Direct action of aldosterone on transmembrane 22Na efflux from arterial smooth muscle. Rapid and delayed effects.

Moura, A M; Worcel, Manuel

doi:10.1161/01.hyp.6.3.425

Cited by 104 publications

(43 citation statements)

References 23 publications

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“…This confirmed earlier work by these investigators showing a rapid increase in passive sodium efflux that was insensitive to actinomycin D in intact rat tail artery. 32 These data suggest that aldosterone has a membrane effect that is not mediated by Na + ,K + -ATPase. In our previous study 15 acute administration of aldosterone (15 minutes) caused a depression in carotid sinus baroreceptor function.…”

Section: Discussionmentioning

confidence: 86%

Chronic administration of aldosterone depresses baroreceptor reflex function in the dog.

Wang

1994

Hypertension

138

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In a previous study it was shown that acute perfusion of aldosterone into the isolated carotid sinus decreased baroreceptor activity. The aim of the present study was to determine whether chronic, systemic administration of aldosterone also depresses baroreflex function. In six conscious dogs, the baroreflex was determined before and 10 days after an osmotic minipump containing aldosterone (100 ixg/kg in 2 mL) was implanted. The slope of the relation between systolic arterial pressure and heart rate was significantly blunted after aldosterone administration (9.1±0.7 versus 13.3±1.2 for nitroglycerin, P<.0l; 23.4+5.0 versus 40.1+5.0 for phenylephrine, P<.01). Baroreflex slopes did not change in a sham group (minipump with saline) and an aldosterone plus spironolactone (600 mg/d) group. Plasma aldosterone levels were significantly elevated after the aldosterone minipump was implanted (443±72 versus 37±11 pg/mL, f<.001). Mean arterial pressure was not significantly increased after aldosterone (106.5 ±3.8 versus 100.4±2.6 mm Hg, P=2). On the 10th day after aldo-

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Section: Discussionmentioning

confidence: 86%

Chronic administration of aldosterone depresses baroreceptor reflex function in the dog.

Wang

1994

Hypertension

138

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“…Discrepancies in reports may result from indirect effects of other transporters on Na + -K + -ATPase pump activity or from different isoforms expressed in different models and tissues (Summa et al 2004). Again just like for ENaC, Na + -K + -ATPase response to aldosterone seems to involve trafficking of preexisting subunits to the membrane as well as de novo synthesis (El Mernissi & Doucet 1984, BlotChabaud et al 1990, Kolla & Litwack 2000, Summa et al 2001, Musch et al 2008. SGK, an MR target gene, and aldosterone were shown to stimulate long-term effects synergistically but independently (Alvarez de la Rosa et al 2006).…”

Section: Nongenomic Aldosterone Effects In the Kidneymentioning

confidence: 99%

“…Although the effect is persistent and lasting over several days, the involvement of the EGFR signaling pathways indicates a possible nongenomic mechanism (Krug et al 2003, Drumm et al 2006. Furthermore, it has been demonstrated that NHE3 expression is increased via SGK1 and genomic effects on the long-term (Musch et al 2008). Conversely, aldosterone inhibited maximal velocity of NHE3 via ERK1/2 in MTAL, thus reducing bicarbonate reabsorption (Good et al 2006, Watts et al 2006.…”

Section: :1mentioning

confidence: 99%

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Nongenomic effects via the mineralocorticoid receptor

Ruhs

Nolze

Hübschmann

et al. 2017

Journal of Endocrinology

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The mineralocorticoid receptor (MR) belongs to the steroid hormone receptor family and classically functions as a ligand-dependent transcription factor. It is involved in water-electrolyte homeostasis and blood pressure regulation but independent from these effects also furthers inflammation, fibrosis, hypertrophy and remodeling in cardiovascular tissues. Next to genomic effects, aldosterone elicits very rapid actions within minutes that do not require transcription or translation and that occur not only in classical MR epithelial target organs like kidney and colon but also in nonepithelial tissues like heart, vasculature and adipose tissue. Most of these effects can be mediated by classical MR and its crosstalk with different signaling cascades. Near the plasma membrane, the MR seems to be associated with caveolin and striatin as well as with receptor tyrosine kinases like EGFR, PDGFR and IGF1R and G proteincoupled receptors like AT1 and GPER1, which then mediate nongenomic aldosterone effects. GPER1 has also been named a putative novel MR. There is a close interaction and functional synergism between the genomic and the nongenomic signaling so that nongenomic signaling can lead to long-term effects and support genomic actions. Therefore, understanding nongenomic aldosterone/MR effects is of potential relevance for modulating genomic aldosterone effects and may provide additional targets for intervention.

