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Review
. 2015 May 19:6:72.
doi: 10.3389/fendo.2015.00072. eCollection 2015.

Chemical Communication between Heart Cells is Disrupted by Intracellular Renin and Angiotensin II: Implications for Heart Development and Disease

Affiliations
Review

Chemical Communication between Heart Cells is Disrupted by Intracellular Renin and Angiotensin II: Implications for Heart Development and Disease

Walmor C De Mello. Front Endocrinol (Lausanne). .

Abstract

HighlightsIntracellular renin and angiotensin disrupts chemical communication in heart.Epigenetic modification of renin angiotensin aldosterone system (RAAS) and heart disease.Intracrine renin angiotensin and metabolic cooperation.Gap junction, intracellular renin and angiotensin, cellular patterns, and heart development. The finding that intracellular renin and angiotensin II (Ang II) disrupts chemical communication and impairs metabolic cooperation between cardiomyocytes induced by aldosterone, hyperglycemia, and pathological conditions like myocardial ischemia is discussed. The hypothesis is presented that epigenetic changes of the renin angiotensin aldosterone system (RAAS) are responsible for cardiovascular abnormalities, including the expression of RAAS components inside cardiac myocytes (intracrine RAAS) with serious consequences including inhibition of electrical and chemical communication in the heart, resulting in metabolic disarrangement and cardiac arrhythmias. Moreover, the inhibition of gap junctional communication induced by intracellular Ang II or renin can contribute to the selection of cellular patterns during heart development.

Keywords: cell; chemical; communication; heart; metabolic cooperation.

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Figures

Figure 1
Figure 1
Diagram illustrating the influence of intracellular renin due to internalization or to expression of renin transcript on chemical communication between heart cells. The interaction between renin and pro (renin) receptor occurring inside a cytoplasmic vesicle can induce: the formation of Ang II, and the translocation of PLZF to the nucleus [see Ref. (38)], and consequent generation of oxidative stress through PI3K-Akt pathway with consequent decline of gap junction communication.
Figure 2
Figure 2
Diagram illustrating the role of epigenetic factors, hyperglycemia, aldosterone and heart failure on the expression of renin and angiotensin II in heart cells with consequent disruption of chemical communication and metabolic cooperation.

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