Neuromedin U (NMU) is a neuropeptide first demonstrated to drive smooth muscle contraction.1Translated as a 174 amino acid propeptide, NMU is cleaved to different lengths in different animals. It has diverse receptor-mediated rolesin vivo, as it regulates feeding, vasoconstriction, nociception, and bone remodeling and contributes to obesity, cancer and septic shock.2,2NMU-25 is the active form of NMU in humans. It binds with high affinity to receptors on human left ventricle and coronary artery (KDs = 0.26 and 0.11 nM, respectively), eliciting endothelium-independent vasoconstriction.3NMU-25 also suppresses glucose-stimulated insulin secretion in human islets, and this effect is lost in NMU R165W mutants, resulting in early-onset obesity.4
1.Mitchell, J.D., Maguire, J.J., and Davenport, A.P.Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin SBritish Journal of Pharmacology15887-103(2009) 2.Greenwood, H.C., Bloom, S.R., and Murphy, K.G.Peptides and their potential role in the treatment of diabetes and obesityRev.Diabet.Stud.8(3)355-368(2011) 3.Mitchell, J.D., Maguire, J.J., Kuc, R.E., et al.Expression and vasoconstrictor function of anorexigenic peptides neuromedin U-25 and S in the human cardiovascular systemCardiovascular Research81353-361(2009) 4.Alfa, R.W., Park, S., Skelly, K.R., et al.Suppression of insulin production and secretion by a decretin hormoneCell Metabolism21(2)323-333(2015)
Human Big ET-1 comprises residues 53-90 of the endothelin precursor (preproendothelin). Compared to the mature endothelin-1 (hET-1), the peptide show less vasoconstrictor activity in vitro, but similar pressor effects in vivo. Former CAS-number 121014-53-7.
The big endothelins comprise residues 53-90 (human big ET-1) and 53-91 (porcine big ET-1) of the endothelin precursor (preproendothelin). Compared to the mature endothelin-1 (ET-1), both peptides show less vasoconstrictor activity in vitro, but similar pressor effects in vivo. Former CAS-number 121014-54-8.
Angiotensin II human TFA 是肾素-血管紧张素系统中的强效血管收缩剂,通过与 AT1R 和 AT2R 受体作用调节血压,可激活交感神经、促进醛固酮合成和肾功能,诱导血管平滑肌细胞增殖及成纤维细胞中 I 型和 III 型胶原合成,导致血管和心肌增厚、纤维化,并诱导凋亡及促进毛细血管生成,可用于构建心脏肥大、高血压和腹主动脉瘤模型。
Angiotensin II human acetate 是肾素-血管紧张素系统中的主要血管收缩肽,通过与AT1R和AT2R受体结合调节血压,刺激交感神经,促进醛固酮合成和肾脏功能,诱导血管平滑肌细胞增生和胶原合成,导致血管及心肌增厚和纤维化,同时促进细胞凋亡和内皮毛细血管形成。常用于诱导高血压和心脏肥大模型。