Dietary sodium intake regulates angiotensin II type 1, mineralocorticoid receptor, and associated signaling proteins in heart

Ricchiuti, Vincent; Lapointe, Nathalie; Pojoga, Luminita H.; Yao, Tham M.; Tran, Loc; Williams, Gordon H.; Adler, Gail K.

doi:10.1530/joe-10-0458

Cited by 31 publications

(23 citation statements)

References 33 publications

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“…Information concerning the cardiovascular roles of striatin family members is beginning to emerge regarding their roles in rapid estrogen signaling (25) and MR activation. We have recently shown increased striatin levels in heart and aortas from mouse and rat models of MR activation, eg, with sodium restriction (7,21). In addition, we studied 2 previously described mouse models of increased ALDO levels: 1) ip ALDO administration and 2) a model of chronic ALDO-mediated cardiovascular damage after treatment with N(G)-nitro-L-arginine methyl ester plus angiotensin II.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone's Rapid, Nongenomic Effects Are Mediated by Striatin: A Modulator of Aldosterone's Effect on Estrogen Action

et al. 2014

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The cellular responses to steroids are mediated by 2 general mechanisms: genomic and rapid/nongenomic effects. Identification of the mechanisms underlying aldosterone (ALDO)'s rapid vs their genomic actions is difficult to study, and these mechanisms are not clearly understood. Recent data suggest that striatin is a mediator of nongenomic effects of estrogen. We explored the hypothesis that striatin is an intermediary of the rapid/nongenomic effects of ALDO and that striatin serves as a novel link between the actions of the mineralocorticoid and estrogen receptors. In human and mouse endothelial cells, ALDO promoted an increase in phosphorylated extracellular signal-regulated protein kinases 1/2 (pERK) that peaked at 15 minutes. In addition, we found that striatin is a critical intermediary in this process, because reducing striatin levels with small interfering RNA (siRNA) technology prevented the rise in pERK levels. In contrast, reducing striatin did not significantly affect 2 well-characterized genomic responses to ALDO. Down-regulation of striatin with siRNA produced similar effects on estrogen's actions, reducing nongenomic, but not some genomic, actions. ALDO, but not estrogen, increased striatin levels. When endothelial cells were pretreated with ALDO, the rapid/nongenomic response to estrogen on phosphorylated endothelial nitric oxide synthase (peNOS) was enhanced and accelerated significantly. Importantly, pretreatment with estrogen did not enhance ALDO's nongenomic response on pERK. In conclusion, our results indicate that striatin is a novel mediator for both ALDO's and estrogen's rapid and nongenomic mechanisms of action on pERK and phosphorylated eNOS, respectively, thereby suggesting a unique level of interactions between the mineralocorticoid receptor and the estrogen receptor in the cardiovascular system.

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Section: Discussionmentioning

confidence: 99%

Aldosterone's Rapid, Nongenomic Effects Are Mediated by Striatin: A Modulator of Aldosterone's Effect on Estrogen Action

et al. 2014

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“…MR also acutely inhibits vascular Na + /K + -ATPase activity, an effect that is not altered by inhibitors of gene transcription or protein synthesis, but blocked by inhibitors of the MR and protein kinase C (PKC) (12). Increased transcription of striatin by MR indirectly counters its nongenomic stimulation of vascular smooth muscle proliferation by enhancing nongenomic ER effects (357, 376). …”

Section: Mammalian Adrenocorticosteroids and Their Receptorsmentioning

confidence: 99%

“…In vascular tissue striatin provides an anchor for the membrane association of ERα and is necessary for the vasoprotective ERα-mediated rapid nongenomic signaling through NO synthase (30, 39, 449). MR coprecipitates with both caveolin 1 and striatin (357), suggesting an interaction between the two membrane receptors and the possibility that rapid nongenomic MR effects leading to adaptive repair and hypertrophy that in excess cause deleterious vascular smooth muscle proliferation is countered by nongenomic ER effects inhibiting vascular smooth muscle proliferation, an effect enhanced by transcriptional MR effects increasing the expression of striatin (357, 376). In vitro and in vivo increases in aldosterone, including physiological increases by feeding a low sodium diet, were reported to increase striatin expression in the heart, vessels and cultured endothelial cells, thereby enhance rapid nongenomic ER effects (357,376).…”

