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Chronic ouabain treatment induces Rho kinase activation
Aysun Ozdemir,Gürkan Şahan,Ayşegül Demirtas,Eda Aypar,Gürkan Gözübüyük,Nilüfer Nermin Turan,Mustafa Ark 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.10
Ouabain is an endogenous Na?/K?-ATPaseinhibitor whose chronic administration induces hypertension. Endogenous ouabain levels increase in humanessential hypertension. On the other hand, Rho/Rho kinase(ROCK) pathway has been implicated in various animalmodels of hypertension. In the current work, we evaluatedthe possible involvement of Rho kinase in ouabain-inducedhypertension. Ouabain was administered daily (20 lg/kg,i.p.) to Wistar rats for 6 weeks. After the ouabain treatment,we evaluated the possible changes in vascular responsesto KCl and phenylephrine alone and in thepresence of Rho kinase inhibitor Y27632. We also determinedthe expressions of ROCKs, Rho A and phosphorylationof myosin binding subunit of myosin light chainphosphatase (pMYPT) and activation of Rho A. Agonistinducedcontractions in the presence of Y27632 are significantlydecreased and Y27632-induced relaxations inaortas precontracted with phenylephrine are significantlyenhanced with the chronic treatment of ouabain. Althoughthe expressions of ROCK I and ROCK II remained unchanged,pMYPT expression was significantly increased inouabain-treated group. Moreover, Rho A expression andactivation were decreased after treatment with ouabain. Although Rho kinase expression did not change in aortas,increased basal Rho kinase activation may contribute to thedevelopment of ouabain-induced hypertension. Our currentdata present the first evidence that Rho kinase is involvedin the development of ouabain-induced hypertension inrats.
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