作者: Sung-Moon Kim , Ji-One Kang , Ji Eun Lim , Sue-Yun Hwang , Bermseok Oh
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摘要: BACKGROUND Blood pressure is regulated by a network of diverse physiological pathways. The C-terminal Src kinase (CSK) locus (15q24) associated with blood in various ethnic groups. It was recently reported thatCskinsufficiency increases through Src. mechanisms hypertension inCsk+/-mice are examined further this study.Methods and Results:To identify causal component responsible for inCsk+/-, the heart rate measured electrocardiogram and plasma volume Evans blue dilution. Plasma increased inCsk+/-compared wild-types, while did not change. sodium aldosterone levels rose consistently inCsk+/-vs. spironolactone, mineralocorticoid receptor antagonist, reduced pressure. amounts Sgk1 Na+/K+-ATPase (NKA) kidney ofCsk+/-compared wild-types. also found that Cyp11b2 (aldosterone synthase) upregulated adrenal glands ofCsk+/-, Csk enriched zona glomerulosa adrenals, major site production normal mouse. CONCLUSIONS results present study pathway which regulated, insufficiency ofCskinduces zonal specificity glands, increasing reabsorption thus resulting hypertension.