (2-AG), arachidonic acid and 12S-hydroperoxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12(S)-HPETE) dialysis increased the conductance identical to extracellular Ca(2+)-induced conductance. These results indicate that high extracellular Ca(2+) raises intracellular Ca(2+) concentration through the DAG lipase/lipoxygenase pathway, resulting in the activation of Cl(-) conductance.

Dataset Information

Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells.

Publications

Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells.

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