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“…Initially, the classic cytosolic MR protein was suggested to be involved in mediating both nongenomic and genomic aldosterone signaling 2,8 ; however, some studies reported that these nongenomic effects could not be blocked by MR antagonists such as spironolactone. In addition, although rapid, nongenomic effects were elicited by the mineralocorticoids aldosterone, deoxycorticosterone, and 9␣-fludrocortisone, these rapid effects could not be elicited by the glucocorticoids cortisol and corticosterone.…”

Section: Evidence For a Nonclassic Aldosterone Receptor In The Plasmamentioning

confidence: 99%

Cell Membrane–Associated Mineralocorticoid Receptors?

et al. 2011

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Abstract-The purpose of the present article is to provide an overview of plasma membrane steroid hormone receptors and their implications in nongenomic signaling. We especially focus on recent evidence supporting the notion of a possible membrane-associated aldosterone receptor, whether this receptor is different from the classic nuclear receptor, and the possible implications of such a receptor for nongenomic and genomic aldosterone effects in physiological and pathophysiological processes. (Hypertension. 2011;57:1019-1025.)Key Words: mineralocorticoid receptor Ⅲ aldosterone Ⅲ nongenomic effects Ⅲ plasma membrane A ldosterone is the major physiological regulator of Na ϩ and electrolyte balance and, hence, blood pressure homeostasis. In the kidneys, aldosterone mediates Na ϩ retention and K ϩ excretion via genomic effects through the cytosolic mineralocorticoid receptor (MR), which acts as a transcription factor. 1 In 1984, Moura and Worcel 2 described rapid (within minutes) effects of aldosterone on Na ϩ efflux from smooth muscle cells, and this effect could not be blocked by the transcription inhibitor actinomycin D. Later it was shown that aldosterone can elicit activation of Na ϩ /H ϩ exchanger and signaling cascades, such as mitogen activated protein kinases (MAPKs) or protein kinase C, through nongenomic mechanisms, and these effects may impact cellular functions, such as growth and differentiation. [3][4][5] Several excellent recent reviews have extensively described the physiology and biology of aldosterone action. 5-7 Evidence for a Nonclassic Aldosterone Receptor in the Plasma Membrane and MR-Independent Rapid SignalingInitially, the classic cytosolic MR protein was suggested to be involved in mediating both nongenomic and genomic aldosterone signaling 2,8 ; however, some studies reported that these nongenomic effects could not be blocked by MR antagonists such as spironolactone. In addition, although rapid, nongenomic effects were elicited by the mineralocorticoids aldosterone, deoxycorticosterone, and 9␣-fludrocortisone, these rapid effects could not be elicited by the glucocorticoids cortisol and corticosterone. 5 In analogy to other steroid hormones, such as estrogens, Wehling et al 9 hypothesized an aldosterone receptor that is distinct from the classic MR protein, located at the membrane, and responsible for nongenomic aldosterone effects. This view was initially supported by several studies demonstrating functional evidence for the possible existence of a plasma membranebound MR. For example, presumably membraneimpermeable, BSA-coupled aldosterone showed the same rapid effects as aldosterone, supporting the idea of a plasma membrane-bound receptor 10,11 ; however, aldosterone-BSA conjugates may undergo dissociation into hormone and BSA requiring critical and careful handling, 12 as shown for estrogen-BSA. 13 Additional support for a distinct membrane MR comes from recent work by Wildling et al. 14 Using endothelial cell swelling as an index of an aldosterone effect, it was shown that spironolact...

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Direct action of aldosterone on transmembrane 22Na efflux from arterial smooth muscle. Rapid and delayed effects.

Cited by 104 publications

References 23 publications

Chronic administration of aldosterone depresses baroreceptor reflex function in the dog.

Chronic administration of aldosterone depresses baroreceptor reflex function in the dog.

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Nongenomic effects via the mineralocorticoid receptor

Cell Membrane–Associated Mineralocorticoid Receptors?

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