Section: Mammalian Adrenocorticosteroids and Their Receptorsmentioning

confidence: 99%

The Multifaceted Mineralocorticoid Receptor

Gómez-Sánchez

2014

Comprehensive Physiology

277

224

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The primary adrenal cortical steroid hormones, aldosterone, and the glucocorticoids cortisol and corticosterone, act through the structurally similar mineralocorticoid (MR) and glucocorticoid receptors (GRs). Aldosterone is crucial for fluid, electrolyte, and hemodynamic homeostasis and tissue repair; the significantly more abundant glucocorticoids are indispensable for energy homeostasis, appropriate responses to stress, and limiting inflammation. Steroid receptors initiate gene transcription for proteins that effect their actions as well as rapid non-genomic effects through classical cell signaling pathways. GR and MR are expressed in many tissues types, often in the same cells, where they interact at molecular and functional levels, at times in synergy, others in opposition. Thus the appropriate balance of MR and GR activation is crucial for homeostasis. MR has the same binding affinity for aldosterone, cortisol, and corticosterone. Glucocorticoids activate MR in most tissues at basal levels and GR at stress levels. Inactivation of cortisol and corticosterone by 11β-HSD2 allows aldosterone to activate MR within aldosterone target cells and limits activation of the GR. Under most conditions, 11β-HSD1 acts as a reductase and activates cortisol/corticosterone, amplifying circulating levels. 11β-HSD1 and MR antagonists mitigate inappropriate activation of MR under conditions of oxidative stress that contributes to the pathophysiology of the cardiometabolic syndrome; however, MR antagonists decrease normal MR/GR functional interactions, a particular concern for neurons mediating cognition, memory, and affect.

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“…The unexpected pattern of high RAAS associated with HS loading characterized a group of patients, 10% of the entire study population constituted mostly by females, with increased arterial stiffness. Data from Ricchiuti et al 24 demonstrated that an HS diet plus RAAS activation were necessary for the development of cardiovascular damage in healthy rodents, while those animals on an LS diet showed no cardiovascular impairment in spite of a greater increase in their PRA and aldosterone levels. Hollenberg showed that rapid vascular damage requires both high mineralocorticoid levels and HS intake in high-BP diabetic patients.…”

Section: Discussionmentioning

confidence: 99%

Lack of RAAS inhibition by high-salt intake is associated with arterial stiffness in hypertensive patients

Kotliar

Kempny

González

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Hypothesis/introduction:The relationship between salt intake, blood pressure and RAAS activation is still controversial, being that both high-and low-salt intakes are associated with cardiovascular events in a J-shaped curve pattern. We hypothesized that different patterns of RAAS response to dietary salt intake among hypertensives could be identified, while vascular damage would be related to high-salt intake plus absence of expected RAAS inhibition. Objective: We aim to assess the relationship between sodium intake, RAAS and vascular stiffness in hypertension. Materials and methods: We screened 681 hypertensive patients for urinary/plasma electrolytes, renin, aldosterone and pulse wave velocity (PWV) under their usual salt intake level. Results: After applying exclusion criteria, an inverse relation between urinary sodium and RAAS was observed in the 300 remaining subjects. Additionally, four types of response were identified: 1) Low (L) sodium (S)-Low RAAS, 2) LS-High (H) SRAAS, 3) HS-Low RAAS, 4) HS-High RAAS. We found no differences in age/BP among groups, but type 4 response individuals included more females and a higher pulse wave velocity. Conclusions: We showed a) an inverse salt-RAAS relation, b) an association between HS plus high RAAS with increased PWV that could identify a higher-risk hypertensive condition.

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Dietary sodium intake regulates angiotensin II type 1, mineralocorticoid receptor, and associated signaling proteins in heart

Cited by 31 publications

References 33 publications

Aldosterone's Rapid, Nongenomic Effects Are Mediated by Striatin: A Modulator of Aldosterone's Effect on Estrogen Action

Aldosterone's Rapid, Nongenomic Effects Are Mediated by Striatin: A Modulator of Aldosterone's Effect on Estrogen Action

The Multifaceted Mineralocorticoid Receptor

Lack of RAAS inhibition by high-salt intake is associated with arterial stiffness in hypertensive patients

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