Preserved regulation of renal perfusion pressure by small and intermediate conductance KCa channels in hypertensive mice with or without renal failure
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  • 作者：Ludovic Waeckel (1) (2)
    Florence Bertin (1)
    Nicolas Clavreul (1)
    Thibaut Damery (1)
    Ralf K枚hler (3) (4)
    J茅r么me Paysant (1)
    Patricia Sansilvestri-Morel (1)
    Serge Simonet (1)
    Christine Vayssettes-Courchay (1)
    Heike Wulff (5)
    Tony J. Verbeuren (1)
    Michel F茅l茅tou (1)

    1. Unit茅 de Recherches et de D茅couvertes Cardiovasculaires     ; Institut de Recherches Servier ; 11 rue des Moulineaux ; 92150 ; Suresnes ; France
    2. Centre de Recherche des Cordeliers     ; Inserm UMRS 872 ; Paris ; France
    3. Cardiovascular and Renal Research     ; IMM ; University of Southern and Denmark ; Odense ; Denmark
    4. Aragon Institute of Health Sciences-I + CS and ARAID     ; Zaragoza ; Spain
    5. Department of Pharmacology     ; University of California ; Davis ; CA ; 95616 ; USA
  • 关键词：Calcium ; activated potassium channels ; Endothelium ; dependent vasodilatation ; Endothelium ; dependent hyperpolarization ; Hypertension ; Kidney disease ; SKA ; 31
  • 刊名：Pfl篓鹿gers Archiv - European Journal of Physiology
  • 出版年：2015
  • 出版时间：April 2015
  • 年：2015
  • 卷：467
  • 期：4
  • 页码：817-831
  • 全文大小：4,395 KB
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  • 刊物主题：Human Physiology;
  • 出版者：Springer Berlin Heidelberg
  • ISSN：1432-2013
文摘
The purpose of this study was to assess, in the murine kidney, the mechanisms underlying the endothelium-dependent control of vascular tone and whether or not, in a severe model of hypertension and renal failure, KCa channels contribute to its regulation. Wild-type (BL) and double-transgenic female mice expressing human angiotensinogen and renin (AR) genes received either control or a high-salt diet associated to a nitric oxide (NO) synthase inhibitor treatment (BLSL and ARSL). Changes in renal perfusion pressure (RPP) were measured in isolated perfused kidneys. BLSL and AR were moderately hypertensive without kidney disease while ARSL developed severe hypertension and renal failure. In the four groups, methacholine induced biphasic endothelium-dependent responses, a transient decrease in RPP followed by a cyclooxygenase-dependent increase in RPP. In the presence or not of indomethacin, the vasodilatations were poorly sensitive to NO synthase inhibition. However, in the presence of cyclooxygenase and NO synthase inhibitors, apamin, and/or TRAM-34, blockers of KCa2.3 and KCa3.1, respectively, abolished the decrease in RPP in response to either methacholine or the two activators of KCa2.3/KCa3.1, NS309, and SKA-31. Thus, KCa2/3 channels play a major role in the regulation of murine kidney perfusion and this mechanism is maintained in hypertension, even when severe and associated with kidney damage.

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