Role of Cardiac KATP Channels During Anoxia and Ischemia

Benndorf, Klaus; Thierfelder, S; Doepner, Bettina; Gebhardt, Ch.; Hirche, Hj.

doi:10.1152/physiologyonline.1997.12.2.78

Cited by 8 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Changes in cellular metabolic status resulting from hypoxic or ischaemic conditions are well known to modulate ion channel activity in cardiac and other tissues, for example through altered channel phosphorylation state (Allen & Orchard, 1987; Trautwein & Hescheler, 1990; McDonald et al 1994; Benndorf et al 1997). However, in recent years several studies using a diverse range of tissues have indicated that ion channels are rapidly influenced by local oxygen levels in a membrane‐limited, possibly direct manner (reviewed by Peers, 1997).…”

mentioning

confidence: 99%

Modulation of recombinant human cardiac L‐type Ca²⁺ channel α_1C subunits by redox agents and hypoxia

Fearon

Palmer

Balmforth

et al. 1999

The Journal of Physiology

116

View full text Add to dashboard Cite

1. Whole-cell patch clamp recordings were used to investigate the modulation by reducing and oxidizing agents of recombinant human cardiac L-type Ca¥ channel á1C subunits stably expressed in human embryonic kidney (HEK 293) cells. 2. The oxidizing agents thimerosal (10 ìÒ) and p-chloromercuribenzene sulphonic acid (PCMBS; 2 ìÒ to 2 mÒ) caused irreversible inhibition of Ca¥ channel currents. The reducing agent 1,4-dithiothreitol (DTT; 2 mÒ) was without effect on Ca¥ channel currents, but reversed the inhibitory actions of thimerosal and PCMBS. 3. Ca¥ channel currents were also inhibited by pretreatment with the methanethiosulphonate compound (2-aminoethyl)methanethiosulphonate (MTSEA, 2·5 mÒ), but were unaffected by identical pretreatment with (2-sulphonatoethyl)methanethiosulphonate (MTSES, 10 mÒ). The effects of MTSEA could be fully reversed by DTT (2 mÒ). The degree of current inhibition caused by 200 ìÒ PCMBS was not significantly affected by pretreatment with MTSEA, and following PCMBS treatment, MTSEA caused a similar degree of inhibition to that observed in cells that were not previously treated with PCMBS. These findings suggested that distinct thiol groups were modulated by these two agents. 4. Hypoxic inhibition of Ca¥ channel currents was unaffected by pretreatment of cells with MTSEA but was fully prevented by treatment with PCMBS. Our results indicate that distinct cysteine residues on the á1C subunit can undergo redox modulation and in so doing alter channel function. Some, but not all, of these residues appear to be associated with the mechanism underlying inhibition of this channel by hypoxia.

show abstract

mentioning

confidence: 99%

Modulation of recombinant human cardiac L‐type Ca²⁺ channel α_1C subunits by redox agents and hypoxia

Fearon

Palmer

Balmforth

et al. 1999

The Journal of Physiology

116

View full text Add to dashboard Cite

show abstract

“…SURs are the binding sites for known blockers (e.g., glibenclamide) and activators (e.g., pinacidil and cromakalim) of these channels, which have found valuable therapeutic uses. K ATP channels are classically identified as being inhibited by intracellular ATP and were first described in cardiac myocytes (Noma, 1983) in which they were believed to act under conditions of metabolic stress to shorten action potential durations and so reduce the energy demands of myocytes when intracellular ATP levels are reduced (Benndorf et al, 1997).…”

mentioning

confidence: 99%

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca²⁺Sensitivity of Exocytosis

et al. 1999

View full text Add to dashboard Cite

Electrochemical detection of quantal catecholamine release from PC-12 cells revealed that glibenclamide, an inhibitor of ATP-sensitive K(+) channels, potentiated Ca(2+)-dependent exocytosis evoked by raised extracellular [K(+)] and by exposure of cells to caffeine. Glibenclamide was without effect on voltage-gated Ca(2+) currents, membrane potential, or rises of [Ca(2+)](i) evoked by either raised extracellular [K(+)] or caffeine. The dependence of K(+)-evoked secretion on extracellular Ca(2+) was shifted leftward in the presence of glibenclamide, with a small increase in the plateau level of release, suggesting that glibenclamide primarily increased the Ca(2+) sensitivity of the exocytotic apparatus. Enhancement of secretion by glibenclamide was reversed by pinacidil and cromakalim, indicating that the effects of glibenclamide were mediated via an action on a sulfonylurea receptor. These results demonstrate that sulfonylurea receptors can modulate Ca(2+)-dependent exocytosis via a mechanism downstream of Ca(2+) influx or mobilization.

show abstract

“…Àêòèâàö³ÿ ÀÒÔ-÷óòëèâèõ êàë³ºâèõ (Ê ÀÒÔ ) êàíàë³â êë³òèííèõ ìåìáðàí º îäíèì ³ç ãîëîâíèõ åíäîãåííèõ çàõèñíèõ ìåõàí³çì³â îðãàí³çìó â â³äïîâ³äü íà çìåíøåííÿ âíóò-ð³øíüîêë³òèííîãî âì³ñòó ÀÒÔ íèae÷å â³ä ì³ë³ìîëÿðíèõ ð³âí³â, çîêðåìà ïðè ã³ïîêñ³¿ òà ³øåì³¿ òêàíèíè [22,31]. ¯õ åêçîãåííà àêòèâàö³ÿ ôàðìàêîëîã³÷íèì øëÿõîì çàïóñêàº íå ìåíø ïîòóaeí³, àíàëîã³÷í³ äî åíäîãåííèõ, çàõèñí³ ìåõàí³çìè, îäíèì ³ç ÿêèõ º çìåíøåííÿ âõîäó Ñà 2+ â êë³òèíó ÷åðåç L-òèï êàëüö³ºâèõ êàíàë³â [20,25], à òàêîae íàêîïè÷åííÿ éîãî â ìàòðèêñ³ ì³òîõîíäð³é âíàñë³äîê ïðèãí³÷åííÿ âõîäó ÷åðåç ïîòåí-ö³àëçàëåaeíèé êàëüö³ºâèé óí³ïîðòåð [26,29].…”

