Rapid responses to aldosterone in the kidney and colon

Harvey, Bill; Alzamora, Rodrigo; Stubbs, Adam K.; Irnaten, Mustapha; McEneaney, Victoria; Thomas, Warren

doi:10.1016/j.jsbmb.2007.09.005

Cited by 37 publications

(30 citation statements)

References 71 publications

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“…This rapid effect suggests that aldosterone is signaling through previously synthesized messengers, rather than by regulating the transcription of proteins. Our data add to the growing literature describing rapid, nongenomic effects of aldosterone (2,5,(32)(33)(34)(35). For example, aldosterone activates signaling pathways such as PKA, PKC, PKD, MAPK, and the NADPH oxidase in vascular smooth muscle; and aldosterone activates phosphatidylinositol 3-kinase in endothelial cells (32,34,(36)(37)(38)(39)(40)(45)(46)(47).…”

Section: Aldosterone Activates Endothelial Exocytosis Through a Nongementioning

confidence: 52%

“…In addition to its transcriptional effects, aldosterone can also promote inflammation through nontranscriptional pathways (5,(32)(33)(34)(35). Aldosterone rapidly activates mitogen-activated protein kinase (MAPK) signaling in fibroblasts (36,37).…”

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confidence: 99%

“…Aldosterone rapidly activates mitogen-activated protein kinase (MAPK) signaling in fibroblasts (36,37). Furthermore, aldosterone rapidly activates calcium influx and protein kinase C (PKC), cAMP levels and protein kinase A (PKA), and protein kinase D (PKD) signaling pathways (32,34,(38)(39)(40).…”

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confidence: 99%

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Aldosterone activates endothelial exocytosis

Jeong¹,

Chaupin²,

Matsushita³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Although elevated levels of aldosterone are associated with vascular inflammation, the proinflammatory pathways of aldosterone are not completely defined. We now show that aldosterone triggers endothelial cell exocytosis, the first step in leukocyte trafficking. Exogenous aldosterone stimulates endothelial exocytosis of Weibel-Palade bodies, externalizing P-selectin and releasing von Willebrand factor. Spironolactone, a nonselective mineralocorticoid receptor (MR) blocker, antagonizes aldosterone-induced endothelial exocytosis. Knockdown of the MR also decreases exocytosis, suggesting that the MR mediates exocytosis. Aldosterone triggers exocytosis within minutes, and this effect is not inhibited by actinomycin D, suggesting a nongenomic effect of aldosterone. Aldosterone treatment of endothelial cells increases leukocyte adherence to endothelial cells in culture. Taken together, our data suggest that aldosterone activates vascular inflammation in part through nongenomic, MR-mediated pathways. Aldosterone antagonism may decrease vascular inflammation and cardiac fibrosis in part by blocking endothelial exocytosis.inflammation ͉ mineralocorticoid ͉ P-selectin ͉ vascular ͉ nitric oxide

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Section: Aldosterone Activates Endothelial Exocytosis Through a Nongementioning

confidence: 52%

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confidence: 99%

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Aldosterone activates endothelial exocytosis

Jeong¹,

Chaupin²,

Matsushita³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Acute aldosteronemediated ENaC activation by rapid, nongenomic mechanisms has been observed in isolated rabbit principal duct cells (112) and cortical CD cell lines (see review in Ref. 43), but the relevance of these effects in vivo are unknown. On the contrary, the rapid effects (minutes) of vasopressin on its target tissues are well established and can be reversed quickly because of the short biological half-life of the hormone.…”

Section: Vasopressin Enac and Urinary Sodium Excretionmentioning

confidence: 99%

Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?

