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• W1515952978 endingPage "3603" @default.
• W1515952978 startingPage "3587" @default.
• W1515952978 abstract "Nitric oxide (NO) from endothelium is a major mediator of vasodilatation through cGMP/PKG signals that lead to a decrease in Ca 2+ concentration. In addition, NO‐mediated signals trigger an increase in myosin light chain phosphatase (MLCP) activity. To evaluate the mechanism of NO‐induced relaxation through MLCP deinhibition, we compared time‐dependent changes in Ca 2+ , myosin light chain (MLC) phosphorylation and contraction to changes in phosphorylation levels of CPI‐17 at Thr38, RhoA at Ser188, and MYPT1 at Ser695, Thr696 and Thr853 in response to sodium nitroprusside (SNP)‐induced relaxation in denuded rabbit femoral artery. During phenylephrine (PE)‐induced contraction, SNP reduced CPI‐17 phosphorylation to a minimal value within 15 s, in parallel with decreases in Ca 2+ and MLC phosphorylation, followed by a reduction of contractile force having a latency period of about 15 s. MYPT1 phosphorylation at Ser695, the PKG‐target site, increased concurrently with relaxation. Phosphorylation of RhoA, MYPT1 Thr696 and Thr853 differed significantly at 5 min but not within 1 min of SNP exposure. Inhibition of Ca 2+ release delayed SNP‐induced relaxation while inhibition of Ca 2+ channel, BK Ca channel or phosphodiesterase‐5 did not. Pretreatment of resting artery with SNP suppressed an increase in Ca 2+ , contractile force and phosphorylation of MLC, CPI‐17, MYPT1 Thr696 and Thr853 at 10 s after PE stimulation, but had no effect on phorbol ester‐induced CPI‐17 phosphorylation. Together, these results suggest that NO production suppresses Ca 2+ release, which causes an inactivation of PKC and rapid CPI‐17 dephosphorylation as well as MLCK inactivation, resulting in rapid MLC dephosphorylation and relaxation." @default.
• W1515952978 created "2016-06-24" @default.
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• W1515952978 date "2009-07-14" @default.
• W1515952978 modified "2023-10-17" @default.
• W1515952978 title "Nitric oxide-induced biphasic mechanism of vascular relaxation via dephosphorylation of CPI-17 and MYPT1" @default.
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• W1515952978 doi "https://doi.org/10.1113/jphysiol.2009.172189" @default.
• W1515952978 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2742283" @default.
• W1515952978 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19470783" @default.
• W1515952978 hasPublicationYear "2009" @default.
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