Section: âñòóïunclassified

“…¯õ åêçîãåííà àêòèâàö³ÿ ôàðìàêîëîã³÷íèì øëÿõîì çàïóñêàº íå ìåíø ïîòóaeí³, àíàëîã³÷í³ äî åíäîãåííèõ, çàõèñí³ ìåõàí³çìè, îäíèì ³ç ÿêèõ º çìåíøåííÿ âõîäó Ñà 2+ â êë³òèíó ÷åðåç L-òèï êàëüö³ºâèõ êàíàë³â [20,25], à òàêîae íàêîïè÷åííÿ éîãî â ìàòðèêñ³ ì³òîõîíäð³é âíàñë³äîê ïðèãí³÷åííÿ âõîäó ÷åðåç ïîòåí-ö³àëçàëåaeíèé êàëüö³ºâèé óí³ïîðòåð [26,29]. Îñíîâíèì åíäîãåííèì ðåãóëÿòîðîì àêòèâ-íîñò³ öèõ êàíàë³â º âíóòð³øíüîêë³òèííà êîíöåíòðàö³ÿ ÀÒÔ ³ äåêîëè, ÿê ó ïàíê-ðåàòè÷íèõ β-êë³òèíàõ, ãîëîâíó ðîëü â³ä³ãðàº ñï³ââ³äíîøåííÿ ÀÒÔ/ÀÄÔ [22,33]. ¯õ çíà÷èì³ñòü â óìîâàõ ô³ç³îëîã³÷íî¿ íîðìè äëÿ á³ëüøîñò³ òêàíèí äîñ³ çàëèøàºòüñÿ íåâ³äîìîþ, òîä³ ÿê äëÿ ï³äøëóíêîâî¿ çàëîçè âîíà ïåâíèì ÷èíîì ðîçêðèòà.…”

Section: âñòóïunclassified

“…Ê ÀÒÔ -êàíàëè, çâÿçóþ÷è á³îåíåðãåòè÷íèé ñòàí êë³òèíè ç ¿¿ ìåìáðàííèì ïîòåíö³àëîì, âïëèâàþòü íà ðåàêö³þ êë³òèíè â â³äïîâ³äü íà çì³íè ìåòàáîë³çìó â ¿¿ öèòîïëàçì³ ³ ñåðåäîâèù³, ÿêå îòî÷óº êë³òèíó, ùî ïåðåâàaeàíî ïîâÿçàí³ ç ã³ïîêñ³ºþ òà âì³ñòîì ãëþêîçè â êðîâ³. Çá³ëüøåííÿ âì³ñòó ÀÒÔ â³ä âèùåâêàçàíîãî ð³âíÿ, íàâïàêè, ïðèçâîäèòü äî çàêðèâàííÿ öèõ êàíàë³â [22,30,31]. Âèõîäÿ÷è ç òîãî, ùî ïðè ô³ç³îëîã³÷íèõ óìîâàõ âíóòð³ø-íüîêë³òèííà êîíöåíòðàö³ÿ ÀÒÔ â³äïîâ³äàº ì³ë³ìîëÿðíèì ð³âíÿì (áëèçüêî 35 ììîëü/ ë) Ê ÀÒÔ -êàíàëè ïîñò³éíî ïîâèíí³ áóòè â ³íã³áîâàíîìó ñòàí³ [34].…”

Section: âñòóïunclassified

See 1 more Smart Citation

Effect of a new activator of adenosine triphosphate-sensitive potassium channels flocalin on the glucose level in blood

Strutyns'kyĭ¹,

Rovenets'²,

Op³

2010

Fiziol Zh

View full text Add to dashboard Cite

Role of Cardiac KATP Channels During Anoxia and Ischemia

Cited by 8 publications

References 0 publications

Modulation of recombinant human cardiac L‐type Ca²⁺ channel α_1C subunits by redox agents and hypoxia

Modulation of recombinant human cardiac L‐type Ca²⁺ channel α_1C subunits by redox agents and hypoxia

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca²⁺Sensitivity of Exocytosis

Effect of a new activator of adenosine triphosphate-sensitive potassium channels flocalin on the glucose level in blood

Contact Info

Product

Resources

About

Role of Cardiac KATP Channels During Anoxia and Ischemia

Cited by 8 publications

References 0 publications

Modulation of recombinant human cardiac L‐type Ca2+ channel α1C subunits by redox agents and hypoxia

Modulation of recombinant human cardiac L‐type Ca2+ channel α1C subunits by redox agents and hypoxia

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca2+Sensitivity of Exocytosis

Effect of a new activator of adenosine triphosphate-sensitive potassium channels flocalin on the glucose level in blood

Contact Info

Product

Resources

About

Modulation of recombinant human cardiac L‐type Ca²⁺ channel α_1C subunits by redox agents and hypoxia

Modulation of recombinant human cardiac L‐type Ca²⁺ channel α_1C subunits by redox agents and hypoxia

Potentiation of Quantal Catecholamine Secretion by Glibenclamide: Evidence for a Novel Role of Sulphonylurea Receptors in Regulating the Ca²⁺Sensitivity of Exocytosis