Control of aldosterone secretion: a model for convergence in cellular signaling pathways.

  title={Control of aldosterone secretion: a model for convergence in cellular signaling pathways.},
  author={Andr{\'a}s Sp{\"a}t and L{\'a}szl{\'o} Hunyady},
  journal={Physiological reviews},
  volume={84 2},
Aldosterone secretion by glomerulosa cells is stimulated by angiotensin II (ANG II), extracellular K(+), corticotrophin, and several paracrine factors. Electrophysiological, fluorimetric, and molecular biological techniques have significantly clarified the molecular action of these stimuli. The steroidogenic effect of corticotrophin is mediated by adenylyl cyclase, whereas potassium activates voltage-operated Ca(2+) channels. ANG II, bound to AT(1) receptors, acts through the inositol 1,4,5… 

Signaling Interactions in the Adrenal Cortex

Cross-actions of parallel signal transducing pathways are not mere intracellular curiosities but rather substantial phenomena, which fine-tune the biological response.

Calcium-dependent mitochondrial cAMP production enhances aldosterone secretion

Minireview: aldosterone biosynthesis: electrically gated for our protection.

Aldosterone produced by adrenal zona glomerulosa (ZG) cells plays an important role in maintaining salt/water balance and, hence, blood pressure homeostasis. However, when dysregulated, aldosterone

Regulation of aldosterone production from zona glomerulosa cells by ANG II and cAMP: evidence for PKA-independent activation of CaMK by cAMP.

This work found that Ca(2+)/calmodulin-dependent protein kinases (CaMKs) play a predominant role in the regulation of aldosterone production stimulated by ANG II, ACTH, and cAMP, and provides evidence that cAMP effects in ZG cells do not involve Ca( 2+) or MAPK signaling.

Potassium channels in adrenocortical cells

Effect of aldosterone on BK channel expression in mammalian cortical collecting duct.

It is suggested that aldosterone does not contribute to the regulation of BK channel expression/activity in response to dietary K(+) loading, and the flow-stimulated increase in J(K) was similar in both groups.

D4 dopamine receptor enhances angiotensin II-stimulated aldosterone secretion through PKC-epsilon and calcium signaling.

D4R augmented aldosterone synthesis/secretion induced by AII through enhancing PKC-epsilon phosphorylation and [Ca(2+)](i) elevation, and inhibitory peptide attenuated AII-stimulated ald testosterone secretion, CYP11B2 mRNA expression, and elevation of intracellular IP(3) and[Ca( 2+](i).

Mitochondrial matrix calcium is an activating signal for hormone secretion.




Role of calcium in angiotensin II-mediated aldosterone secretion.

The present discussion will focus on the role of calcium (Ca2+) in the acute (hours vs. days) regulation of aldosterone secretion by Ang II.

The role of tyrosine kinases in capacitative calcium influx-mediated aldosterone production in bovine adrenal zona glomerulosa cells.

Results suggest that, in bovine adrenal glomerulosa cells, Ang II promotes capacitative Ca(2+) influx and aldosterone biosynthesis through tyrosine kinase activation.

Signaling events activated by angiotensin II receptors: what goes before and after the calcium signals.

The sensitivities of both Raf-1 kinase and MAP-kinase stimulation by Ang II to the inhibitors of phosphoinositide kinases, wortmannin and LY 294002, suggest that inositol phospholipids may play a role in these activation events unrelated to their role in Ca2+ signaling.

Angiotensin II stimulates T-type Ca2+ channel currents via activation of a G protein, Gi.

It is observed that ANG II enhances T-type Ca2+ current by shifting the voltage dependence of channel activation to more negative potentials and should increase Ca2- entry in AG cells at physiologically relevant voltages and result in a sustained increase in aldosterone secretion.

A role for T-type Ca2+channels in the synergistic control of aldosterone production by ANG II and K.

It is proposed that synergy in aldosterone secretion results from K+-induced depolarization and ANG II-induced modulation of T-type channel activation, such that together they promote enhanced steady-state Ca2+ flux.

Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells.

It is concluded that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca(2+)-activatable K(+)-conductive pathway likely to be the maxi-K channel.

Angiotensin-II induces changes in the cytosolic sodium concentration in bovine adrenal glomerulosa cells: involvement in the activation of aldosterone biosynthesis.

Results show that Ang II and, to a lesser extent, K+ induce significant changes in [Na+]i in bovine glomerulosa cells, and these changes probably occur through the Na+/H+ andNa+/Ca2+ exchangers and are likely to play a role in activation of the steroidogenic cascade.

FK506 blocks intracellular Ca2+ oscillations in bovine adrenal glomerulosa cells.

It is demonstrated that angiotensin (AngII), phorbol ester (PMA), and FK506 significantly increase the level of InsP(3) receptor phosphorylation in intact bovine adrenal glomerulosa cells and that FK505 causes important changes in the Ca(2+) oscillatory process.