Regulation of cardiac and renal mineralocorticoid receptor expression by captopril following myocardial infarction in rats

Resende, Micheline; Kauser, Katalin; Mill, José Geraldo

doi:10.1016/j.lfs.2005.12.011

Cited by 23 publications

(17 citation statements)

References 39 publications

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“…ACE activity increases in all regions of the infarcted heart, particularly in the scar tissue, leading to high local Ang II concentrations (27,30). ACE inhibition in infarcted rats reduces mortality, attenuates reactive fibrosis and myocyte hypertrophy and prevents HF development (16,26,30,31). In agreement, expression of AT 1 receptors is enhanced during the postinfarction period, being highly detected just 3 days after coronary occlusion (29).…”

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 90%

“…Angiotensinogen is produced in infarcted hearts mainly by macrophages and fibroblasts, and ACE is extensively synthesized in endothelial cells and macrophages (29). ACE activity increases in all regions of the infarcted heart, particularly in the scar tissue, leading to high local Ang II concentrations (27,30). ACE inhibition in infarcted rats reduces mortality, attenuates reactive fibrosis and myocyte hypertrophy and prevents HF development (16,26,30,31).…”

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

“…In fact, in a mouse model with cardiac overexpression of Ang II, fibrosis was spontaneously observed in transgenic animals, showing that Ang II can act locally independently of hemodynamic effects (33). Moreover, infarction caused an upregulation of mineralocorticoid receptor expression in the left ventricle (30). This increase, which was associated with increased aldosterone production, contributed to harmful collagen proliferation in the overall myocardium, including the right ventricle free wall.…”

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

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Remodeling in the ischemic heart: the stepwise progression for heart

Mill¹,

Stefanon

Santos

et al. 2011

Braz J Med Biol Res

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Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.

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Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 90%

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

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Remodeling in the ischemic heart: the stepwise progression for heart

Mill¹,

Stefanon

Santos

et al. 2011

Braz J Med Biol Res

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“…Previous studies that addressed this issue compared DE parameters to non-simultaneously obtained invasive hemodynamic data at a chronic stage after MI (9-12). The importance of LV function analysis soon after MI is emphasized by the fact that in many studies using this model the experimental drug was started as early as 2 days after surgery (4,5,19). Therefore, the present study provides important information permitting selection of animals with recent MI and severe LV dysfunction, expressed as elevated LVEDP, yielding randomization of homogenous populations before the start of the experimental therapy to be evaluated.…”

Section: Discussionmentioning

confidence: 97%

“…Experimentally induced myocardial infarction (MI) in rats is commonly used as a heart failure (HF) model in a variety of settings, such as the study of pathophysiology (1,2) or the evaluation of experimental drugs (3)(4)(5), and non-drug therapies such as stem cells (6,7). However, this model displays a wide variation in infarct size (1), leading to a wide range of left ventricular (LV) function impairment (1,8).…”

Section: Introductionmentioning

confidence: 99%

Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction

Saraiva¹,

Kanashiro‐Takeuchi²,

Antônio³

et al. 2007

Braz J Med Biol Res

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The severity of left ventricular (LV) dysfunction in rats with myocardial infarction (MI) varies widely. Because homogeneity in baseline parameters is essential for experimental investigations, a study was conducted to establish whether Doppler echocardiography (DE) could accurately identify animals with high LV end-diastolic pressure as a marker of LV dysfunction soon after MI. Direct measurements of LV end-diastolic pressure were made and DE was performed simultaneously 1 week after surgically induced MI (N = 16) or shamoperation (N = 17) in female Wistar rats (200 to 250 g). The ratio of peak early (E) to late (A) diastolic LV filling velocities and the ratio of E velocity to peak early (E m ) diastolic myocardial velocity were the best predictors of high LV end-diastolic pressure (>12 mmHg) soon after MI. Cut-off values of 1.77 for the E/A ratio (P = 0.001) identified rats with elevated LV end-diastolic pressure with 90% sensitivity and 80% specificity. Cut-off values of 20.4 for the E/E m ratio (P = 0.0001) identified rats with elevated LV end-diastolic pressure with 81.8% sensitivity and 80% specificity. Moreover, E/A and E/E m ratios were the only echocardiographic parameters independently associated with LV end-diastolic pressure in multiple linear regression analysis. Therefore, DE identifies rats with high LV end-diastolic pressure soon after MI. These findings have implications for using serial DE in animal selection and in the assessment of their response to experimental therapies.

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Compromised regulation of the collecting duct ENaC activity in mice lacking AT_1a receptor

Mamenko

Zaika

Tomilin

et al. 2018

Journal Cellular Physiology

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ENaC-mediated sodium reabsorption in the collecting duct (CD) is a critical determinant of urinary sodium excretion. Existing evidence suggest direct stimulatory actions of Angiotensin II (Ang II) on ENaC in the CD, independently of the aldosterone-mineralocorticoid receptor (MR) signaling. Deletion of the major renal AT receptor isoform, AT R, decreases blood pressure and reduces ENaC abundance despite elevated aldosterone levels. The mechanism of this insufficient compensation is not known. Here, we used patch clamp electrophysiology in freshly isolated split-opened CDs to investigate how AT R dysfunction compromises functional ENaC activity and its regulation by dietary salt intake. Ang II had no effect on ENaC activity in CDs from AT R -/- mice suggesting no complementary contribution of AT receptors. We next found that AT R deficient mice had lower ENaC activity when fed with low (<0.01% Na ) and regular (0.32% Na ) but not with high (∼2% Na ) salt diet, when compared to the respective values obtained in Wild type (WT) animals. Inhibition of AT R with losartan in wild-type animals reproduces the effects of genetic ablation of AT R on ENaC activity arguing against contribution of developmental factors. Interestingly, manipulation with aldosterone-MR signaling via deoxycosterone acetate (DOCA) and spironolactone had much reduced influence on ENaC activity upon AT R deletion. Consistently, AT R -/- mice have a markedly diminished MR abundance in cytosol. Overall, we conclude that AT R deficiency elicits a complex inhibitory effect on ENaC activity by attenuating ENaC P and precluding adequate compensation via aldosterone cascade due to decreased MR availability.

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Regulation of cardiac and renal mineralocorticoid receptor expression by captopril following myocardial infarction in rats

Cited by 23 publications

References 39 publications

Remodeling in the ischemic heart: the stepwise progression for heart

Remodeling in the ischemic heart: the stepwise progression for heart

Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction

Compromised regulation of the collecting duct ENaC activity in mice lacking AT_1a receptor

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Regulation of cardiac and renal mineralocorticoid receptor expression by captopril following myocardial infarction in rats

Cited by 23 publications

References 39 publications

Remodeling in the ischemic heart: the stepwise progression for heart

Remodeling in the ischemic heart: the stepwise progression for heart

Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction

Compromised regulation of the collecting duct ENaC activity in mice lacking AT1a receptor

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Compromised regulation of the collecting duct ENaC activity in mice lacking AT_1a receptor