Adrenocorticotropic hormone inhibits angiotensin II-stimulated inositol phosphate accumulation in rat adrenal glomerulosa cells

@article{Woodcock1989AdrenocorticotropicHI,
  title={Adrenocorticotropic hormone inhibits angiotensin II-stimulated inositol phosphate accumulation in rat adrenal glomerulosa cells},
  author={Elizabeth A. Woodcock},
  journal={Molecular and Cellular Endocrinology},
  year={1989},
  volume={63},
  pages={247-253}
}
  • E. Woodcock
  • Published 1 May 1989
  • Biology, Medicine
  • Molecular and Cellular Endocrinology

Modulation of agonist-induced inositol phosphate metabolism by cyclic adenosine 3',5'-monophosphate in adrenal glomerulosa cells.

Activation of the cAMP messenger system was found to cause specific changes in angiotensin-II (All)-induced inositol phosphate production and metabolism in bovine adrenal glomerulosa cells.

Role of rat adrenal antioxidant defense systems in the aldosterone turn-off phenomenon

Potentiation of [Ca2+]i response to angiotensin III by cAMP in cortical thick ascending limb.

In CTAL, there is a positive crosstalk between the adenylyl cyclase and phosphoinositide pathways mediated by V2- and AT1A-R, respectively, through activation of PKA.

Angiotensin and Aldosterone Biosynthesis

The present chapter reviews the current knowledge on the events that are triggered by angiotensin II, from the interaction with membrane receptors to the final output of aldosterone.

References

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Adrenocorticotropin regulates angiotensin II receptors in bovine adrenal cells in vitro.

Inhibition of adenylate cyclase in rat adrenal glomerulosa cells by angiotensin II.

The presence in rat adrenal glomerulosa cells of angiotensin receptors coupled to adenylate cyclase inhibition is demonstrated and it is shown that their properties are similar to those of adrenal angiotENSin receptors described previously.

Angiotensin II-stimulated phosphatidylinositol turnover in rat adrenal glomerulosa cells has a complex dependence on calcium.

While the increase in cytosolic Ca2+ may have a direct role in the stimulation of aldosterone synthesis, it is also required to sustain the PI turnover response to angiotensin II.

The rapid desensitization of glucagon-stimulated adenylate cyclase is a cyclic AMP-independent process that can be mimicked by hormones which stimulate inositol phospholipid metabolism.

It is proposed that protein kinase C activation plays a pivotal role in the molecular mechanism of desensitization of glucagon-stimulated adenylate cyclase in intact hepatocytes.