Nucleotide regulation of ATP sensitive potassium channels

Terzic, André; Tung, Robert; Kurachi, Yoshihisa

doi:10.1093/cvr/28.6.746

Cited by 60 publications

(51 citation statements)

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“…As discussed in detail elsewhere, a complex set of cellular constituents seems to determine the activity state of these metabolism-related K+ channels (Trapp & Ballanyi, 1995; see also Terzic, Kung & Kurachi, 1994). For example, it was reported for muscle tissue that lactate, as well as the anoxiainduced fall in pHi, counteract ATP inhibition of KATP channels, even in the presence of millimolar concentrations of intracellular ATP (Terzic et al 1994). We showed recently that anoxia-induced activation of KATP channels in DVNs is observed prior to the accompanying fall in intracellular pH and that reoxygenation leads to inactivation of these channels when the cells are still subject to a substantial intracellular acidosis (Trapp et al 1996a).…”

Section: Effects Of Energy Depletionmentioning

confidence: 92%

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Ballanyi

Doutheil

Brockhaus

1996

The Journal of Physiology

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1. Brainstem slices were taken from mature rats. In the dorsal vagal nucleus (DVNX), membrane potentials (Em) of neurons (DVNs) and glia, as well as extracellular oxygen, K+ and pH (Po2, aKO, pHO), were analysed during metabolic disturbances.2. Postsynaptic potentials of DVNs, elicited by repetitive electrical stimulation of the solitary tract (TS), led to a secondary glial depolarization of up to 25 mV, a fall in Po. of up to 150 mmHg, a rise in extracellular aKo of up to 9 mm, and a fall in pHo of about 0-2 pH units.3. Hypoxic superfusates produced tissue anoxia, leading to an aK. increase of less than 2 mM and a pHo fall of 024 + 0 04 pH units (mean + S.D.). Glucose-free solution evoked, after a delay of more than 8 min, a slow rise in aKo of 1-9 + 0-8 mm, accompanied by a mean increase in pHo of 0-24 + 0-13 pH units. After pre-incubation in glucose-free solution, anoxia elevated aKo by up to 15 mm, whereas the anoxia-induced pHo decrease was completely blocked. 4. In 45 of 118 DVNs, anoxia elicited a persistent hyperpolarization of 15'6 + 5 0 mV. In the remaining DVNs, anoxic exposure either did not produce a change in Em (37 %) or led to a depolarization of less than 10 mV (25 %). A stable depolarization of 9 + 3 8 mV was detected in glial cells during anoxia. Similar responses were revealed in oxygenated glucose-free solution after a delay of 12-60 min.5. The metabolism-related hyperpolarizations were blocked by 100-500 /uM tolbutamide or 20-100 AM glibenclamide, leading to recovery of spontaneous (0-5-6 Hz) spike discharge. In these cells, 400-500 uM diazoxide evoked hyperpolarizations and blockade of spontaneous activity. 6. In DVNs and glial cells, a progressive depolarization of up to 40 mV in amplitude developed during anoxic exposure after pre-incubation in glucose-free solution. 7. The results show that oxygen or glucose depletion does not impair the viability of DVNX cells. The contribution of neuronal ATP-sensitive K+ (KATP) channels to this tolerance is discussed.

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Section: Effects Of Energy Depletionmentioning

confidence: 92%

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Ballanyi

Doutheil

Brockhaus

1996

The Journal of Physiology

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“…Voltagegated K ϩ channels include a major subunit that consists of one pore domain and six transmembrane segments (1P/6TMS) (12). A second family that consists of channel subunits containing a single pore domain and two membrane-spanning segments (1P/ 2TMS) includes inward rectifiers many of which contribute to the resting potential and some of which are inhibited directly by intracellular ATP (12)(13)(14). K ϩ -selective leak or background channels comprise the third and most recently described family of K ϩ channels.…”

Section: Bovine Adrenal Zona Fasciculata (Azf) Cells Express a Backgrmentioning

confidence: 99%

An ACTH- and ATP-regulated Background K+ Channel in Adrenocortical Cells Is TREK-1

