S Hojna

Summary

Affiliation: Charles University
Country: Czech Republic

Publications

  1. ncbi request reprint Alterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension
    S Hojna
    Cardiovascular Research Center, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
    Physiol Res 59:997-1009. 2010
  2. ncbi request reprint Age-dependent salt hypertension in Dahl rats: fifty years of research
    J Zicha
    Centre for Cardiovascular Research, Prague, Czech Republic
    Physiol Res 61:S35-87. 2012
  3. ncbi request reprint Apolipoprotein A5 and hypertriglyceridemia in Prague hypertriglyceridemic rats
    M Kadlecov√°
    Institute of Physiology AS CR and Cardiovascular Research Center, Prague, Czech Republic
    Physiol Res 55:373-9. 2006

Collaborators

Detail Information

Publications3

  1. ncbi request reprint Alterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension
    S Hojna
    Cardiovascular Research Center, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
    Physiol Res 59:997-1009. 2010
    ..Decreased nNOS expression was associated with increased blood pressure due to enhanced sympathetic tone...
  2. ncbi request reprint Age-dependent salt hypertension in Dahl rats: fifty years of research
    J Zicha
    Centre for Cardiovascular Research, Prague, Czech Republic
    Physiol Res 61:S35-87. 2012
    ..On the contrary, moderate salt hypertension in adult Dahl rats is attenuated by superoxide scavenging or endothelin-A receptor blockade which do not affect salt hypertension development in young animals...
  3. ncbi request reprint Apolipoprotein A5 and hypertriglyceridemia in Prague hypertriglyceridemic rats
    M Kadlecov√°
    Institute of Physiology AS CR and Cardiovascular Research Center, Prague, Czech Republic
    Physiol Res 55:373-9. 2006
    ..The absence of significant changes in Apoa5 gene expression during chronic fructose-induced TG elevation excludes its major role in mechanisms compensating severe hypertriglyceridemia...