Abstract—

Proliferative effects of vasopressin belong to the least studied field of molecular biochemistry of peptide hormones. At the same time, synthetic preparations of vasopressin are widely used in the treatment of vascular diseases and in oncology. In a number of cases, vasopressin has proliferative effects; however, emerging information about the antiproliferative properties of the hormone is currently being more actively discussed. Any proliferation is accompanied by tissue neovascularization. Two main types of vasopressin receptors are expressed in the blood vessels. In this regard, analysis of how the vasopressin effect works with access to mitogenic and secretory effects in blood vessel cells is topical. The review considers tissue-specific peculiarities of vasopressin receptor expression and recent data concerning the organization of signal transduction of hormonal reception. Attention is focused on smooth muscle cells and platelets expressing V_1А-type receptors and on endotheliocytes expressing V₂ vasopressin receptors. The structure of glycopeptides and enzymes playing the role of mediators in noncanonical transduction of the hormonal signal was analyzed in detail. Particular attention was paid to the molecular organization of platelet/endothelial cell adhesion protein (PECAM-1). The integral glycopeptide PECAM-1 performs simultaneously structural and signaling functions, converting the vasoconstrictor effect of V_1А vasopressin receptors into the reaction of other membrane receptors and intracellular enzymes of blood vessels. The cytoplasmic department of PECAM-1 is involved in the inhibition of VEGFR-2 receptor of vascular endothelial growth factor (VEGF), the main stimulator of endotheliocyte proliferation. Intercellular dimers of PECAM-1 activate integrins. The integrin αVβ3 and von Willebrand factor are expressed in endotheliocytes. Multimeric molecules of von Willebrand factor are involved in cooperation between the endothelium and interstitium with local reorganization of the vascular network accompanying the repair of blood vessels in trauma and tumor progression. The von Willebrand factor aggregates the complexes of ανβ3 integrins with other ligands and membrane receptors of endotheliocytes and platelets, fixing the cells to the basement membrane. V_1А vasopressin receptors activate VEGF secretion in platelets and proliferation of myocytes. V₂ receptors stimulate exocytosis of Weibel–Palade bodies and secretion of von Willebrand factor in endotheliocytes, inducing chemotaxis of smooth muscle cells and endotheliocytes. Activated ανβ3 integrins physically interact with VEGFR-2 receptors of endotheliocytes and modulate the stimulation of angiogenic effects.

中文翻译：

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血管中的加压素受体和内皮细胞的增殖

摘要——

加压素的增殖作用属于肽类激素分子生物化学研究最少的领域。同时，血管加压素的合成制剂广泛用于血管疾病的治疗和肿瘤学。在许多情况下，加压素具有增殖作用；然而，目前正在更积极地讨论有关激素抗增殖特性的新信息。任何增殖都伴随着组织新血管形成。血管中表达两种主要类型的加压素受体。在这方面，关于血管加压素作用如何与血管细胞中的促有丝分裂和分泌作用有关的分析是局部的。该综述考虑了加压素受体表达的组织特异性特性和有关激素接收信号转导组织的最新数据。注意力集中在表达 V 的平滑肌细胞和血小板上_1-型受体和表达 V ₂加压素受体的内皮细胞。详细分析了在激素信号的非经典转导中起中介作用的糖肽和酶的结构。特别注意血小板/内皮细胞粘附蛋白 (PECAM-1) 的分子组织。积分糖肽PECAM-1进行同时结构和信令功能，转换V的血管收缩作用_1А血管加压素受体与其他膜受体和血管细胞内酶反应。PECAM-1的细胞质部参与抑制血管内皮生长因子(VEGF)的VEGFR-2受体，血管内皮细胞增殖的主要刺激物。PECAM-1 的细胞间二聚体激活整合素。整合素 αVβ3 和血管性血友病因子在内皮细胞中表达。血管性血友病因子的多聚体分子参与内皮和间质之间的合作，血管网络的局部重组伴随着创伤和肿瘤进展中的血管修复。von Willebrand 因子将 ανβ3 整联蛋白与内皮细胞和血小板的其他配体和膜受体的复合物聚集在一起，将细胞固定在基底膜上。伏_1-加压素受体激活血小板中的VEGF分泌和肌细胞增殖。V ₂受体刺激内皮细胞中 Weibel-Palade 小体的胞吐作用和血管性血友病因子的分泌，诱导平滑肌细胞和内皮细胞的趋化性。活化的 ανβ3 整联蛋白与内皮细胞的 VEGFR-2 受体发生物理相互作用并调节血管生成效应的刺激。