Arginine-vasopressin, as an important hormone in the regulation of plasma osmolality and blood volume/pressure, always is used in the treatment of septic shock and decompensated cirrhosis.[1]
In vitro experiment it shown that treatment with 5-10 μM argipressin (vasopressin) in RN46A cells decreased RN46A proliferation, while 10 μM argipressin (vasopressin) decreased the number of cells extending neurites. [2] In vitro, treatment with 0.1 μM and 1 μM. argipressin (vasopressin)in PV cardiomyocytes, there had a faster dose dependent beating rate than control PV cardiomyocytes by 4 and 37% respectively. [3] In vitro, Arginine vasopressin (10-12M-10-6M) can induce markedly concentration-dependent increases of insulin release from both rodent and human beta-cells, as well as mouse islets.[4] Moreover, treatment with 100 pM to 1 μM Arginine-vasopressin in the non-neuronal cells evoked [Ca2+](i) responses and had concentration-dependent responses increased with days in vitro in culture, reaching a maximum amplitude after 4-5 day. [5]
In vivo efficacy test it exhibited that argipressin (vasopressin) shown antinociception in the hot-plate test after intracerebroventricular injection (0.5 ug) and in the acetic acid abdominal constriction test after intraperitoneal injection (0.1 mg/kg).[6] In vivo experiment it demonstrated that treatment with 0.5 u/kg arginine vasopressin intravenously significantly increased the levels of IL-6 mRNA in rat hearts with the maximum level occurred at 6 h.[7]
References:
[1] Wagener G, Bakker J. Vasopressin in cirrhosis and sepsis: physiology and clinical implications. Minerva Anestesiol. 2015 Dec;81(12):1377-83. Epub 2014 Nov 11.
[2] Marinova Z, et al. Effects of oxytocin and Argipressin (Vasopressin) on the proliferation and differentiation of a serotonergic cell line. J Neural Transm (Vienna). 2018 Jan;125(1):103-106.
[3] Huang JH, et al. Argipressin (Vasopressin) modulates electrical activity and calcium homeostasis in pulmonary vein cardiomyocytes. J Biomed Sci. 2019 Sep 17;26(1):71.
[4] Mohan S, et al. Vasopressin receptors in islets enhance glucose tolerance, pancreatic beta-cell secretory function, proliferation and survival. Biochimie. 2019 Mar;158:191-198.
[5] Moriya T, et al. Vasopressin-induced intracellular Ca2? concentration responses in non-neuronal cells of the rat dorsal root ganglion. Brain Res. 2012 Nov 5;1483:1-12.
[6] Hart SL, Oluyomi AO. Vasopressin and stress-induced antinociception in the mouse. Br J Pharmacol. 1990 Feb;99(2):243-6.
[7] Sun SZ, et al. β-Arrestin 2 mediates Argipressin (Vasopressin)-induced IL-6 induction via the ERK1/2-NF-κB signal pathway in murine hearts. Acta Pharmacol Sin. 2020 Feb;41(2):198-207.
精氨酸加压素作为调节血浆渗透压和血容量/血压的重要激素,一直被用于治疗感染性休克和失代偿性肝硬化。[1]
体外实验表明,用 5-10 μM argipressin（血管加压素）处理 RN46A 细胞会降低 RN46A 的增殖,而 10 μM argipressin（血管加压素）会减少延伸轴突的细胞数量。 [2] 在体外,用 0.1 μM 和 1 μM 处理。 PV 心肌细胞中的 argipressin（血管加压素）,其剂量依赖性搏动率比对照 PV 心肌细胞分别快 4% 和 37%。 [3] 在体外,精氨酸加压素 (10-12M-10-6M) 可显着增加胰岛素释放的浓度依赖性来自啮齿动物和人类 β 细胞以及小鼠胰岛。[4] 此外,在非神经元细胞中用 100 pM 至 1 μM 精氨酸加压素处理可诱发 [Ca2+ ](i) 反应和浓度依赖性反应随着体外培养天数的增加而增加,在 4-5 天后达到最大幅度。 [5]
体内药效试验表明,argipressin（血管加压素）在侧脑室注射（0.5 ug）后的热板试验和腹腔注射（0.1 mg/kg）后的醋酸缩腹试验中均表现出镇痛作用。 [6] 体内实验表明,静脉注射0.5 u/kg精氨酸加压素可显着提高大鼠心脏IL-6 mRNA水平,并在6 h时达到最大值。[7]