Enyeart

Danthi³

et al. 2002

Journal of Biological Chemistry

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Bovine adrenal zona fasciculata (AZF) cells express a background K؉ channel (I AC ) that sets the resting potential and acts pivotally in ACTH-stimulated cortisol secretion. We have cloned a bTREK-1 (KCNK2) tandempore K ؉ channel cDNA from AZF cells with properties that identify it as the native I AC . The bTREK-1 cDNA is expressed robustly in AZF cells and includes transcripts of 4.9, 3.6, and 2.8 kb. In patch clamp recordings made from transiently transfected cells, bTREK-1 displayed distinctive properties of I AC in AZF cells. Specifically, bTREK-1 currents were outwardly rectifying with a large instantaneous and smaller time-dependent component. Similar to I AC , bTREK-1 increased spontaneously in amplitude over many minutes of whole cell recording and was blocked potently by Ca 2؉ antagonists including penfluridol and mibefradil and by 8-(4-chlorophenylthio)-cAMP. Unitary TREK-1 and I AC currents were nearly identical in amplitude. The native I AC current, in turn, displayed properties that together are specific to TREK-1 K ؉ channels. These include activation by intracellular acidification, enhancement by the neuroprotective agent riluzole, and outward rectification. bTREK-1 current differed from native K ؉ current only in its lack of ATP dependence. In contrast to I AC , the current density of bTREK-1 in human embryonic kidney-293 cells was not increased by raising pipette ATP from 0.1 to 5 mM. Further, the enhancement of I AC current in AZF cells by low pH and riluzole was facilitated by, and dependent on, ATP at millimolar concentrations in the pipette solution. Overall, these results establish the identity of I AC K ؉ channels, demonstrate the expression of bTREK-1 in a specific endocrine cell, identify potent new TREK-1 antagonists, and assign a pivotal role for these tandem-pore channels in the physiology of cortisol secretion. The activation of I AC by ATP indicates that native bTREK-1 channels may function as sensors that couple the metabolic state of the cell to membrane potential, perhaps through an associated ATP-binding protein.

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“…Although the defining property of KATP channels is their inhibition by intracellular ATP (ATP1) (Noma, 1983), a reduction in [ATP]i appears not to be the sole mechanism responsible for channel opening (reviewed by Nichols & Lederer, 1991;Weiss & Venkatesh, 1993;Findlay, 1994;Terzic, Tung & Kurachi, 1994c). Indeed, in membrane patches excised from a cardiac cell, half-maximal inhibition of KATP channel activity is usually produced by 20-30 /uM ATPi (see Nichols & Lederer, 1991;Terzic, Jahangir & Kurachi, 1995), whereas the concentration of ATP, remains in the millimolar range in all but the most pathological of circumstances (Weiss & Venkatesh, 1993).…”

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confidence: 99%

“…Therefore, it appears that the mechanism responsible for the opening of KATP channels is complex (see Ashcroft & Ashcroft, 1990; Davies et at. 1991;Findlay, 1994;Terzic et at. 1994c).…”

mentioning

confidence: 99%

“…1994c). Major variations in the sensitivity of KATP channels towards ATP1-induced channel inhibition have been reported following excision of a patch from a cardiac cell membrane, which cannot be explained by changes in the concentration of intracellular nucleotides and/or in the intrinsic properties of the channel protein (Findlay & Faivre, 1991;Terzic et al 1994c). This observation may indicate that previously unrecognized mechanism(s) associated with the patch membrane could participate in the regulation of KATP channel gating in cardiac cells.…”

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confidence: 99%

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Actin microfilament disrupters enhance K(ATP) channel opening in patches from guinea‐pig cardiomyocytes.

Terzic

Kurachi

1996

The Journal of Physiology

101

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1. To determine whether actin filament networks are associated with the regulation of ATP‐sensitive K+ (K(ATP)) channel activity, single channel currents were measured in the inside‐out configuration, and cytoskeletal disrupters applied to the internal side of patches excised from guinea‐pig ventricular myocytes. 2. Treatment of patches with DNase I (10‐200 micrograms ml(‐1)), which forms complexes with G‐actin and prevents actin filament formation, antagonized the ATP‐induced inhibition of K(ATP) channels. 3. In the absence of ATP, DNase I did not increase K(ATP) channel activity. 4. When denatured by boiling or co‐incubated with purified actin subunits (200 mu g ml(‐1)), DNase I(100 mu g ml(‐1)) did not antagonize the ATP‐induced inhibition of K(ATP) channels. 5. The DNase I‐induced decrease in the sensitivity of K(ATP) channels towards ATP‐induced inhibition was partially restored by addition of purified actin subunits (200 micrograms ml(‐1)). 6. Cytochalasin B (10 microM), another actin filament disrupter, but neither taxol nor nocodazole (30‐100 microM), two antimicrotubule agents, enhanced K(ATP) channel activity in the presence of ATP. 7. Hence, actin filament disrupters can attenuate the ATP‐dependent inhibitory gating of K(ATP) channels. This suggests that subsarcolemmal actin filament networks may be associated with the regulation of cardiac K(ATP) channels.

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Nucleotide regulation of ATP sensitive potassium channels

Cited by 60 publications

References 0 publications

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

An ACTH- and ATP-regulated Background K+ Channel in Adrenocortical Cells Is TREK-1

Actin microfilament disrupters enhance K(ATP) channel opening in patches from guinea‐pig cardiomyocytes.

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