2012
DOI: 10.1016/j.ejphar.2012.07.006
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Abstract: HMG-CoA reductase inhibitors, or statins, are widely used as cholesterol-lowering agents in the treatment of dyslipidemias. Statins have also been reported to have pleiotropic effects, independent of their effects on cholesterol synthesis, possibly through inhibition of the monomeric G proteins Ras and Rho, which are able to signal through ERK and Rho kinase activities, respectively. We have previously demonstrated that inhibition of ERK activation enhances β-adrenoceptor-mediated vasodilatation in the porcine… Show more

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Cited by 6 publications
(6 citation statements)
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“…Activation of cardiac K ATP channels by statins has been reported [14], [35], [36]. However, a recent study [37] and our current study demonstrated that simvastatin inhibits pinacidil-induced relaxation in porcine isolated coronary artery. Furthermore, our result illustrate that simvastatin consistently suppressed, instead of enhanced, cromakalim- and pinacidil-induced K ATP channel openings of arterial myocytes of pig coronary artery and human left internal mammary artery.…”
Section: Discussioncontrasting
confidence: 51%
“…Activation of cardiac K ATP channels by statins has been reported [14], [35], [36]. However, a recent study [37] and our current study demonstrated that simvastatin inhibits pinacidil-induced relaxation in porcine isolated coronary artery. Furthermore, our result illustrate that simvastatin consistently suppressed, instead of enhanced, cromakalim- and pinacidil-induced K ATP channel openings of arterial myocytes of pig coronary artery and human left internal mammary artery.…”
Section: Discussioncontrasting
confidence: 51%
“…For example, lovastatin has been shown to inhibit calcium influx through L-type calcium channels in rat basilar artery (Bergdahl et al, 2003), although it is not clear how this inhibition occurs. Rosuvastatin has been proposed to improve Ca 2+ -activated K + channel function (Miller et al, 2004) and rosuvastatin-induced relaxation of rat aorta may be due to opening of Ca 2+ -activated K + channels (Lopez et al, 2008), which in turn could lead to reduced calcium influx However, in contrast to this, simvastatin has been shown to inhibit Ca 2+ -activated K + channels in coronary artery smooth muscle (Seto et al, 2007) which may be responsible for the inhibition of β-adrenoceptor-mediated relaxations that we have observed (Uhiara et al, 2012).…”
Section: Introductionmentioning
confidence: 54%
“…However, in this current study we have demonstrated that neither the selective K ATP potassium channel inhibitor glibenclamide, nor the non-selective inhibitor of K + channels TEA altered the simvastatin relaxation, suggesting that activation of K + channels is not involved in the relaxation response. In fact, our previous studies demonstrate that simvastatin actually inhibits K + channel-mediated relaxations in the porcine coronary artery (Uhiara et al, 2012). Other studies have suggested that simvastatin increases mitochondrial K ATP channel activity (Jones et al, 2003;Zhao et al, 2006).…”
Section: Control Treatedmentioning
confidence: 95%
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“…Statins can mobilize bone marrow endothelial stem cells and promote recovery from nerve injury. Mobilization of autologous BMSCs has improved treatment of ischemic cerebrovascular diseases to a certain extent (Almansob et al, 2012;Uhiara et al, 2012). Vasculogenesis and neurogenesis are two major pathophysiologic processes that occur in the brain after cerebral ischemia.…”
Section: Introductionmentioning
confidence: 99%