Angiotensin effects
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Angiotensin Effects: A Comprehensive Overview
Angiotensin II and Cardiac Hypertrophy
Angiotensin II (Ang II) plays a crucial role in the progression of myocardial hypertrophy to heart failure. It exerts its effects through different isoforms of the angiotensin-converting enzyme (ACE) and at least two different AT receptors, which are differentially expressed in cardiomyocytes from neonatal, adult, and failing hearts. The intracellular effects of Ang II are influenced by nitric oxide (NO)/cGMP-dependent cross-talk and are mediated by the release of autocrine factors such as transforming growth factor (TGF)-beta1 and interleukin (IL)-6. Additionally, Ang II interacts with systemic networks including aldosterone, parathyroid hormone, and adrenomedullin, which can modify, amplify, or antagonize its primary effects .
Angiotensin-(1-7) and Vascular Effects
Angiotensin-(1-7), a heptapeptide fragment of Ang II, has been shown to counteract the vasoconstrictive effects of Ang II. In human forearm resistant vessels, Ang-(1-7) antagonizes Ang II-induced vasoconstriction, suggesting it acts as an endogenous Ang II antagonist . In hypertensive rats, Ang-(1-7) failed to enhance the hypotensive responses evoked by bradykinin but did show a depressor effect after long-term treatment, although this effect waned over time . Furthermore, Ang-(1-7) counteracts the effects of Ang II on vascular smooth muscle cells (VSMCs) and intracerebral hemorrhagic stroke (ICH) through the NFκB inflammatory pathway, reducing VSMC proliferation, migration, and apoptosis, and decreasing blood pressure and hemorrhage volume in ICH mice .
Angiotensin II and Metabolic Effects
Ang II also affects adipose and skeletal muscle tissue. It decreases local blood flow in a dose-dependent manner and inhibits lipolysis in both tissues. These effects are consistent in both normal-weight and obese subjects, indicating that Ang II's metabolic effects are not significantly influenced by body weight .
Central Nervous System Effects
Ang II has significant effects on the central nervous system (CNS), particularly in influencing cardiovascular activity. It stimulates structures within the CNS, resulting in increased peripheral blood pressure. This effect is mediated through the sympathetic nervous system, where Ang II facilitates ganglionic transmission and sensitizes neurovascular effectors, augmenting the effects of sympathetic vasomotor discharge 89.
Angiotensin-(1-7) and Renal Protection
In diabetic mice, Ang-(1-7) prevents systemic hypertension, attenuates oxidative stress, and reduces kidney injury. It achieves these protective effects by decreasing renal oxidative stress-mediated signaling and normalizing the expression of ACE2 and the Mas receptor. These findings suggest that Ang-(1-7) plays a protective role in systolic hypertension and renal proximal tubular cell injury in diabetes .
Conclusion
Angiotensin II and its fragments, particularly Angiotensin-(1-7), have diverse and significant effects on cardiovascular, metabolic, and central nervous systems. While Ang II primarily promotes vasoconstriction, hypertrophy, and metabolic inhibition, Ang-(1-7) often counteracts these effects, providing vasoprotective, antihypertensive, and renal protective benefits. Understanding these interactions is crucial for refining therapeutic strategies targeting the renin-angiotensin system.
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