Aldosterone Induces Angiotensin-Converting-Enzyme Gene Expression in Cultured Neonatal Rat Cardiocytes

Harada, Eisaku; Yoshimura, Michihiro; Yasue, Hirofumi; Nakagawa, Osamu; Nakagawa, Masataka; Hara, Masaki; Mizuno, Yuji; Nakayama, Masafumi; Shimasaki, Yukio; Ito, Taeko; Nakamura, Shota; Kuwahara, Koichiro; Saito, Yoshihiko; Nakao, Kazuwa; Ogawa, Hisao

doi:10.1161/01.cir.104.2.137

Cited by 195 publications

(134 citation statements)

References 23 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…Aldosterone, as already mentioned, increases tissue ACE activity 45 and upregulates angiotensin receptors. 40 This suggests the potential for a vicious cycle in which Ang II, through the AT 1 receptor, stimulates the production of aldosterone, which, in turn, leads to an increase in tissue ACE activity, an additional increase in Ang II, and, therefore, an additional elevation in aldosterone levels.…”

Section: Integrative Molecular Physiology Of Vascular Effects Of Aldomentioning

confidence: 59%

“…[42][43][44] More recently, it has been demonstrated that aldosterone upregulates components of the renin-angiotensin system, specifically angiotensin-converting enzyme (ACE), resulting in increased local generation of Ang II (Figure 1). 45 Furthermore, aldosterone exerts direct effects on signaling in VSMCs, upregulating mitogen-activated protein (MAP) kinases. 46 -48 In salt-loaded stroke-prone spontaneously hypertensive rats (SHRSPs) fed high-(4.2%), normal-(0.28%), or low-salt (0.03%) diets with or without eplerenone, BP rise was prevented by eplerenone in the salt-loaded rats, with little effect on control and low-salt SHRSPs.…”

Section: Schiffrinmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Aldosterone on the Vasculature

2006

View full text Add to dashboard Cite

Section: Integrative Molecular Physiology Of Vascular Effects Of Aldomentioning

confidence: 59%

Section: Schiffrinmentioning

confidence: 99%

Effects of Aldosterone on the Vasculature

2006

View full text Add to dashboard Cite

“…A previous study indicated the existence of a positive feedback pathway from MR activation to ACE within the local cardiac renin-angiotensin-aldosterone system. 37 These results suggested the existence and the importance of local tissue regulation of the rennin-angiotensin-aldosterone system in the atrium. Further study is needed to clarify the mechanism of MR activation in DS rats.…”

Section: Discussionmentioning

confidence: 87%

Role of mineralocorticoid receptor on atrial structural remodeling and inducibility of atrial fibrillation in hypertensive rats

et al. 2011

View full text Add to dashboard Cite

Hypertension is well known to increase atrial fibrillation (AF) and the development of AF is associated with atrial chamber remodeling. Although mineralocorticoid receptor (MR) inhibition provides cardiovascular protection, the role of MR on atrial structural remodeling and inducibility of AF in hypertension remains unclear. Here, we investigated roles of the MR on atrial structural remodeling and inducibility of AF in hypertensive rats by using MR antagonist eplerenone (EPL). Dahl salt-sensitive (DS) rats were fed a normal-salt or a high-salt (HS) diet from 7 weeks, and a non-antihypertensive dose of EPL or vehicle was administrated from 13 weeks, at which time myocytes hypertrophy, interstitial fibrosis in the atrium and AF inducibility had increased, until 20 weeks. There was no significant difference in systolic blood pressure between DS+HS (186±4 mm Hg) and DS+HS+EPL (184±5 mm Hg) at 20 weeks. Burst atrial pacing demonstrated decreased AF inducibility in DS+HS+EPL (0 of 10) compared with DS+HS (7 of 10). Fibrosis and myocytes hypertrophy in the atrium were decreased in DS+HS+EPL with the reduction of atrial inflammatory cytokines. These beneficial effects of EPL were associated with less atrial oxidative stress, as assessed by 4-hydroxy-2-nonenal staining, and reduced activation of the Rho GTPase Rac1 in the atrium. Thus, MR has important roles in atrial structural remodeling and AF inducibility in Dahl rats. The effects of MR are associated, at least in part, with activation of Rac1-oxidative stress/inflammatory axis.

show abstract

“…Ang II induces aldosterone synthesis through stimulation of AT1 (Ang II type 1) receptors in the adrenal cortex. Aldosterone increases tissue ACE (angiotensin converting enzyme) activity and up-regulates angiotensin receptors [62], which suggests the existence of a vicious cycle that may potentiate the effect of the RAAS.…”

Section: Part II -Role Of the Renin-angiotensin-aldosterone System Onmentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

111

View full text Add to dashboard Cite

Abstract:The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosteron system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Recpetor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflmmatory effect of drugs bocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.

show abstract

Aldosterone Induces Angiotensin-Converting-Enzyme Gene Expression in Cultured Neonatal Rat Cardiocytes

Abstract: Aldosterone upregulates ACE mRNA expression, which is blocked by spironolactone in neonatal rat cardiocytes. Thus, spironolactone may suppress the progression of heart failure by blocking the effects of aldosterone and angiotensin II.

Cited by 195 publications

References 23 publications

Effects of Aldosterone on the Vasculature

Effects of Aldosterone on the Vasculature

Role of mineralocorticoid receptor on atrial structural remodeling and inducibility of atrial fibrillation in hypertensive rats

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Contact Info

Product

Resources

About