Specific block of the anti-ischemic actions of cromakalim by sodium 5-hydroxydecanoate.

McCullough, Judith; Normandin, Diane E.; Conder, Mary Lee; Sleph, Paul G.; Dzwonczyk, Steven; Grover, Gary J.

doi:10.1161/01.res.69.4.949

Cited by 126 publications

(55 citation statements)

References 16 publications

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“…Although initially thought to be a blocker of the plasma membrane K ATP channel [24], 5-HD has subsequently been shown to act as a highly selective inhibitor of the mitochondrial K ATP channel [25][26][27][28]; and as such, 5-HD has been used to explore the relation of the ouabain-sensitive Na + /K + -ATPase to mitochondrial K ATP channels [5][6][7]. From this point of view, the important findings of the present study are: (1) 5-HD concentrations that may have significant inhibitory effects on Na + /K + -ATPase (Figs.…”

Section: Discussionmentioning

confidence: 99%

Interactions of K+ ATP channel blockers with Na+/K+-ATPase

et al. 2007

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Two K + ATP channel blockers, 5-hydroxydecanoate (5-HD) and glyburide, are often used to study crosstalk between Na + /K + -ATPase and these channels. The aim of this work was to characterize the effects of these blockers on purified Na + /K + -ATPase as an aid to appropriate use of these drugs in studies on this cross-talk. In contrast to known dual effects (activating and inhibitory) of other fatty acids on Na + /K + -ATPase, 5-HD only inhibited the enzyme at concentrations exceeding those that block mitochondrial K + ATP channels. 5-HD did not affect the ouabain sensitivity of Na + /K + -ATPase. Glyburide had both activating and inhibitory effects on Na + /K + -ATPase at concentrations used to block plasma membrane K + ATP channels. The findings justify the use of 5-HD as specific mitochondrial channel blocker in studies on the relation of this channel to Na + /K + -ATPase, but question the use of glyburide as a specific blocker of plasma membrane K + ATP channels, when the relation of this channel to Na + /K + -ATPase is being studied.

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Section: Discussionmentioning

confidence: 99%

Interactions of K+ ATP channel blockers with Na+/K+-ATPase

et al. 2007

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“…5-HD (5 mg kg-'), an ischaemia selective blocker of ATP-sensitive potassium (KATP) channels (McCullough et al, 1991;Auchampach et al, 1992;Hide et al, 1995), was administered as a bolus injection (2 ml volume) into the left ventricle 10 min before infusion of sulprostone or vehicle.…”

Section: Myocardial Ischaemia and Reperfusionmentioning

confidence: 99%

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

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Thiemermann

1996

British J Pharmacology

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1 This study examined whether (i) a 1 h pretreatment with or (ii) a continuous infusion of sulprostone reduces myocardial infarct size arising from coronary artery occlusion (60 min) and reperfusion (120 min) in the anaesthetized rabbit. In addition, we investigated whether the observed cardioprotective effect of this selective agonist of prostanoid EP,/EP3 receptors were due to the activation of ATPsensitive potassium (KATP) channels.2 In anaesthetized rabbits pretreated with vehicle (5% ethanol in 0.9% saline; 0.05 ml min-', i.v.) infarct size (expressed as a percentage of the area at risk) after 60 min of coronary artery occlusion followed by 120 min of reperfusion was 59 + 4% (n = 10). Pretreatment of rabbits with sulprostone (1.0 ug kg-' min-' for 1 h, discontinued immediately prior to coronary artery occlusion) did not reduce infarct size (60 + 4%; n = 4). In contrast, a continuous infusion of sulprostone (1.0 ig kg-' min-') starting 10 min prior to the onset of LAL occlusion and continued throughout the experiment, significantly reduced infarct size (41 + 5%, n = 6) when compared to the respective vehicle-treated controls (57 + 4%, n = 10; P <0.05). Sulprostone (pretreatment or continuous infusion) had no effect on any of the haemodynamic parameters measured. 3 The reduction in infarct size afforded by continuous infusion of sulprostone was abolished by pretreatment of rabbits with the KATP channel blocker 5-hydroxydecanoate (5-HD 5 pg kg-'; 63+4%; n =6). When administered alone, 5-HD had no effect on infarct size when compared to control (52+6, n=10). 4 We propose that a continuous infusion of the selective EP,/EP3 prostanoid receptor agonist, sulprostone, reduces infarct size in the anaesthetized rabbit by a mechanism that involves the opening of KATP channels.

