Aldosterone Nongenomically Produces NADPH Oxidase−Dependent Reactive Oxygen Species and Induces Myocyte Apoptosis

Hayashi, Hironori; Kobara, Miyuki; Abe, Masaki; Tanaka, N; Gouda, Eri; Toba, Hiroe; Yamada, Hiroyuki; Tatsumi, Tomohide; Nakata, Tetsuo; Matsubara, Hiroaki

doi:10.1291/hypres.31.363

Cited by 101 publications

(89 citation statements)

References 52 publications

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“…NADPH oxidase is one of the major sources of aldosterone-induced ROS production in renal cells (19,23,39). In agreement with this, we observed that NADPH oxidase activation leads to aldosterone-mediated Nrf2 activation.…”

Section: Discussionsupporting

confidence: 89%

Aldosterone Activates Transcription Factor Nrf2 in Kidney Cells both In Vitro and In Vivo

Queisser¹,

Oteiza²,

Hey³

et al. 2013

Free Radical Biology and Medicine

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Section: Discussionsupporting

confidence: 89%

Aldosterone Activates Transcription Factor Nrf2 in Kidney Cells both In Vitro and In Vivo

Queisser¹,

Oteiza²,

Hey³

et al. 2013

Free Radical Biology and Medicine

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“…Likewise, TNFα-induced apoptosis of cultured mouse cardiomyocytes was reported to involve an NOS/NADPH oxidase-dependent, peroxynitrite-mediated signaling pathway [75]. In neonatal rat cardiomyocytes, aldosterone was shown to induce apoptosis by activating NADPH oxidase-mediated O2−radical dot production and ASK-1 [76]. Collectively, these studies suggest that NADPH oxidase-derived ROS may play a role in cardiomyocyte apoptosis in response to a number of pathogenic stimuli.…”

Section: Apoptosismentioning

confidence: 89%

NADPH oxidase signaling and cardiac myocyte function

Akki

Zhang

Murdoch

et al. 2009

Journal of Molecular and Cellular Cardiology

124

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“…36 It was suggested that some effects of salt loading might depend on MR activation occurring as a consequence of increased generation of reactive oxygen species. 37 It has been shown that aldosterone affects intracellular redox potential in myocytes, 38 an effect that is potentiated by exposure to high concentrations of salt, 39 leading to increased production of reactive oxygen species and thereby to tissue damage. Therefore, the effects of salt might depend, at least in part, on MR activation providing a possible explanation for the interaction with aldosterone.…”

Section: Discussionmentioning

confidence: 99%

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

et al. 2016

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Primary aldosteronism is associated with increased left ventricular (LV) mass independently of blood pressure. Previous studies suggest that elevated aldosterone causes cardiac damage only in the presence of an inappropriate salt status. We examined the relevance of dietary salt intake on cardiac changes in patients with primary aldosteronism before and after treatment. Sixty-five patients with tumoral or idiopathic primary aldosteronism were recruited at a University medical center and followed after either surgical (n=30) or medical (n=35) treatment. At baseline and 1 year after treatment, cardiac morphology and functional variables were measured by echocardiography together with duplicate 24-hour urinary sodium collections. At baseline, LV mass index was associated with urinary sodium excretion and plasma aldosterone levels. During follow-up, blood pressure (from 167/102–135/83 mm Hg; P <0.001) and LV mass index (from 50.5±13.0–44.4±8.9 g/m 2.7 ; P <0.001) decreased significantly with nonsignificant changes in LV geometry and functional properties. At the end of follow-up, percentage decrease in LV mass index was significantly greater in patients who had >10% reduction in urinary sodium excretion (15.0±12.5%) than in the remaining patients (5.5±9.3%; P <0.001). Changes in LV mass index induced by both surgical and medical treatment were directly and independently correlated with changes in blood pressure (β=0.419; P =0.009) and urinary sodium excretion (β=0.334; P =0.012) observed at follow-up. These findings strongly support the hypothesis that dietary salt intake has a crucial role in aldosterone-related LV changes and could contribute to cardiac damage in patients with primary aldosteronism.

show abstract

Aldosterone Nongenomically Produces NADPH Oxidase−Dependent Reactive Oxygen Species and Induces Myocyte Apoptosis

Cited by 101 publications

References 52 publications

Aldosterone Activates Transcription Factor Nrf2 in Kidney Cells both In Vitro and In Vivo

Aldosterone Activates Transcription Factor Nrf2 in Kidney Cells both In Vitro and In Vivo

NADPH oxidase signaling and cardiac myocyte function

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

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