Nongenomic Actions of Aldosterone on the Renal Tubule

Good, David W.

doi:10.1161/01.hyp.0000259797.48382.b2

Cited by 52 publications

(55 citation statements)

References 115 publications

(203 reference statements)

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“…3 Animal studies have confirmed that mineralocorticoid receptors are present in the renal tubule and partial glomerular cells. 4 One study showed that along with angiotensin-converting enzyme inhibitors, aldosterone also causes cardiovascular and renal damage, and spironolactone (even with injection of Ang II) can exert obvious cardiovascular and renal protective roles. Moreover, many research data have shown that the aldosterone system, inhibited in DN, has a beneficial effect independent of blockade of the renin-angiotensin system.…”

Section: Introductionmentioning

confidence: 99%

Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors

Hao

Ren

Zhang

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Introduction: In this study, we investigated whether AngII receptors (AT1a and AT2) contributed to the development of the aldosterone-induced inflammatory response of rat mesangial cells (RMCs). Materials and methods: RMCs were isolated from the glomeruli of normal or diabetic rats which were produced by injection of streptozotocin, and cultured in high-glucose media. In order to evaluate the effects of aldosterone, the expression of AT1a, AT2, NF-κB and MCP-1 was detected. In addition, in order to evaluate the role of Ang II receptors, AT1a and AT2 genes were blocked and the expression of NF-κB and MCP-1 was detected. Moreover, for assessing the relationship between NF-κB and MCP-1, the NF-κB gene was blocked and MCP-1 expression was detected. Results: Aldosterone significantly increased AT1a, AT2, NF-κB and MCP-1 levels in RMCs in a dose-dependent manner, whereas eplerenone (EPI), a selective aldosterone antagonist, partly inhibited the effects of aldosterone. When AT1a and AT2 genes were blocked, the expression of NF-κB and MCP-1 was greatly inhibited. Moreover, when the NF-κB gene was silenced, the expression of MCP-1 was reduced. Conclusion: We demonstrated that aldosterone induced an inflammatory response in RMCs cultured in high-glucose media via the AT1a and AT2 pathways.

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Section: Introductionmentioning

confidence: 99%

Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors

Hao

Ren

Zhang

et al. 2014

J Renin Angiotensin Aldosterone Syst

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“…Genomic effects of aldosterone are generally thought to be mediated by the MR and involve transcription, while nongenomic effects occur without gene transcription (32), but occasionally involve the MR (17). Aldosterone induced an increase in intracellular calcium and sodium and an increased potassium flux within 1 min in Madin-Darby canine kidney cells, which are similar to renal cortical collecting duct cells (16) and M-1 kidney cell lines (20), which were likely due to a nongenomic effect of aldosterone.…”

Section: Discussionmentioning

confidence: 95%

Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback

Zhang

Lin

Liu

et al. 2013

American Journal of Physiology-Renal Physiology

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Ϫ production, we exposed the O 2 Ϫ cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKC␣ inhibitor Go6976, or a PKC␣ siRNA, and the aldosterone-induced increase in O 2 Ϫ production was blocked. These data indicate that aldosterone-stimulated O 2 Ϫ production in the MD buffers the effect of NO in control of TGF response, an effect that was mediated by PKC␣. tubuloglomerular feedback; renal hemodynamics; nitric oxide; kidney KIDNEYS PLAY A CENTRAL ROLE in control of salt-water balance and blood pressure. Tubuloglomerular feedback (TGF) is an important mechanism in regulation of renal microcirculation and hemodynamics (9, 44). TGF regulates distal tubular sodium load by adjusting tone of the afferent arteriole and glomerular filtration rate in response to changes in NaCl concentration at the macula densa (MD) (5, 9, 44). Responsiveness of TGF can be regulated by a number of factors, including ANG II (44), adenosine (40), arachidonic acid metabolites (24), ATP (22, 36), atrial natriuretic factor (21), NO (30), and O 2 Ϫ (31). Recently, we found that aldosterone plays an important role in control of TGF response (12).Aldosterone is a mineralocorticoid primarily produced in the zona glomerulosa of the adrenal gland. The best known physiological role of aldosterone is to increase sodium reabsorption in the distal nephron to maintain sodium balance. In recent years, aldosterone has been associated with obesity and metabolic syndrome in selected populations, and these associations may further contribute to the higher cardiovascular risk of subjects with elevated aldosterone levels. The role of aldosterone in renal and cardiovascular injury, including inflammation, tissue remodeling, and fibrosis, has been demonstrated in various animal models of hypertension and kidney failure (18, 35), independent of its salt-water retention and hypertensive effects (8, 15).We found recently that mineralocorticoid receptors (MR) are expressed in the MD cells. Activating MR in the macula densa blunted TGF response both in vivo and in vitro by enhancing NO generation (12). These findings provide a novel mechanism for regulation of renal hemodynamics and salt-water balance by aldosterone, especially the hyperfiltration in primary aldosteronism and obesity patients. We also found that aldosterone stimulated superoxide (O 2 Ϫ ) generation by activating NOX2 and NOX4 isoforms of NAD(P)H oxidase in cultured MD cells (46). O 2 Ϫ in the MD enhances TGF response by scavenging NO (31). However, their interactions and the net effect on TGF are not clarified. In the present study we further investigated the interaction between NO and O 2 Ϫ in the MD in response to aldosterone and their effect on aldosterone-induced TGF alterations. In addition, the previous study (46) was performed in cultured cells. The goal was to determine if aldosterone has the same effect on O 2 Ϫ generation in native MD cells using isolated perfused rabbit macula densa.The present study was designed to test the hypothesis that aldosterone stimulates O 2...

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“…The existence of a "non-classical" membrane receptor for thenongenomic actions of aldosterone separate from the classical mineralocorticoid receptor (MR) has been postulated [49], but none has been identified or characterized. On the other hand attempts made to explain all actions of aldosterone through its binding to MR have not been convincing [50,51].…”

Section: Receptor Independent Actions Of Egfmentioning

confidence: 99%

“…Since the recognition of the non-genomic actions of aldosterone [49], more questions than answers have arisen about the identity and behaviour of its receptors and the mechanisms of aldosterone actions onnonepithelial tissues. A critical review of the vast and conflicting literature on the subject is far beyond the present scope.…”

Section: Aldosterone Receptorsmentioning

confidence: 99%

“…It has been suggested that rapid non genomic actions of aldosterone (Rap Lo NG Aldo R) potentiate the inhibitory actions of EGF on sodium reabsorption [49] and EGF signalling has been viewed as a negative feedback control of aldosterone induced Na+ reabsorption [106]. The other important component of Pathway, AT2r inhibits Na+ reabsorption in the proximal tubule via mediation of angiotensin III [70].…”

Section: Physiological Role Of Pathway 1 To Inhibit Renal Sodium Reabmentioning

confidence: 99%

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A Single Initiating Cause of Hypertension; Potential for Primary Prevention

Sambhi¹

2014

J Hypertens

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Nongenomic Actions of Aldosterone on the Renal Tubule

Cited by 52 publications

References 115 publications

Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors

Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors

Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback

A Single Initiating Cause of Hypertension; Potential for Primary Prevention

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