IndraLab

Statements


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"Thus NO may modulate BK channel opening directly or by inducing cytosolic Ca 2+ increase."

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"In nerve terminals of the posterior pituitary, NO increases BK channel conductance, generating spike after hyperpolarization and also Na + channels recovery from inactivation, so reducing action potential failures."

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"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."

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"With the approach of the present study, especially at lower levels of contractility, NO induces a PKG mediated increase in BK channel activity that is weaker than the large [Ca 2+] i decrease mediated decrease in BK channel activity."

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"In human dermal fibroblast, PKA is involved in activation of the KCNMA1 by nitric oxide through cGMP xref ."

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"However, they also limit NO‐induced relaxation at intermediate and low contractility levels, which is caused by a predominant NO‐induced reduction in activator calcium influx and deactivation of the BK channel."

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"Although not examined in the present study, it is likely that the observed NO induced BK channel activity results from an increase in Ca 2+ spark frequency."

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"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."

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"XREF_BIBR, XREF_BIBR In addition, to NO mediated BK channel activation, it is also possible that other mechanisms 13 involving cGMP dependent decreases in SM Ca 2+ may contribute to TBI induced cerebral artery dilation."

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"Ciorba et al. 1999 showed that NO could promote methionine oxidation in Shaker channels, and it would be interesting to see if NO could increase hSlo currents."

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"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."

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"Thus, the degree of contribution of PKG to the NO-induced activation of the BK channel is still not completely clear."

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"These results suggest that NO can modulate Maxi-K channel via direct interaction and chemical modification, such as Snitrosylation in the brain."

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"Finally, this study provides another important piece of evidence supporting the idea that an NO induced reduction of calcium influx via VOC enables the BK channel to limit the anticontractile effect of NO."

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"NO is found to stimulate rapid surface trafficking of the BK channel β1 subunit via cGMP-PKG- and cAMP-PKA-dependent pathways, resulting in increased channel Ca sensitivity/channel activity, and vasodilation [137]."

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"Moreover, NO is able to directly activate the BK channel in VSMCs [138,139]."

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"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 ."

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"NO and EDHFs released from ECs subsequently trigger BK channel activation in VSMCs, leading to vasorelaxation [139,157,158,159]."

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"These findings suggest that blockade of L-type Ca (2+) channels is not a major mechanism responsible for the vascular relaxation due to NO mediated MaxiK (Ca) channel activation in guinea pig aorta."

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"Here, we describe a unique mechanism by which NO and ET-1 modulate BK channel activity in myocytes to control arterial contractility."

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"Leo et al. [137] demonstrate that NO stimulates rapid trafficking of the BK channel β1 subunit to the plasma membrane via a PKG-dependent pathway."

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"NO is a potent stimulator of the BK channel in VSMCs [139]."

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"We investigated whether nitric oxide (NO) directly activates the cloned alpha-subunit of large conductance Ca2 +-activated K+ (Maxi-K) channels from rat brain (rSlo), expressed either in HEK293 cells or Xenopus oocytes."

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"We investigated whether nitric oxide (NO) directly activates the cloned alpha-subunit of large conductance Ca2 +-activated K+ (Maxi-K) channels from rat brain (rSlo), expressed either in HEK293 cells or Xenopus oocytes."

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"Although different mechanisms account for CO- and NO mediated BK channel stimulation [XREF_BIBR], considerable evidence supports interactions between HO/CO and NOS/NO systems in vasoregulation [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."

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"BK channel activation by NO was inhibited in SP-SHR myocytes and restored by Rab11A S177A expression."

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"In summary, data indicate that spontaneously active PKC inhibits Rab11A mediated beta1 subunit trafficking in arterial myocytes of SP-SHRs, leading to dysfunctional NO induced BK channel activation and vasodilation."

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"Both arachidonic acid and nitric oxide potentiate BK channel activity by slowing inactivation kinetics and enhancing channel opening, respectively [XREF_BIBR, XREF_BIBR]."

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"At a high contraction level, NO induces a PKG mediated increase in BK channel activity, well established by many studies,1, 5, 6 that is stronger than the small [Ca 2+] i decrease mediated decrease of BK channel activity."