Angiotension ii
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The Role of Angiotensin II in Cardiovascular and Renal Diseases
Angiotensin II and Myocardial Hypertrophy
Angiotensin II (Ang II) is a critical hormone in the progression of myocardial hypertrophy, which can lead to heart failure. The hormone's effects on cardiomyocytes are mediated through different isoforms of the angiotensin-converting enzyme (ACE) and at least two distinct AT receptors, which are differentially expressed in neonatal, adult, and failing hearts. Ang II's intracellular effects involve nitric oxide (NO)/cGMP-dependent cross-talk and the release of autocrine factors like transforming growth factor (TGF)-beta1 and interleukin (IL)-6. Additionally, Ang II interacts with other systemic hormones such as aldosterone and parathyroid hormone, which can modify its primary effects on cardiomyocytes.
Angiotensin II and Atherosclerosis
Increased plasma concentrations of Ang II have been directly linked to the promotion of atherosclerotic lesions and aneurysms, particularly in hyperlipidemic conditions. Studies in apolipoprotein E-deficient mice have shown that Ang II infusions lead to more severe aortic atherosclerotic lesions, characterized by lipid-laden macrophages and lymphocytes. Moreover, Ang II can induce abdominal aortic aneurysms, highlighting its profound impact on vascular pathology.
Molecular Mechanisms in Cardiovascular and Renal Diseases
Ang II plays a central role in the etiology of hypertension and the pathophysiology of cardiovascular and renal diseases. It causes cellular phenotypic changes, cell growth, and regulates gene expression of various bioactive substances. These actions are mediated through the AT1 receptor and involve multiple intracellular signaling cascades, including mitogen-activated protein kinase (MAPK) cascades and tyrosine kinases. These pathways contribute to cardiac hypertrophy, heart failure, vascular thickening, atherosclerosis, and glomerulosclerosis.
Angiotensin II Receptors and Vascular Tone
Ang II exerts its effects through AT1 and AT2 receptors, which couple to various signaling molecules. Acute Ang II stimulation induces vasoconstriction by altering intracellular calcium concentrations, while long-term stimulation leads to cell proliferation and proinflammatory responses. Novel mechanisms such as RhoA/Rho kinase, transient receptor potential (TRP) channels, and reactive oxygen species are involved in regulating vasomotor tone.
Angiotensin II and Vascular Smooth Muscle Cells
Ang II stimulates DNA and protein synthesis in vascular smooth muscle cells (VSMCs) from human arteries, promoting both hyperplasia and hypertrophy. These growth effects are mediated via AT1 receptors linked to extracellular signal-regulated kinase (ERK)-dependent signaling pathways. Ang II significantly increases ERK phosphorylation, which is essential for its growth-promoting effects.
Angiotensin II and Angiogenesis
Ang II enhances vascular endothelial growth factor (VEGF)-induced angiogenic activity in retinal microcapillary endothelial cells. It increases the expression of VEGF receptors, particularly KDR/Flk-1, and potentiates VEGF-induced cell growth and tube formation. This suggests that Ang II can amplify VEGF-induced angiogenesis through upregulation of VEGF receptors.
Angiotensin II and Oxidative Stress
Ang II stimulates NADH and NADPH oxidase activity in VSMCs, leading to increased superoxide anion formation. This oxidative stress is a key factor in the long-term metabolic effects of Ang II, contributing to hypertrophy and hyperplasia. The activation of these oxidases suggests that superoxide generation may function as a second messenger in Ang II-induced cellular responses.
Conclusion
Angiotensin II is a multifaceted hormone with significant roles in cardiovascular and renal diseases. Its effects are mediated through complex signaling pathways involving various receptors and intracellular mechanisms. Understanding these pathways provides insights into potential therapeutic targets for conditions such as hypertension, atherosclerosis, and heart failure.
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