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“…10 min before infusion of PGE1, PGEo or vehicle. Sodium 5-hydroxydecanoate (5-HD), an ischaemia-selective inhibitor of (KATP) channels (McCullough, et al, 1991), was administered as a bolus injection (2 ml volume) into the left ventricle 10 min before infusion of PGE1 or vehicle. As the different vehicle groups (methanol and methyl acetate) had no significant effect on any of the haemodynamic parameters or on infarct size, the data of these groups were pooled to form one vehicle-control group.…”

Section: Measurements Of Area At Risk and Infarct Sizementioning

confidence: 99%

“…Pretreatment of rabbits with an infusion of PGEI (1.0 jug kg-1 min 1) resulted in a significant reduction in infarct size (P< 0.05, n = 6; Figure 1). This reduction in infarct size was abolished by pretreatment of rabbits with either glibenclamide (0.3 mg kg-, n = 8) or 5-HD (5 mg kg-', n =6) (Figure 1), both blockers of KATP channels (Gross & Auchampach, 1990;McCullough et al, 1991). When administered alone, neither glibenclamide (54+10%; n=8, P>0.05) nor 5-HD (55+7%; n=8, P>0.05) had any effect on myocardial infarct size when compared to vehicle control.…”

Section: Area At Risk and Infarct Sizementioning

confidence: 99%

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

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Ney

Piper

et al. 1995

British J Pharmacology

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1 This study examined whether pretreatment of rabbits with infusions of prostaglandin El (PGEI) or prostaglandin Eo (PGEO) (which were terminated prior to the onset of ischaemia) reduce myocardial infarct size arising from coronary artery occlusion (60 min) and reperfusion (120 min). In addition, we investigated whether the observed cardioprotective effects of these two prostaglandins were due to the activation of ATP-sensitive potassium (KATP) channels. 2 In the anaesthetized rabbit, infarct size (expressed as a percentage of the area at risk) after 60 min of coronary artery occlusion followed by 2 h of reperfusion was 59 + 4% (n = 10). PGEI or PGEo treatment (1.0 ,yg kg-' min-'), administered as 1 h pretreatments (0.05 ml min-', i.v.), significantly reduced infarct size to 44 + 6% (n = 6) or 42 + 1 % (n = 6), respectively. PGE, or PGEo pretreatment resulted in a significant reduction in mean arterial blood pressure, which returned to baseline within 15 min of discontinuation of the infusion (i.e. prior to LAL ligation). 3 The reduction in infarct size afforded by PGE, was abolished by pretreatment of rabbits with the KATP channel blockers, glibenclamide (60 + 4%; n =8) or 5-hydroxydecanoate (58 + 6%; n = 6). Similarly, glibenclamide also largely attenuated the reduction in infarct size afforded by PGEo (52 + 3%; n = 8).4 We propose that a 1 h pretreatment of PGEI or PGEO reduces infarct size by activating protein kinase C resulting in the opening of KATP channels.

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Specific block of the anti-ischemic actions of cromakalim by sodium 5-hydroxydecanoate.

Cited by 126 publications

References 16 publications

Interactions of K+ ATP channel blockers with Na+/K+-ATPase

Interactions of K+ ATP channel blockers with Na+/K+-ATPase

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

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Specific block of the anti-ischemic actions of cromakalim by sodium 5-hydroxydecanoate.

Cited by 126 publications

References 16 publications

Interactions of K+ ATP channel blockers with Na+/K+-ATPase

Interactions of K+ ATP channel blockers with Na+/K+-ATPase

Sulprostone‐induced reduction of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Reduction by prostaglandin E1 or prostaglandin E0 of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

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Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels