Somatostatin activates glibenclamide‐sensitive and ATP‐regulated K<sup>+</sup> channels in insulinoma cells via a G‐protein

Fosset, Michel; Schmid-Antomarchi, Heidy; Weille, Jan R. de; Lazdunski, Michel

doi:10.1016/0014-5793(88)80992-x

Cited by 58 publications

(26 citation statements)

References 15 publications

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“…One of the important properties of KATP channels is that, once they have been opened (e.g., by KCOs), they can be blocked with high potency by sulfonylureas such as glibenclamide or glipizide (17,18,22,40,42,47,52,53). Indeed the beneficial effects of KCOs against the series of events produced by ischemia were suppressed when openers were administered in the presence ofglipizide before ischemia was started.…”

Section: Resultsmentioning

confidence: 99%

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K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

Heurteaux

Bertaina

Widmann

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

173

105

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Communicated by Jean-Marie Lehn, June 1, 1993 (received for review March 8, 1993) ABSTRACT Transient global forebrain ischemia induces in rat brain a large increase of expression of the immediate early genes c-fos and c-jun and of the mRNAs for the 70-kDa heat-shock protein and for the form of the amyloid ,-protein precursor including the Kunitz-type protease-inhibitor domain. At 24 hr after ischemia, this increased expression is particularly observed in regions that are vulnerable to the deleterious effects of ischemia, such as pyramidal cells of the CAl field in the hippocampus. In an attempt to find conditions which prevent the deleterious effects of ischemia, representatives of three different classes of K+ channel openers, (-)-cromakalim, nicorandil, and pinacidil, were administered both before ischemia and during the reperfusion period. This treatment totally blocked the ischemia-induced expression of the different genes. In addition it markedly protected neuronal cells against degeneration. The mechanism of the neuroprotective effects involves the opening of ATP-sensitive K+ channels since glipizide, a specific blocker of that type of channel, abolished the beneficial effects of K+ channel openers. The various classes of K+ channel openers seem to deserve attention as potential drugs for cerebral ischemia.Global forebrain ischemia leads to a complete neuronal death in the CAl field of the hippocampus after 7 days of recovery, whereas the adjacent CA3 sector and the dentate gyrus are largely more resistant (1, 2). The main factors involved in the damage of neuronal tissue following ischemia are ATP depletion (3), intracellular acidosis (4), enhanced release and/or diminished reuptake of the excitatory transmitters glutamate and aspartate (5), generation of free radicals (6), and increased Ca2+ influx and K+ efflux (7,8).N-Methyl-D-aspartate (NMDA) antagonists and Ca2+ channel blockers have exhibited little ability to reduce tissue damage in animals with global ischemia (7, 9). They seem to be more helpful in focal ischemia (10,11 were administered intracerebroventricularly 30 min before the induction of cerebral ischemia and once each day during the recovery period. These doses of KCOs are similar to those previously shown to prevent seizures (31). Glipizide (1 ttmol/5 ul; Pfizer Diagnostics) was injected intracerebroventricularly 20 min prior to openers. Control experiments were performed with intracerebroventricular injection of 0.9% NaCl under conditions used for openers.Cerebral Ischemia Model. Forebrain ischemia involved occlusion of all four major extracranial arteries ("four-vessel occlusion" model) (2).The first day, the rats were anesthesized by inhalation of 2% halothane mixed with 30% oxygen/70% nitrous oxide. Body temperature was maintained at 37°C. The vertebral arteries were irreversibly occluded by electrocoagulation. After a delay of 1 day for recovery, both common carotid arteries were clamped during 20 min in awake and spontaneously ventilating animals. Rats lost their righting refle...

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Section: Resultsmentioning

confidence: 99%

“…[14][15][16]. The cardioprotective effects of these drugs are completely reversed by antidiabetic sulfonylureas such as glibenclamide, which are blockers of KATP channels (17,18).…”

mentioning

confidence: 99%

K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

Heurteaux

Bertaina

Widmann

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

173

105

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“…To further test this we determined if activating KATP through lowering cellular ATP [26] also regulates Kir6.1. Ventricular myocytes were treated for 3 h with the metabolic inhibitors oligomycin (0.2 |4,g/ml) and 2-deoxy-D-glucose (5 mM), which decreased intracellular ATP concentrations to 0.2 mM from 1 mM (data not shown).…”

Section: Regulation Of Kir61 Mrna By Atp Depletionmentioning

confidence: 99%

Channel activators regulate ATP‐sensitive potassium channel (KIR6.1) expression in chick cardiomyocytes

Changwan

Halvorsen

1997

FEBS Letters

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“…Therefore, the opening of sarc-K ATP channels, such as in an ischemic heart, can significantly shorten the action potential and promote arrhythmia, and if enough channels open, can render cells unexcitable (26,109). These reductions in the action potential duration are exacerbated by K ATP channel agonists (68,122) and blocked by the K ATP inhibitors such as glibenclamide, HMR 1833, or HMR 1098 (69,81,223). Various K ATP inhibitors also reduce the incidence of postischemic ventricular arrhythmia in rat, rabbit, pig, dog, and in humans (15,80,254,265); however, this blockade of the sarc-K ATP causes increase in the infarct sizes of heart postischemia (95).…”

Section: Aggarwal and Makielskimentioning

confidence: 99%

Redox Control of Cardiac Excitability

Aggarwal

Makielski

2013

Antioxidants & Redox Signaling

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Reactive oxygen species (ROS) have been associated with various human diseases, and considerable attention has been paid to investigate their physiological effects. Various ROS are synthesized in the mitochondria and accumulate in the cytoplasm if the cellular antioxidant defense mechanism fails. The critical balance of this ROS synthesis and antioxidant defense systems is termed the redox system of the cell. Various cardiovascular diseases have also been affected by redox to different degrees. ROS have been indicated as both detrimental and protective, via different cellular pathways, for cardiac myocyte functions, electrophysiology, and pharmacology. Mostly, the ROS functions depend on the type and amount of ROS synthesized. While the literature clearly indicates ROS effects on cardiac contractility, their effects on cardiac excitability are relatively under appreciated. Cardiac excitability depends on the functions of various cardiac sarcolemal or mitochondrial ion channels carrying various depolarizing or repolarizing currents that also maintain cellular ionic homeostasis. ROS alter the functions of these ion channels to various degrees to determine excitability by affecting the cellular resting potential and the morphology of the cardiac action potential. Thus, redox balance regulates cardiac excitability, and under pathological regulation, may alter action potential propagation to cause arrhythmia. Understanding how redox affects cellular excitability may lead to potential prophylaxis or treatment for various arrhythmias. This review will focus on the studies of redox and cardiac excitation. Antioxid. Redox Signal. 18, 432-468.

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Somatostatin activates glibenclamide‐sensitive and ATP‐regulated K⁺ channels in insulinoma cells via a G‐protein

Cited by 58 publications

References 15 publications

K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

Channel activators regulate ATP‐sensitive potassium channel (KIR6.1) expression in chick cardiomyocytes

Redox Control of Cardiac Excitability

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Somatostatin activates glibenclamide‐sensitive and ATP‐regulated K+ channels in insulinoma cells via a G‐protein

Cited by 58 publications

References 15 publications

K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

Channel activators regulate ATP‐sensitive potassium channel (KIR6.1) expression in chick cardiomyocytes

Redox Control of Cardiac Excitability

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Somatostatin activates glibenclamide‐sensitive and ATP‐regulated K⁺ channels in insulinoma cells via a G‐protein