
IndraLab
Statements
Nitric oxide activates KCNMA1. 29 / 29
|
1
27
1
reach
"It has been suggested that, particularly at lower levels of vessel contractility, NO-induced PKG-mediated activation of the BK channel is weaker than NO-induced [Ca ] decrease–mediated deactivation of the BK channel and that the overall decrease in BK channel activity determines the role of BK channels as limiters of the effect of NO."
reach
"It was suggested that at higher levels of vessel contractility, NO-induced PKG-mediated activation of the BK channel is stronger than NO-induced [Ca ] decrease–mediated deactivation of the BK channel and that the overall increase in BK channel activity determines the role of BK channels as facilitators of the effect of NO."
reach
"This leads to an overall decrease in BK channel activity, which defines the role of BK channels as limiters of the effect of NO.Alternatively, the observed shifts in methoxamine-induced concentration response relationships could be explained by an NO-induced increase in BK channel activity that overcomes the iberiotoxin-induced decrease in BK channel activity."
eidos
"Because L-NAME prevented hyperpolarization to SP in SMCs ( Figure 4 ) , we suggest that KCa channels ( likely BK ) on SMCs are activated by endothelium-derived NO to mediate hyperpolarization , which can occur through cGMP - and PKG-dependent phosphorylation.37 ,39 Alternatively , direct activation of BK channels by NO has been reported in vascular smooth muscle independent of guanylate cyclase signaling.40 Because SK and IK channels can regulate NO synthesis in ECs ,30,41 it is possible KCa inhibition in ECs prevents SMC hyperpolarization by limiting NO production ."