IndraLab

Statements


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

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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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"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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"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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"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."

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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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"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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"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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"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."

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

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

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 ."

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