Bankir

Bichet

Bouby

2010

American Journal of Physiology-Renal Physiology

106

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Excessive sodium reabsorption by the kidney has long been known to participate in the pathogenesis of some forms of hypertension. In the kidney, the final control of NaCl reabsorption takes place in the distal nephron through the amiloride-sensitive epithelial sodium channel (ENaC). Liddle's syndrome, an inherited form of hypertension due to gain-of-function mutations in the genes coding for ENaC subunits, has demonstrated the key role of this channel in the sodium balance. Although aldosterone is classically thought to be the main hormone regulating ENaC activity, several studies in animal models and in humans highlight the important effect of vasopressin on ENaC regulation and sodium transport. This review summarizes the effect of vasopressin V2 receptor stimulation on ENaC activity and sodium excretion in vivo. Moreover, we report the experimental and clinical data demonstrating the role of renal ENaC in water conservation at the expense of a reduced ability to excrete sodium. Acute administration of the selective V2 receptor agonist dDAVP not only increases urine osmolality and reduces urine flow rate but also reduces sodium excretion in rats and humans. Chronic V2 receptor stimulation increases blood pressure in rats, and a significant correlation was found between blood pressure and urine concentration in healthy humans. This led us to discuss how excessive vasopressin-dependent ENaC stimulation could be a risk factor for sodium retention and resulting increase in blood pressure. water conservation; antidiuresis; sodium excretion; collecting duct VASOPRESSIN WAS FIRST IDENTIFIED as a pressor hormone and later recognized to be also a potent antidiuretic hormone. Today, these early historical discoveries have been explained by the identification of different receptor types. V1a receptors (V1aR), abundantly expressed in vascular smooth muscle cells, and signaling through calcium and phosphatidylinositol transducer pathways, are responsible for the pressor effects. V2 receptors (V2R), expressed mainly in principal cells of the renal collecting duct (CD), and signaling through cAMP, mediate the antidiuretic actions of the hormone (113).Vasopressin is elevated in some forms of human hypertension (26,92,111) and in animal models of hypertension (see reviews in Refs. 91 and 108). This hormone has long been suspected to play a role in blood pressure control because of its vasoconstrictive effects, well demonstrated in vitro. However, the studies trying to evaluate the contribution of V1aR-dependent effects in hypertension are inconclusive [either in favor of (27,35,70) or against (59, 98)].Excessive sodium reabsorption by the kidney is known to participate in the pathogenesis of some forms of hypertension.Among the genes responsible for monogenic forms of blood pressure disorders identified to date, the majority either mediate renal sodium transport in the distal part of the nephron or are involved in its regulation. Loss of function of the corresponding proteins leads to salt-wasting states with hypotension (48), ...

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“…However, the action of this hormone on H ϩ -ATPase in the proximal tubule is not known. In the cortical and outer medullary collecting duct, prolonged exposure to aldosterone stimulates H ϩ secretion directly through the H ϩ -ATPase and indirectly through increased absorption of Na ϩ (9,13,33); in addition, a rapid activation of H ϩ -ATPase has also been described in intercalated renal tubule cells (38). The nongenomic effect of aldosterone, which has been shown in several epithelial and nonepithelial tissues, has the following characteristics: it is not sensitive to inhibitors of gene transcription and synthesis of protein and, in general, has a rapid effect (seconds to a few minutes) (11,20,36).…”

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confidence: 99%

Genomic and nongenomic stimulatory effect of aldosterone on H⁺-ATPase in proximal S3 segments

Dellova¹,

Malnic

Mello-Aires

2011

American Journal of Physiology-Renal Physiology

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The genomic and nongenomic effects of aldosterone on the intracellular pH recovery rate (pHirr) via H+-ATPase and on cytosolic free calcium concentration ([Ca2+]i) were investigated in isolated proximal S3 segments of rats during superfusion with an Na+-free solution, by using the fluorescent probes BCECF-AM and FLUO-4-AM, respectively. The pHirr, after cellular acidification with a NH4Cl pulse, was 0.064 ± 0.003 pH units/min ( n = 17/74) and was abolished with concanamycin. Aldosterone (10−12, 10−10, 10−8, or 10−6 M with 1-h or 15- or 2-min preincubation) increased the pHirr. The baseline [Ca2+]i was 103 ± 2 nM ( n = 58). After 1 min of aldosterone preincubation, there was a transient and dose-dependent increase in [Ca2+]i and after 6-min preincubation there was a new increase in [Ca2+]i that persisted after 1 h. Spironolactone [mineralocorticoid (MR) antagonist], actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min preincubation) on pHirr and on [Ca2+]i but inhibited the effects of aldosterone (1-h preincubation) on these parameters. RU 486 [glucocorticoid (GR) antagonist] and dimethyl-BAPTA (Ca2+ chelator) prevented the effect of aldosterone on both parameters. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on the H+-ATPase and on [Ca2+]i. The results are compatible with stimulation of the H+-ATPase by increases in [Ca2+]i (at 10−12-10−6 M aldosterone) and inhibition of the H+-ATPase by decreases in [Ca2+]i (at 10−12 or 10−6 M aldosterone plus RU 486).

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Rapid responses to aldosterone in the kidney and colon

Cited by 37 publications

References 71 publications

Aldosterone activates endothelial exocytosis

Aldosterone activates endothelial exocytosis

Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?

Genomic and nongenomic stimulatory effect of aldosterone on H⁺-ATPase in proximal S3 segments

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Rapid responses to aldosterone in the kidney and colon

Cited by 37 publications

References 71 publications

Aldosterone activates endothelial exocytosis

Aldosterone activates endothelial exocytosis

Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?

Genomic and nongenomic stimulatory effect of aldosterone on H+-ATPase in proximal S3 segments

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Genomic and nongenomic stimulatory effect of aldosterone on H⁺-ATPase in proximal S3 segments