Hypertension in Cardiovascular and Kidney Disease

Botdorf, Joshua; Chaudhary, Kunal; Whaley‐Connell, Adam

doi:10.1159/000329927

Cited by 50 publications

(39 citation statements)

References 102 publications

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“…1 The relationship between HTN and CKD is cyclic in nature. Uncontrolled HTN is a risk factor for developing CKD, is associated with a more rapid progression of CKD, and is the second leading cause of ESRD in the U.S. 2 Meanwhile, progressive renal disease can exacerbate uncontrolled HTN due to volume expansion and increased systemic vascular resistance. Multiple guidelines discuss the importance of lowering blood pressure (BP) to slow the progression of renal disease and reduce cardiovascular morbidity and mortality.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress and Antioxidant Enzyme levels In Hypertensive Chronic Kidney Disease patients

Kachhawa

Varma

Sahu

et al. 2014

Int J of Biomed & Adv Res

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Section: Introductionmentioning

confidence: 99%

Oxidative stress and Antioxidant Enzyme levels In Hypertensive Chronic Kidney Disease patients

Kachhawa

Varma

Sahu

et al. 2014

Int J of Biomed & Adv Res

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“…Pharmacologic intervention targeting renin-angiotensin-aldosterone system (RAAS) interruption has been shown to slow progression of heart failure [1,2]. However, these anti-hypertensive strategies only attenuate heart failure morbidity and mortality across trials which suggest a significant remaining amount of residual risk for heart disease [3,4].…”

Section: Introductionmentioning

confidence: 99%

Renin Inhibition and AT1R blockade improve metabolic signaling, oxidant stress and myocardial tissue remodeling

et al. 2013

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Objective Strategies that block angiotensin II actions on its angiotensin type 1 receptor or inhibit actions of aldosterone have been shown to reduce myocardial hypertrophy and interstitial fibrosis in states of insulin resistance. Thereby, we sought to determine if combination of direct renin inhibition with angiotensin type 1 receptor blockade in vivo, through greater reductions in systolic blood pressure (SBP) and aldosterone would attenuate left ventricular hypertrophy and interstitial fibrosis to a greater extent than either intervention alone. Materials/Methods We utilized the transgenic Ren2 rat which manifests increased tissue expression of murine renin which, in turn, results in increased renin-angiotensin system activity, aldosterone secretion and insulin resistance. Ren2 rats were treated with aliskiren, valsartan, the combination (aliskiren+valsartan), or vehicle for 21 days. Results Compared to Sprague-Dawley controls, Ren2 rats displayed increased systolic blood pressure, elevated serum aldosterone levels, cardiac tissue hypertrophy, interstitial fibrosis and ultrastructural remodeling. These biochemical and functional alterations were accompanied by increases in the NADPH oxidase subunit Nox2 and 3-nitrotyrosine content along with increases in mammalian target of rapamycin and reductions in protein kinase B phosphorylation. Combination therapy contributed to greater reductions in systolic blood pressure and serum aldosterone but did not result in greater improvement in metabolic signaling or markers of oxidative stress, fibrosis or hypertrophy beyond either intervention alone. Conclusions Thereby, our data suggest that the greater impact of combination therapy on reductions in aldosterone does not translate into greater reductions in myocardial fibrosis or hypertrophy in this transgenic model of tissue renin overexpression.

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“…Hypertension is the second leading cause of end stage renal disease (ESRD) in the United States following diabetes 1 . In 2009, more than half a million people in the U.S. had ESRD, with nearly 400,000 on dialysis and over 17,000 with kidney transplants 2 .…”

mentioning

confidence: 99%