Key result
Melatonin and ramelteon caused a rightward shift of Angiotensin II in both endothelium-intact and endothelium-denuded rat aorta.
Why the study?
To examine the involvement of ACE2 inhibitor, melatonin, and ramelteon in the vascular response to Ang II activities in endothelial denuded and intact rat isolated thoracic aortic rings.
Melatonin and ramelteon attenuate angiotensin II-induced vascular contractility in rat aortic rings, suggesting a vasomodulatory role.
MEL/RAM modulate Ang II responses in endothelium- and diabetes-dependent manner; leaves open clinical relevance of ACE2-melatonin interactions.
Background The pineal product melatonin (MEL) modulates blood vessels through G protein-coupled receptors (GPCRs) called melatonin type 1 receptor (MT1R) and melatonin type 2 receptor (MT2R), in that order. The renin-angiotensin system (RAS), which breaks down angiotensin II (Ang II) to create Ang 1–7, is thought to be mostly controlled by angiotensin-converting enzyme-2 (ACE2).Aim The current work examines the involvement of ACE2 inhibitor, MEL, and ramelteon (RAM) in the vascular response to Ang II activities in the endothelial denuded (E-) and intact (E+) rat isolated thoracic aortic rings.Method The isometric tension was measured to evaluate the vascular Ang II contractility using dose response curve (DRC).Results MEL and RAM caused a rightward shift of Ang II in endothelium E + and endothelium E- aorta.Conclusion According to the current study, the distribution of MEL receptors and the endothelium’s condition are related to the vasomodulatory effect of MEL and ACE2 on Ang II attenuation. These physiological interactions can control vascular tone and increase Ang II reactivity denude endothelial layaer.
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Mahmood et al. (2024) studied this question. Melatonin and ramelteon was evaluated on Vascular Angiotensin II contractility. Melatonin and ramelteon caused a rightward shift of Angiotensin II in both endothelium-intact and endothelium-denuded rat aorta.
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