Effect of Male Sex and Obesity on Platelet Arachidonic Acid in Spontaneous Hypertensive Heart Failure Rats

Park, Sonhee C.; Liu-Stratton, Yiwen; Medeiros, Lydia C.; McCune, Sylvia A.; Radin, M. Judith

doi:10.1177/153537020422900710

Cited by 5 publications

(3 citation statements)

References 65 publications

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“…The time for the development of HF depends on facp gene dosage and gender (male animals are more prone to HF than females [96]) but, in general, SHHF rats present HF earlier than the SHR strain, with loss of cardiac function starting at the age of 15 months [100]. These animals present alterations in the renin-angiotensin-aldosterone system (RAAS) and also in calcium metabolism [82,107,188,222]. The greatest advantage of this strain is the possibility of studying drug interventions in an extended range of cardiovascular risk factors like obesity, diabetes and renal dysfunction [259].…”

Section: Spontaneously Hypertensive Hf-prone Rats (Shhf)mentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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Heart failure (HF) is one of the major health and economic burdens worldwide, and its prevalence is continuously increasing. The study of HF requires reliable animal models to study the chronic changes and pharmacologic interventions in myocardial structure and function and to follow its progression toward HF. Indeed, during the past 40 years, basic and translational scientists have used small animal models to understand the pathophysiology of HF and find more efficient ways of preventing and managing patients suffering from congestive HF (CHF). Each species and each animal model has advantages and disadvantages, and the choice of one model over another should take them into account for a good experimental design. The aim of this review is to describe and highlight the advantages and drawbacks of some commonly used HF rodents models, including both non-genetically and genetically engineered models, with a specific subchapter concerning diastolic HF models.

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Section: Spontaneously Hypertensive Hf-prone Rats (Shhf)mentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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“…Heart, left ventricle plus interventricular septum (LVS), right ventricle (RV), left atria (LA), right atria (RA), and brain were weighed. Because of the marked difference in body fat mass between lean and obese SHHF, the ratio of organ weight to brain weight was calculated as an index of organ to lean body weight (20). Brain weight is correlated with lean body mass and tibial length in SHHF rats (R = 0.92, p < 0.05, personal communication, S. McCune), is easy to measure and reproducible.…”

Section: Methodsmentioning

confidence: 99%

Salt-Induced Cardiac Hypertrophy Is Independent of Blood Pressure and Endothelin in Obese, Heart Failure-Prone SHHF Rats

Radin

Holycross

Hoepf

et al. 2008

Clinical and Experimental Hypertension

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The interaction of salt sensitivity and obesity in development of cardiac hypertrophy is incompletely understood. The SHHF/Mcc-fa(cp) (SHHF) rat model was used to examine the effect of high salt on cardiac hypertrophy and expression of endothelin (ET) and nitric oxide synthase (NOS) isoforms. Homozygous lean (+/+) and obese (fa(cp)/fa(cp)) SHHF were fed a low-salt diet (0.3% NaCl) for seven days followed by a high-salt diet (8.0% NaCl) for seven days. To assess the role of ET in mediating cardiac hypertrophy and gene expression with high salt, additional groups were treated with an ET(A)/ET(B) receptor antagonist (bosentan) while on high salt. Obese SHHF showed an increase in systolic blood pressure and cardiac hypertrophy in response to the high-salt diet. High salt resulted in decreased expression of preproET as well as all three NOS isoforms in the Obese, while cytokine induced NOS (iNOS) and neuronal NOS (nNOS) increased in Leans. Though the salt-sensitive component of the hypertension observed in the Obese was prevented by bosentan, cardiac hypertrophy still occurred and expression of all NOS isoforms remained lower in Obese compared to Lean. Endothelial NOS (eNOS) expression increased in the Lean with bosentan. These studies suggest that cardiac hypertrophy is independent of the level of hypertension and may be mediated by altered production of NOS isoforms in salt-sensitive, obese SHHF.

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“…When compared to SHR rats, SHHF rats would have suffer from HF earlier with loss of cardiac function begins at age of 15 months (Heyen et al, 2002). And similar to SHRs, male animals are more likely to suffer from HF than female animals (Park, Liu-Stratton, Medeiros, Mccune, & Radin, 2004). During the same period SHR rat emerged, a model of salt sensitivity, namely the Dahl-salt-sensitive (DS) rat was also developed, characterized by susceptibility to develop different degrees of hypertension depending on the variations in sodium intake (Dahl, Heine, & Tassinari, 1962).…”

Section: Transgenic Animal Modelsmentioning

confidence: 99%

Insights in animal models for translational cardiovascular research：A pharmaceutical industry perspective

Cao

et al. 2021

Preprint

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The pathological mechanisms involved in Heart failure (HF) are complex and remain controversial. Caused by a variety of predisposing and exacerbating factors for HF development, the selection of animal models in current preclinical R&D has been a major challenge. In this review, we give a comprehensive overview of different models in various species currently used in HF research, and discuss their general applicability. In addition, we summarize the preclinical research review of approved drugs for HF, which provides theoretical and practical guidance for researchers considering preclinical studies for the treatment of HF.

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Effect of Male Sex and Obesity on Platelet Arachidonic Acid in Spontaneous Hypertensive Heart Failure Rats

Cited by 5 publications

References 65 publications

Rodent models of heart failure: an updated review

Rodent models of heart failure: an updated review

Salt-Induced Cardiac Hypertrophy Is Independent of Blood Pressure and Endothelin in Obese, Heart Failure-Prone SHHF Rats

Insights in animal models for translational cardiovascular research：A pharmaceutical industry perspective

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