PubMed Health⌕ Search

PubMed · 11850323

Aldosterone.

Abstract

Aldosterone plays a pivotal role in electrolyte and fluid homeostasis and thus control of blood pressure. The "classical" view of aldosterone action is that it targets epithelia of the distal colon and renal nephron to stimulate Na(+) (re)absorption and K(+) secretion. In these cells, aldosterone binds steroid receptors, promoting translocation to the nucleus, where they modulate gene expression with the induced proteins stimulating transport. This "genomic" action is dependent on transcription and translation and has a latency of 0.5-1.0 h. Recently, more rapid actions of aldosterone that are independent of transcription and translation have been described. These "nongenomic" actions are mediated by a distinct receptor that is insensitive to inhibitors of the classical mineralocorticoid receptor, such as spironolactone. The present review describes advances in our understanding of the classical model of aldosterone action as well as those that broaden this model to encompass nongenomic actions, nonepithelial targets, production of aldosterone outside of the adrenal gland, novel mechanisms of specificity, and novel mechanisms for mediating genomic actions.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Rachell E Booth, John P Johnson, James D Stockand. 2002. Aldosterone.. https://doi.org/10.1152/advan.00051.2001

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Effects of different angiotensins during acute, double blockade of the renin system in conscious dogs.

Evidence of biological activity of fragments of ANG II is accumulating. Fragments considered being inactive degradation products might mediate actions previously attributed to ANG II. The study aimed to determine whether angiotensin fragments exert biological activity when administered in amounts equimolar to physiological doses of ANG II. Cardiovascular, endocrine, and renal effects of ANG II, ANG III, ANG IV, and ANG-(1-7) (6 pmol.kg-1.min-1) were investigated in conscious dogs during acute inhibition of angiotensin I-converting enzyme (enalaprilate) and aldosterone (canrenoate). Furthermore, ANG III was investigated by step-up infusion (30 and 150 pmol.kg-1.min-1). Arterial plasma concentrations [ANG immunoreactivity (IR)] were determined by an ANG II antibody cross-reacting with ANG III and ANG IV. Metabolic clearance rates were higher for ANG III and ANG IV (391 +/- 19 and 274 +/- 13 ml.kg-1.min-1, respectively) than for ANG II (107 +/- 13 ml.kg-1.min-1). ANG II increased ANG IR by 60 +/- 7 pmol/ml, blood pressure by 30%, increased plasma aldosterone markedly (to 345 +/- 72 pg/ml), and plasma vasopressin transiently, while reducing glomerular filtration rate (40 +/- 2 to 33 +/- 2 ml/min), sodium excretion (50 +/- 7 to 16 +/- 4 micromol/min), and urine flow. Equimolar amounts of ANG III induced similar antinatriuresis (57 +/- 8 to 19 +/- 3 micromol/min) and aldosterone secretion (to 268 +/- 71 pg/ml) at much lower ANG IR increments ( approximately 1/7) without affecting blood pressure, vasopressin, or glomerular filtration rate. The effects of ANG III exhibited complex dose-response relations. ANG IV and ANG-(1-7) were ineffective. It is concluded that 1) plasma clearances of ANG III and ANG IV are higher than those of ANG II; 2) ANG III is more potent than ANG II in eliciting immediate sodium and potassium retention, as well as aldosterone secretion, particularly at low concentrations; and 3) the complexity of the ANG III dose-response relationships provides indirect evidence that several effector mechanisms are involved.

Aldosterone↗

Effect of extracellular and intracellular angiotensins on heart cell function; on the cardiac renin-angiotensin system.

In this manuscript, I presented up-to-date evidence that intracellular and extracellular angiotensins have an important regulatory effect on the processes of heart cell communication and inward calcium current and that aldosterone modulates the effect of angiotensin II (Ang II) on the electrical properties of the heart. Moreover, I discussed the most relevant information about the origin of cardiac renin, the presence of a cardiac renin-angiotensin aldosterone system and its possible relevance for heart cell physiology and pathology.

Aldosterone↗

Aldosterone potentiates 1,25-dihydroxyvitamin D3 action in renal thick ascending limb via a nongenomic, ERK-dependent pathway.

Recently, we demonstrated that aldosterone inhibits HCO3- absorption in the rat medullary thick ascending limb (MTAL) via a nongenomic pathway blocked by inhibitors of extracellular signal-regulated kinase (ERK) activation. Here we examined the effects on the MTAL of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], which regulates cell functions through nongenomic mechanisms in nonrenal systems. Addition of 1 nM 1,25(OH)2D3 to the bath decreased HCO3- absorption by 24%, from 15.0 +/- 0.3 to 11.4 +/- 0.5 pmol. min-1. mm-1 (P < 0.001). This inhibition was maximal within 60 min and was eliminated by pretreatment with actinomycin D, cycloheximide, or inhibitors of protein kinase C. In MTAL bathed with 1 nM aldosterone [added 15-20 min before 1,25(OH)2D3], the absolute (5.6 +/- 0.3 vs. 3.6 +/- 0.3 pmol. min-1. mm-1) and fractional (49 +/- 2 vs. 24 +/- 2%) decreases in HCO3- absorption induced by 1,25(OH)2D3 were significantly greater than those in the absence of aldosterone (P < 0.05). The effect of aldosterone to potentiate inhibition by 1,25(OH)2D3 was not affected by spironolactone but was eliminated by the MAPK kinase/ERK inhibitor U-0126. U-0126 did not affect inhibition of HCO3- absorption by 1,25(OH)2D3 alone. Aldosterone induced rapid activation of ERK via a transcription-independent pathway. We conclude that 1) 1,25(OH)2D3 inhibits HCO3- absorption in the MTAL via a genomic pathway involving protein kinase C, which may contribute to 1,25(OH)2D3-induced regulation of urinary net acid and/or Ca2+ excretion and 2) aldosterone potentiates inhibition by 1,25(OH)2D3 through an ERK-dependent, nongenomic pathway. These results identify a novel regulatory interaction whereby aldosterone acts via nongenomic mechanisms to enhance the genomic response to 1,25(OH)2D3. Aldosterone may influence a broad range of biological processes, including epithelial transport, by modifying the response of target tissues to 1,25(OH)2D3 stimulation.

Aldosterone↗