Do the K+ channel openers relax smooth muscle by opening K+ channels?

Quast, Ulrich

doi:10.1016/0165-6147(93)90006-6

Cited by 193 publications

(125 citation statements)

References 34 publications

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“…Their findings suggest that high K+ can activate phospholipase C in some vascular muscles. The mechanism by which a depolarizing agent, such as K+, activates membranebound or intracellular enzymes is not known but such a phenomenon has been previously reported (Itoh et al, 1992;Quast, 1993). This interesting phenomenon in excitationcontraction coupling warrants further investigation.…”

Section: Concentration Of H7 (>M)mentioning

confidence: 86%

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K⁺ contracture in rat and guinea‐pig aorta

Low

Loke

Kwan

et al. 1994

British J Pharmacology

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Section: Concentration Of H7 (>M)mentioning

confidence: 86%

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K⁺ contracture in rat and guinea‐pig aorta

Low

Loke

Kwan

et al. 1994

British J Pharmacology

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“…In several vascular beds, it is opened by local or circulating vasodilator transmitters (5), and its opening leads to vasorelaxation by a variety of pathways (22). In addition, there is a K ATP channel in endothelial cells consisting of SUR2B ϩ Kir6.1 and/or Kir6.2 (23).…”

Section: Function Of K Atp Channels In the Coronary Vascular Bed In Nmentioning

confidence: 99%

The Impact of ATP-Sensitive K+ Channel Subtype Selectivity of Insulin Secretagogues for the Coronary Vasculature and the Myocardium

et al. 2004

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Insulin secretagogues (sulfonylureas and glinides) increase insulin secretion by closing the ATP-sensitive K ؉ channel (K ATP channel) in the pancreatic ␤-cell membrane. K ATP channels subserve important functions also in the heart. First, K ATP channels in coronary myocytes contribute to the control of coronary blood flow at rest and in hypoxia. Second, K ATP channels in the sarcolemma of cardiomyocytes (sarcK ATP channels) are required for adaptation of the heart to stress. In addition, the opening of sarcK ATP channels and of K ATP channels in the inner membrane of mitochondria (mitoK ATP channels) plays a central role in ischemic preconditioning. Opening of sarcK ATP channels also underlies the STsegment elevation of the electrocardiogram, the primary diagnostic tool for initiation of lysis therapy in acute myocardial infarction. Therefore, inhibition of cardiovascular K ATP channels by insulin secretagogues is considered to increase cardiovascular risk. Electrophysiological experiments have shown that the secretagogues differ in their selectivity for the pancreatic over the cardiovascular K ATP channels, being either highly selective (ϳ1,000؋; short sulfonylureas such as nateglinide and mitiglinide), moderately selective (10 -20؋; long sulfonylureas such as glibenclamide [glyburide]), or essentially nonselective (<2؋; repaglinide). New binding studies presented here give broadly similar results. In clinical studies, these differences are not yet taken into account. The hypothesis that the in vitro selectivity of the insulin secretagogues is of importance for the cardiovascular outcome of diabetic patients with coronary artery disease needs to be tested. Diabetes 53 (Suppl. 3):S156 -S164, 2004 I nsulin secretagogues are widely prescribed in the treatment of type 2 diabetes. They close the ATPsensitive K ϩ channel (K ATP channel) in the membrane of the pancreatic ␤-cell, thereby depolarizing the cell and triggering insulin secretion. K ATP channels are gated by intracellular nucleotides with ATP inducing channel closure and MgADP channel opening. The ␤-cell is special in that physiological changes in plasma glucose change the intracellular ATP and ADP concentrations such that the channel opens and closes; hence, the channel functions as the glucose sensor in this cell (1-3). K ATP channel subtypes are found in many cell types. The generation of mice in which the genes for the K ATP channel subunits were deleted have shed new light on the diverse functions of the K ATP channels in various tissues in physiological and pathophysiological conditions (1). In brain, K ATP channels are involved in actions as diverse as the control of glucose homeostasis and the regulation of neuronal excitability in hypoxia (1); however, the insulin secretagogues do not cross the blood-brain barrier easily enough to affect these channels at therapeutic plasma levels (4). In several vascular beds, the K ATP channel in the vascular myocytes is involved in the regulation of vessel tone; opening is triggered in particular by stimuli inc...

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“…Ba21 inhibits (-)Ckm-induced 86Rb+-flux with an IC50 of 30 JiM (Quast, 1993). We compared the effects of bathapplied Ba2+ on IK(-Ckn) and IK(DR) (Figure 3).…”

Section: Effects Of Ba2+mentioning

confidence: 99%

Inhibition of delayed rectifier K⁺‐current by levcromakalim in single intestinal smooth muscle cells: effects of cations and dependence on K⁺‐flux

McHugh

Beech

1995

British J Pharmacology

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1 Whole-cell voltage-clamp recordings were made from single smooth muscle cells isolated from the longitudinal layer of the guinea-pig small intestine.2 Levcromakalim ((-)Ckm) inhibited delayed rectifier K-current (IK(DR)) and induced a voltageindependent K-current (IK(Ckm)). Both effects were inhibited similarly by glibenclamide. In some cells, however, IK(-ckm) could be induced without any effect on IK(DR)-3 Ba2" caused a voltage-dependent block of IK(dckm). The IC50 was 0.2 mM at -40 mV (6 cells), but at 0 mV 2 mM Ba2" caused only a 26 ± 7% inhibition (n = 5). Ba2+ had much less effect on IK(DR), 2 mM Ba2" having no inhibitory effect on current elicited by depolarization to -30 mV (n = 6) or 0 mV (n = 5).

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Do the K+ channel openers relax smooth muscle by opening K+ channels?

Cited by 193 publications

References 34 publications

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K⁺ contracture in rat and guinea‐pig aorta

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K⁺ contracture in rat and guinea‐pig aorta

The Impact of ATP-Sensitive K+ Channel Subtype Selectivity of Insulin Secretagogues for the Coronary Vasculature and the Myocardium

Inhibition of delayed rectifier K⁺‐current by levcromakalim in single intestinal smooth muscle cells: effects of cations and dependence on K⁺‐flux

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Do the K+ channel openers relax smooth muscle by opening K+ channels?

Cited by 193 publications

References 34 publications

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K+ contracture in rat and guinea‐pig aorta

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K+ contracture in rat and guinea‐pig aorta

The Impact of ATP-Sensitive K+ Channel Subtype Selectivity of Insulin Secretagogues for the Coronary Vasculature and the Myocardium

Inhibition of delayed rectifier K+‐current by levcromakalim in single intestinal smooth muscle cells: effects of cations and dependence on K+‐flux

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Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K⁺ contracture in rat and guinea‐pig aorta

Sensitivity to protein kinase C inhibitors of nicardipine‐insensitive component of high K⁺ contracture in rat and guinea‐pig aorta

Inhibition of delayed rectifier K⁺‐current by levcromakalim in single intestinal smooth muscle cells: effects of cations and dependence on K⁺‐flux