Crosstalk Between Abnormal Electrical Activity and Angiotensin II Cell Signaling in the Hyperglycemic Mammalian Heart

It has been well-accepted that an up-regulation of not only the systemic but also local cardiac renin angiotensin systemRenin angiotensin system (RAS) leads to end-stage damage in the heart under pathological conditions. So, a well-controlled RAS has an important impact on the prevention of morbidity and mortality of patients with cardiovascular disorders. Local cardiac RAS is composed of renin, angiotensin-converting enzyme (ACE), angiotensin IAngiotensin I (Ang I), and it products Ang(1–9), angiotensin IIAngiotensin II (Ang II), and its product Ang(1–7), while the main effector peptide of the RASRenin angiotensin system is Ang II. Ang II plays prominent roles in cardiovascular pathology through its fundamental roles in the modulation of cellular signaling mechanisms, such as participation in immunity, lipid peroxidation, and insulin resistanceInsulin resistance. An overall insight to the literature data, activation of cardiac RASRenin angiotensin system may be pivotal in the pathogenesis of cardiac dysfunction in diabetesDiabetes, metabolic syndromeMetabolic syndrome, obesityObesity, and/or other types of pathological conditions. Herein, the aim of this review article is particularly focused to discuss the evidence on the role of crosstalk between Ang II cell signaling and abnormal electrical activity and in the hyperglycemic mammalian heart. In the content of the article, it will be discussed characteristics and mechanisms of Ang II-related cardiac remodelingCardiac remodeling such as effects of Ang II receptor activation on electrical and mechanical activities of the heart under pathological stimuli, in both cellular and organelle level alterations. It will be also documented the literature data related to the roles of Ang IIAngiotensin II receptors on structural and electrophysiological remodeling in the hyperglycemic and insulin-resistant heart.