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Renin overexpression leads to increased titin-based stiffness contributing to diastolic dysfunction in hypertensive mRen2 rats.

Am. J. Physiol. Heart Circ. Physiol.. 2016; 
KovácsÁrpád,FülöpGábor Á,KovácsAndrea,CsípőTamás,BódiBeáta,PrikszDániel,JuhászBéla,BekeLívia,HendrikZoltán,MéhesGábor,GranzierHenk L,ÉdesIstván,FagyasMiklós,PappZoltán,BartaJudit,TóthAt
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摘要

Hypertension (HTN) is a major risk factor for heart failure. We investigated the influence of HTN on cardiac contraction and relaxation in transgenic renin overexpressing rats (carrying mouse Ren-2 renin gene, mRen2, n = 6). Blood pressure (BP) was measured. Cardiac contractility was characterized by echocardiography, cellular force measurements, and biochemical assays were applied to reveal molecular mechanisms. Sprague-Dawley (SD) rats (n = 6) were used as controls. Transgenic rats had higher circulating renin activity and lower cardiac angiotensin-converting enzyme two levels. Systolic BP was elevated in mRen2 rats (235.11 ± 5.32 vs. 127.03 ± 7.56 mmHg in SD, P < 0.05), resulting in increased l... More

关键词

RAAS,diastolic dysfunction,hypertension,passive stiffness,renin-angiotensin-aldosterone system,titin phosphoryla
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