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Na,K-ATPase as a target for endogenous cardiotonic steroids:What’s the evidence?

Genes & Diseases 2021年第3期8卷 259-271页

作者： Sergei N.orlov Artem M.Tverskoi Svetlana V.Sidorenko Larisa V.Smolyaninova olga D.Lopina nickolai o.dulin Elizaveta A.Klimanova MV Lomonosov Moscow State University Moscow119234Russia National Research Tomsk State University Tomsk634050Russia Siberian State Medical University Tomsk634050Russia University of Chicago IL60637USA

With an exception of few reports,the plasma concentration of ouabain and mari-nobufagenin,mostly studied cardiotonic steroids(CTS)assessed by immunoassay techniques,is less than 1 *** the last 3 decades,the implication of these endogenous CTS in the path-ogenesis of hypertension and other volume-expanded disorders is widely *** threshold for inhibition by CTS of human and rodent a1-Na,K-ATPase is~1 and 1000 nM,respectively,that rules out the functioning of endogenous CTS(ECTS)as natriuretic hormones and regulators of cell adhesion,cell-to-cell communication,gene transcription and transla-tion,which are mediated by dissipation of the transmembrane gradients of monovalent *** several types of cells ouabain and marinobufagenin at concentrations corresponding to its plasma level activate Na,K-ATPase,decrease the[Na^(+)]i;/[K^(+)]i;-ratio and increase cell *** physiological significance and mechanism of non-canonical Na^(+)/K^(+)-depen-dent and Nai^(+)/Ki^(+)independent cell responses to CTS are discussed.

关键词： Cell proliferation Cellular signaling Endogenous cardiotonic steroids Na+,K+-ATPase Transcription Translation

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NKCC1 and NKCC2:The pathogenetic role of cation-chloride cotransporters in hypertension

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Genes & Diseases 2015年第2期2卷 186-196页

作者： Sergei N.orlov Svetlana V.Koltsova Leonid V.Kapilevich Svetlana V.Gusakova nickolai o.dulin Faculty of Biology M.V.Lomonosov Moscow State UniversityRussia Tomsk State University Russia Siberian State Medical University Russia University of Chicago Department of Medicine USA

This review summarizes the data on the functional significance of ubiquitous(NKCC1)and renal-specific(NKCC2)isoforms of electroneutral sodium,potassium and chloride *** carriers contribute to the pathogenesis of hypertension via regulation of intracellular chloride concentration in vascular smooth muscle and neuronal cells and via sensing chloride concentration in the renal tubular fluid,*** NKCC1 and NKCC2 are inhibited by furosemide and other high-ceiling diuretics widely used for attenuation of extracellular fluid ***,the chronic usage of these compounds for the treatment of hypertension and other volume-expanded disorders may have diverse side-effects due to suppression of myogenic response in microcirculatory beds.

关键词： Hypertension Intracellular chloride Myogenic tone Neuronal cell NKCC cotransport Smooth muscle

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Skeletal muscle as an endocrine organ:Role of[Na+]i/[K+]i-mediated excitation-transcription coupling

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Genes & Diseases 2015年第4期2卷 328-336页

作者： Leonid V.Kapilevich Tatyana A.Kironenko Anna N.Zaharova Yuri V.Kotelevtsev nickolai o.dulin Sergei N.orlov National Research Tomsk State University TomskRussia Skolkovo Institute of Science and Technology Moscow RegionRussia University of Chicago ILUSA Siberian Medical University TomskRussia M.V.Lomonosov Moscow State University MoscowRussia

During the last two decadesnumerous research teams demonstratedthat skeletalmuscles function as an exercise-dependent endocrine organ secreting dozens of *** of physiological and pathophysiological implications of skeletalmusclemyokines secretion has been described;however,upstream signals and sensing mechanisms underlying this phenomenon remain poorly *** is well documented that in skeletal muscles intensive exercise triggers dissipation of transmembrane gradient of monovalent cations caused by permanent activation of voltage-gated Nat and Kt ***,we demonstrated that sustained elevation of the[Nat]i/[Kt]i ratio triggers expression of dozens ubiquitous genes including several canonical myokines,such as interleukin-6 and cyclooxygenase 2,in the presence of intra-and extracellular Ca2t *** data allowed us to suggest a novel[Nat]i/[Kt]i-sensitive,Ca2t i-independent mechanism of excitation-transcription coupling which triggers myokine *** pathway exists in parallel with canonical signaling mediated by Ca2t i,AMP-activated protein kinase and hypoxia-inducible factor 1a(HIF-1a).In ourmini-reviewwe briefly summarize data supporting this hypothesis as well as unresolved issues aiming to forthcoming studies.

关键词： Myokines Secretion Skeletal muscle Transcription Translation

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