Evaluation of the renin-angiotensin system in cardiac tissues of cats with pressure-overload cardiac hypertrophy

Uechi, Masami; Tanaka, Yoshiyuki; Aramaki, Yoshitaka; Hori, Yuichi; Ishikawa, Yojiro; Ebisawa, Takashi; Yamano, Shigeki

doi:10.2460/ajvr.69.3.343

Cited by 12 publications

(7 citation statements)

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“…In humans, differences in the clinical efficacy of ACEI has been hypothesized to be associated with variation in tissue‐ACE affinity and this might also hold true for dogs and cats. Chymase has a greater catalytic efficiency than ACE and is thought to serve as the primary generator of AngII in the tissues however, and likely contributes to apparent inefficacy of ACEI . Additional explanations for the sporadic failure of ACEI to prevent abnormal remodeling as a class include inadequate aldosterone suppression (aldosterone breakthrough), underdosing, and poor compliance.…”

Section: Suppression Of Raasmentioning

confidence: 99%

The renin‐angiotensin‐aldosterone system and its suppression

Ames

Atkins

Pitt

2019

Veterinary Internal Medicne

300

264

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Chronic activation of the renin‐angiotensin‐aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro‐fibrotic, ‐inflammatory, and ‐hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.

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Section: Suppression Of Raasmentioning

confidence: 99%

The renin‐angiotensin‐aldosterone system and its suppression

Ames

Atkins

Pitt

2019

Veterinary Internal Medicne

300

264

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“…Ang II, especially when it is expressed locally, is a crucial mediator of pressure overload-induced cardiac hypertrophy (Lachance et al 2008;Uechi et al 2008;Kumar et al 2008). Local activation of intracardiac RAS results in increased levels of Ang II in the heart, which indu- In cardiac tissue of the AC group, ROS levels increased and GSH/GSSG ratio decreased relative to SO animals.…”

Section: Discussionmentioning

confidence: 95%

Apocynin attenuates pressure overload-induced cardiac hypertrophy in rats by reducing levels of reactive oxygen species

Liu

Zhou

et al. 2010

Can. J. Physiol. Pharmacol.

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It has been shown that angiotensin II (Ang II) is involved in cardiac remodeling mediated by NADPH oxidase-dependent reactive oxygen species (ROS). Accordingly, NADPH oxidase-dependent ROS may play a role in cardiac hypertrophy induced by pressure overload. In the present study, we sought to determine whether inhibition of NADPH oxidase prevents cardiac hypertrophy. After abdominal aorta banding to induce cardiac hypertrophy, rats were treated for 8 weeks with apocynin (Apo) or captopril (Cap). Measures of cardiac hypertrophy were evaluated. Treatment with Cap or Apo reduced the left ventricle/body weight ratio (LV/BW), LV transnuclear myocyte diameter, and atrial natriuretic factor (ANF) mRNA expression relative to those of untreated rats subjected to aorta banding. The activity of NADPH oxidase and the ROS levels were decreased in treated animals. Cap, but not Apo, decreased Ang II levels and inhibited expression of p22phox and p67phox in LVs. In conclusion, local expression of Ang II appears to contribute to pressure overload-induced cardiac hypertrophy by upregulating NADPH oxidase expression and promoting ROS synthesis. Inhibition of NADPH oxidase and elimination of ROS may prevent or repair damage due to cardiac hypertrophy.

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“…Dogs with MMVD, as opposed to DCM, do not suffer the same decline in forward stroke volume (and forward cardiac output), which could be one reason for the difference in RAAS response between diseases. The formation of ANG II in the heart is mediated by a local RAAS, acting independently of the circulating RAAS, and is upregulated by haemodynamic wall stress [83]. Nevertheless, urinary aldosterone concentration has recently been shown to increase with increasing heart dimensions in dogs with MMVD, indicating an association between aldosterone and degree of cardiac remodelling (eccentric hypertrophy and dilatation) [81].…”

Section: The Renin-angiotensin-aldosterone System and Endothelin-1 Asmentioning

confidence: 99%

Cardiovascular endocrinology in naturally occurring canine and feline models

Häggström¹,

Ljungvall²,

Höglund

2014

Cardiovascular Endocrinology

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Rodents are frequently used to study aspects of cardiovascular endocrinology. The present review focuses on opportunities offered by naturally occurring heart disease in dogs and cats, that is larger animal models. In particular, the benefits of using these species include the possibility of studying the same types of naturally occurring diseases as those occurring in humans, and carrying out studies in genetically similar individuals (i.e. breeds) sharing the same environment as humans. Recent findings in neuroendocrine hormones, that is natriuretic peptides, components of the renin-angiotensinaldosterone system, and endothelin-1, in dogs and cats are reviewed in this article. As in humans, all these hormones have been evaluated as cardiovascular biomarkers in dogs and cats, and natriuretic peptides have shown promise in the diagnosis, staging and prognostication of heart disease. However, components of the renin-angiotensin-aldosterone system and endothelin-1 appear to be more useful as functional biomarkers for monitoring compensatory responses to naturally occurring heart diseases and their treatments.Percent of angiotensin II (ANG II) formation from angiotensinconverting enzyme (ACE) and chymase in hearts from multiple species showing that more than 90% of ANG II formation was from chymase in dogs and humans, whereas more than 90% was from ACE in rat, mouse and rabbit. The green bar indicates chymase and the yellow bar represents ACE. From Dell'Italia [8] with permission from publisher.Neuroendocrines in canine and feline models Hä ggströ m et al. 33

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Evaluation of the renin-angiotensin system in cardiac tissues of cats with pressure-overload cardiac hypertrophy

Abstract: Chronic pressure overload on the heart of cats can activate the RA system in cardiac tissues. A local increase in angiotensin II was one of the factors that sustained myocardial remodeling.

Cited by 12 publications

References 50 publications

The renin‐angiotensin‐aldosterone system and its suppression

The renin‐angiotensin‐aldosterone system and its suppression

Apocynin attenuates pressure overload-induced cardiac hypertrophy in rats by reducing levels of reactive oxygen species

Cardiovascular endocrinology in naturally occurring canine and feline models

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