scholarly journals Animal Models to Study Links between Cardiovascular Disease and Renal Failure and Their Relevance to Human Pathology

2015 ◽  
Vol 6 ◽  
Author(s):  
Tim D. Hewitson ◽  
Stephen G. Holt ◽  
Edward R. Smith
Keyword(s):  
Cardiovascular Disease ◽  
Renal Failure ◽  
Animal Models ◽  
Human Pathology

Reno-protective mechanisms of epoxyeicosatrienoic acids in cardiovascular disease

2012 ◽  
Vol 302 (3) ◽  
pp. R321-R330 ◽  
Author(s):  
Ahmed A. Elmarakby
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Animal Models ◽  
Vascular Function ◽  
Organ Damage ◽  
Reduce Blood Pressure ◽  
Experimental Models ◽  
Epoxyeicosatrienoic Acids ◽  
Protective Effects ◽  
Protective Mechanisms

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, and it is well known that end-stage renal disease (ESRD) is a profound consequence of the progression of CVD. Present treatments only slow CVD progression to ESRD, and it is imperative that new therapeutic strategies are developed to prevent the incidence of ESRD. Because epoxyeicosatrienoic acids (EETs) have been shown to elicit reno-protective effects in hypertensive animal models, the current review will focus on addressing the reno-protective mechanisms of EETs in CVD. The cytochrome P-450 epoxygenase catalyzes the oxidation of arachidonic acid to EETs. EETs have been identified as endothelium-derived hyperpolarizing factors (EDHFs) with vasodilatory, anti-inflammatory, antihypertensive, and antiplatelet aggregation properties. EETs also have profound effects on vascular migration and proliferation and promote angiogenesis. The progression of CVD has been linked to decreased EETs levels, leading to the concept that EETs should be therapeutically targeted to prevent end-organ damage associated with CVD. However, EETs are quickly degraded by the enzyme soluble epoxide hydrolase (sEH) to their less active diols, dihydroxyeicosatrienoic acids (DHETs). As such, one way to increase EETs level is to inhibit their degradation to DHETs by using sEH inhibitors. Inhibition of sEH has been shown to effectively reduce blood pressure and organ damage in experimental models of CVD. Another approach to target EETs is to develop EET analogs with improved solubility and resistance to auto-oxidation and metabolism by sEH. For example, stable ether EET analogs dilate afferent arterioles and lower blood pressure in hypertensive rodent animal models. EET agonists also improve insulin signaling and vascular function in animal models of metabolic syndrome.

Do Current Animal Models of Intracerebral Hemorrhage Mirror the Human Pathology?

2010 ◽  
Vol 2 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Opeolu Adeoye ◽  
Joseph F. Clark ◽  
Pooja Khatri ◽  
Kenneth R. Wagner ◽  
Mario Zuccarello ◽  
...  
Keyword(s):  
Animal Models ◽  
Intracerebral Hemorrhage ◽  
Human Pathology

Renal Effects of 1,4-Dihydropyridines in Animal Models of Hypertension and Renal Failure

1987 ◽  
Vol 9 ◽  
pp. S8-S13 ◽  
Author(s):  
B. Garthoff ◽  
C. Hirth ◽  
A. Federmann ◽  
S. Kazda ◽  
J.-P. Stasch
Keyword(s):  
Renal Failure ◽  
Animal Models ◽  
Renal Effects

Abstract 15642: Race Sex Disparities in Atherosclerotic Cardiovascular Disease in Hospitalized Patients With Diabetes, 2005-2015 Potential Warning Signs for Future U.S. Public Health

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Gursukhman Sidhu ◽  
Charisse J Ward ◽  
Keith Ferdinand
Keyword(s):  
Cardiovascular Disease ◽  
Renal Failure ◽  
Black Women ◽  
Black Men ◽  
Odds Ratio ◽  
White Men ◽  
The United States ◽  
Atherosclerotic Cardiovascular Disease ◽  
Secondary Diagnosis ◽  
The U.S

Introduction: Despite a recent gradually slowing and perhaps recent increase in the burden of atherosclerotic cardiovascular disease (ASCVD) related hospitalization in the United States population with diabetes, it is unclear whether the prior downward trend was uniform or there was an unbalanced division amongst sex and race. Methods: Adults aged ≥40 years old with comorbid diabetes as a secondary diagnosis were identified using the U.S. 2005-2015 National (Nationwide) Inpatient Sample (NIS) data. The prevalence of other modifiable cardiovascular risk factors (hypertension, dyslipidemia, smoking/substance abuse, obesity, and renal failure), procedures like major amputations in the secondary diagnosis field and their association with ASCVD (acute coronary syndrome (ACS), coronary artery disease (CAD), stroke, or peripheral arterial disease (PAD)) as the first-listed diagnosis were determined. Complex samples multivariate regression was used to determine the odds ratio (O.D.) with 95% confidence limits (C.L.s). Sex and race risk-adjusted ASCVD related in-hospital mortality rates were estimated. Results: The rate of total ASCVD hospitalizations adjusted to the U.S. census population increased by 5.7% for black men compared to 4% for black women cumulatively compared to a stable downtrend in white men and white women. There was a higher odd of an ASCVD hospitalizations if there was comorbid hypertension (Odds Ratio (OR 1.29; 95% Confidence Interval (CI) 95% 1.28 - 1.31), dyslipidemia (OR 2.03; 95% CI 2.01 - 2.05), renal failure (OR 1.84; 95% CI 1.82 - 1.86), and smoking/substance use disorder (OR 1.31; 95% CI 1.29 - 1.33). When compared to white men, black men (OR 1.43; 95% CI 1.3 - 1.57) and black women (OR 1.15; 95% CI 1.04 - 1.27) had a higher likelihood of undergoing a major limb amputation during an ASCVD hospitalization. Conclusions: Blacks with diabetes continue to have a higher hospitalizations burden with a concomitant disparity in procedures and outcomes.

Roles of metabolic and endocrinological alterations in atherosclerosis and cardiovascular disease in renal failure: Another form of metabolic syndrome

2004 ◽  
Vol 24 (5) ◽  
pp. 423-425 ◽  
Author(s):  
Yoshiki Nishizawa ◽  
Tetsuo Shoji ◽  
Masanori Emoto ◽  
Hideki Koyama ◽  
Hideki Tahara ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Renal Failure

scholarly journals Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jeanie Park
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Nervous System ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Renal Disease ◽  
Left Ventricular ◽  
Sympathetic Nervous

Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications.

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