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• W2010382458 abstract "Vascular contraction is an important determinant of the peripheral vascular resistance and blood pressure. The mechanisms underlying vascular smooth muscle (VSM) contraction and the pathological changes that occur in hypertension have been the subject of numerous studies and interpretations. Activation of VSM by vasoconstrictor stimuli at the cell surface causes an increase in [Ca2+]i, Ca2+-dependent activation of myosin light chain (MLC) kinase, MLC phosphorylation, actin–myosin interaction and VSM contraction. Additional signaling pathways involving Rho-kinase and protein kinase C (PKC) may increase the myofilament force sensitivity to [Ca2+]i and MLC phosphorylation, and thereby maintain vascular contraction. PKC is a particularly intriguing protein kinase as it comprises a family of Ca2+-dependent and Ca2+-independent isoforms, which have different tissue and subcellular distribution, and undergo differential translocation during cell activation. PKC translocation to the cell surface may trigger a cascade of protein kinases, such as mitogen-activated protein kinase (MAPK) and MAPK kinase (MEK) that ultimately interact with the contractile myofilaments and cause VSM contraction. Also, PKC translocation to the nucleus may promote VSM growth and proliferation. Increased PKC expression and activity have been identified in several forms of hypertension. The subcellular location of PKC may determine the state of VSM activity, and may be useful in the diagnosis/prognosis of hypertension. Vascular PKC isoforms may represent specific targets for modulation of VSM hyperactivity, and isoform-specific PKC inhibitors may be useful in treatment of Ca2+ antagonist-resistant forms of hypertension." @default.
• W2010382458 created "2016-06-24" @default.
• W2010382458 creator A5008198798 @default.
• W2010382458 creator A5063840461 @default.
• W2010382458 date "2005-11-01" @default.
• W2010382458 modified "2023-10-17" @default.
• W2010382458 title "Protein kinase C isoforms as specific targets for modulation of vascular smooth muscle function in hypertension" @default.
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• W2010382458 doi "https://doi.org/10.1016/j.bcp.2005.07.017" @default.
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