AngiotensinII is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure. Angiotensin also potentiates the release of norepinephrine by a direct action on postganglionic sympathetic fibers.
[Sar1, Ile8]-AngiotensinII (TFA) is a peptide compound that exerts various effects on vascular smooth muscle. These effects include the contraction of normal arteries as well as the hypertrophy or hyperplasia of cultured cells or diseased vessels.
AngiotensinII human (AngiotensinII) TFA 作为肾素/血管紧张素系统中关键的生物活性肽,扮演着血管收缩剂的角色并在调节人体血压中发挥中心作用。其主要通过与 G 蛋白偶联受体 (GPCRs)、血管紧张素 II 1型受体 (AT1R) 和血管紧张素 II 2型受体 (AT2R) 的相互作用来介导效应,包括刺激交感神经系统、增加醛固酮的生物合成和肾脏功能。此外,AngiotensinII human TFA 促进血管平滑肌细胞的生长和 I 型及 III 型胶原在成纤维细胞中的合成,导致血管壁与心肌增厚及纤维化,并诱导细胞凋亡。还通过LOX-1依赖的氧化还原敏感路径诱导内皮细胞中的毛细血管形成。
[Tyr(P)4] AngiotensinII is a peptide that exerts a multitude of effects on vascular smooth muscle. These effects include the contraction of normal arteries, as well as the induction of hypertrophy or hyperplasia in cultured cells or diseased vessels.
Angiotensin I II (1-6) TFA is a chemical compound comprising amino acids 1-6. It is derived from the Angiotensin I II peptide, which is formed by the cleavage of the precursor angiotensinogen by renin. The resulting Angiotensin I is then hydrolyzed by angiotensin-converting enzyme (ACE) to produce biologically active AngiotensinII. AngiotensinII has been extensively studied for its potential applications in the treatment of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy[1][2][3].
Alamandine can be formed from angiotensin A by action of ACE-2 or directly from angiotensin-(1-7) by decarboxylation of its aspartate residue. The angiotensin A analog produces effects resembling those of Ang II (1-7). However, it acts independently of the two known vasodilators receptors of the RAS (Mas and angiotensinII type 2). To produce its effects, alamandine binds to the Mas-related receptor, MrgD. A novel orally active formulation of alamandine produced a long-term antihypertensive effect in spontaneously hypertensive rats and cardioprotective effects. These novel findings will be helpful for developing a new understanding of the RAS, a key regulator of blood pressure and fluid balance. The heptapeptide could serve as a model peptide, e.g. in the development and evaluation of analytical methods.
Angiotensin 1/2 (1-8) amide (H2N-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-amide) is a peptide analog to angiotensinII that is used as a vasopressor agent in the treatment of certain types of shock and circulatory collapse. It is a potent vasoconstrictor and is us
Angiotensin (1-7) (ASP-ARG-VAL-TYR-ILE-HIS-PRO) 是肾素-血管紧张素系统中的内源性七肽。Angiotensin 1-7在心肌细胞中具有抗炎和抗纤维化活性,因此具有心脏保护作用。它能抑制血管紧张素转换酶和释放一氧化氮,是激肽诱导的血管舒张的局部协同调节剂。它阻断 Ang II 诱导的平滑肌细胞增殖和肥大,并显示对内皮的抗血管生成和生长抑制作用。它显示出抗炎活性。
TRV056 is a Gq-biased agonist of the angiotensinII type 1 receptor (AT1R), demonstrating efficacy in stimulating Gq-mediated cellular signaling. It can serve as a foundation for the development of Gq-biased AT1R agonists.
TRV055 is a Gq-biased ligand of the angiotensinII receptor type 1 (AT1R). TRV055 is efficacious in stimulating cellular Gq-mediated signaling. TRV055 can be used to develop the Gq-biased AT1R agonists.
Adrenomedullin (13-52) is a truncated form of adrenomedullin (1-52) . It induces nitric oxide-dependent relaxation of and inhibits release of angiotensinII and endothelin-1 from isolated rat aorta. In vivo, adrenomedullin (13-52) decreases mean arterial pressure (MAP) in spontaneously and renal hypertensive rats in a dose-dependent manner. Adrenomedullin (13-52) (10-3,000 ng per animal) reverses increases in lobar arterial pressure induced by U-46619 in a dose-dependent manner in cats but has no effect on basal lobar arterial pressure or systemic arterial pressure. It also potentiates inflammatory edema and neutrophil accumulation in rats.
TRV120027 is a β-arrestin-1-biased agonist of the angiotensinII receptor type 1. TRV120027 inhibits angiotensinII-mediated vasoconstriction and increases cardiomyocyte contractility.