Non-genomic convergent and divergent signalling of rapid responses to aldosterone and estradiol in mammalian colon

Harvey, Bill; Doolan, Christina M.; Condliffe, Steven B.; Renard, Céline; Alzamora, Rodrigo; Urbach, V.

doi:10.1016/s0039-128x(01)00169-6

Cited by 53 publications

(37 citation statements)

References 20 publications

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“…At the same time, 17-estradiol stimulates an ATP-sensitive basolateral K + conductance involved in Na + absorption. These findings suggest that the nongenomic effects of 17-estradiol in the intestine lead to a rapid decrease in epithelial secretory capacity while increasing the potential for Na + absorption [14,15].…”

mentioning

confidence: 89%

Estrogen inhibits chloride secretion caused by cholera and Escherichia coli enterotoxins in female rat distal colon

2011

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mentioning

confidence: 89%

Estrogen inhibits chloride secretion caused by cholera and Escherichia coli enterotoxins in female rat distal colon

2011

Self Cite

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“…22 However, it is widely suggested that non-genomic actions of aldosterone are largely mediated through the classic MR. Also, non-genomic actions of mineralocorticoids appear to be mediated via activation of the protein kinase C (PKC) pathway, increased sodium/hydrogen interchange activity and intracellular calcium. [23][24][25] In addition, mineralocorticoid-induced stimulation of c-Src induces activation MAPKs (P38 MAPK, JNK, ERK1/2) associated with cellular growth, apoptosis and collagen deposition. 26 Also, Ang II induces cardiovascular tissue remodelling, proliferation, migration and hypertrophy through activation of several small G proteins including Ras, Rho and Rac.…”

Section: Non-genomic Actions Of Aldosterone and The Metabolic Syndrommentioning

confidence: 99%

Role of aldosterone and angiotensin II in insulin resistance: an update

Lastra-Lastra

Sowers

Restrepo-Erazo

et al. 2009

Clinical Endocrinology

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SummaryThe role of the Renin-Angiotensin-Aldosterone system (RAAS) on the development of insulin resistance and cardiovascular disease is an area of growing interest. Most of the deleterious actions of the RAAS on insulin sensitivity appear to be mediated through activation of the Angiotensin II (Ang II) Receptor type 1 (AT 1 R) and increased production of mineralocorticoids. The underlying mechanisms leading to impaired insulin sensitivity remain to be fully elucidated, but involve increased production of reactive oxygen species and oxidative stress. Both experimental and clinical studies also implicate aldosterone in the development of insulin resistance, hypertension, endothelial dysfunction, cardiovascular tissue fibrosis, remodelling, inflammation and oxidative stress. There is abundant evidence linking aldosterone, through non-genomic actions, to defective intracellular insulin signalling, impaired glucose homeostasis and systemic insulin resistance not only in skeletal muscle and liver but also in cardiovascular tissue. Blockade of the different components of the RAAS, in particular Ang II and AT 1 R, results in attenuation of insulin resistance, glucose homeostasis, as well as decreased cardiovascular disease morbidity and mortality. These beneficial effects go beyond to those expected with isolated control of hypertension. This review focuses on the role of Ang II and aldosterone in the pathogenesis of insulin resistance, as well as in clinical relevance of RAAS blockade in the prevention and treatment of the metabolic syndrome and cardiovascular disease.

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“…Aldosterone has been reported to selectively increase the activity of PKC␣ in a cell-free assay system using a purified commercial enzyme, suggesting that a direct aldosterone-PKC␣ interaction may contribute to nongenomic signaling. 28,90 In MDCK cells, rapid aldosterone signaling involved interaction with the epidermal growth factor receptor (EGFR), in which aldosterone increased EGFR phosphorylation on tyrosine, and inhibitors of EGFR tyrosine kinase activity decreased aldosterone-induced activation of ERK. 32 These effects appear to depend on the presence of epidermal growth factor and may involve aldosterone acting indirectly via Src to potentiate epidermal growth factor-EGFR signaling.…”

Section: Possible Receptor Mechanisms: Insights From Estrogen Signalingmentioning

confidence: 99%

Nongenomic Actions of Aldosterone on the Renal Tubule

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2007

Hypertension

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Non-genomic convergent and divergent signalling of rapid responses to aldosterone and estradiol in mammalian colon

Cited by 53 publications

References 20 publications

Estrogen inhibits chloride secretion caused by cholera and Escherichia coli enterotoxins in female rat distal colon

Estrogen inhibits chloride secretion caused by cholera and Escherichia coli enterotoxins in female rat distal colon

Role of aldosterone and angiotensin II in insulin resistance: an update

Nongenomic Actions of Aldosterone on the Renal Tubule

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