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RAASRenin-Angiotensin-Aldosterone System
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References in periodicals archive ?
Dudley Jr, "The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias," Heart Rhythm, vol.
When Vitamin D is sufficient, the Vitamin D receptor would bind to the ligand site of the c-AMP response element binding protein and occupy the binding site, thereby blocking their binding and activation of downstream gene promoters.[19] To study whether the regulation of the renin-angiotensin-aldosterone system by 1,25(OH)[sub]2D[sub]3 was dependent on calcium-phosphorus metabolism, Zhou et al .
Wang et al., "Renin-angiotensin system blockade for the risk of cancer and death," Journal of the Renin-Angiotensin-Aldosterone System, vol.
The reduction in effective arterial blood volume caused by heart failure, kidney disease or severe hypoproteinemia, activates the renin-angiotensin-aldosterone system. This physiological response is called secondary hyperaldosteronism or hyperreninemic hyperaldosteronism (DJAJADININGRAT-LAANEN et al., 2011).
Abbreviations AKI: Acute kidney Injury APK: Acute Page Kidney RAAS: Renin-angiotensin-aldosterone system HTN: Hypertension.
Regarding antihypertensive drug selection, the new statement endorses a focus on treating hypertensive patients with established coronary artery disease with a beta-blocker, a renin-angiotensin-aldosterone system blocker such as an ACE inhibitor or angiotensin-receptor blocker, and a thiazide or thiazide-like diuretic.
Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension.
Among the predisposing genetic factors, renin-angiotensin-aldosterone system (RAAS) disruption is clearly involved in ESRD development [3].
ACE-Is act by inhibiting the renin-angiotensin-aldosterone system (RAAS), specifically the conversion of angiotensin-I to angiotensin-II, thereby causing vasodilatation of the efferent renal arterioles and thus decreasing the intraglomerular pressures [17].
However the role of renin-angiotensin-aldosterone system (RAAS) blocking agents, angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) in the pathophysiology of CIN remains controversial, as the available literature is conflicted and discordant.