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(Hypertension. 2008;52:1016.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Networking Between Systemic Angiotensin II and Cardiac Mineralocorticoid Receptors

Augusto C. Montezano; Rhian M. Touyz

From the Kidney Research Centre, Ottawa Health Research Institute, University of Ottawa, Ottawa, Ontario, Canada.

Correspondence to Rhian M. Touyz, Kidney Research Centre, University of Ottawa/Ottawa Health Research Institute, 451 Smyth Rd, Ottawa, Ontario KIH 8M5, Canada. E-mail rtouyz@uottawa.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The traditional view of the renin-angiotensin-aldosterone system as a circulating system with a linear organization, where angiotensin (Ang) II, the final effector peptide of the renin angiotensin system, mediates effects through Ang II type 1 receptor (AT1R) to induce aldosterone production (reninangiotensinogenAng IAng IIaldosterone), has been challenged recently. It is becoming increasingly evident that, in addition to circulating Ang II, there is a rich and dynamic local (tissue) renin-angiotensin-aldosterone system, that the system is circuitous in that Ang II and its peptide derivatives feed back to influence upstream and downstream components of the renin-angiotensin-aldosterone system, that Ang II signals through multiple receptor subtypes, and that an intracellular (intracrine) renin-angiotensin system may contribute to extracrine Ang II actions.¹ The paradigm appears to be even more complex with the recent observations that not only does Ang II/AT1R mediate effects in part through transactivation of receptor tyrosine kinases, such as the epidermal growth factor receptor (EGFR) in a cell-specific manner, but that Ang II may induce some of its actions through aldosterone and its mineralocorticoid receptor (MR).² This interaction was first identified in the 1980s, where it was shown that, in rats, aldosterone administration increases expression of vascular Ang II receptors³ and, more recently, that aldosterone upregulates angiotensin I–converting enzyme (ACE), resulting in increased generation of Ang II.⁴ Moreover, there is intracellular networking between aldosterone and Ang II, resulting in modulation of mitogen-activated protein kinase activity, c-Src phosphorylation, NADPH oxidase–driven generation of reactive oxygen species, Rho kinase activation, EGFR . . . [Full Text of this Article]

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