Cell lines

PV cardiomyocytes

Preparation Method

For the measurement of SR Ca2+ leak, PV cardiomyocytes were incubated with argipressin (vasopressin)(1 μM) or Argipressin (Vasopressin)(1 μM) plus KN-93 (a Ca2+/calmodulin-dependent protein kinase II, CaMKII inhibitor, 1 μM) for 4~6 h before experiments.

Reaction Conditions

1 μM; 4~6 h

Applications

Spontaneous Ca2+ transients in argipressin (vasopressin) (1 μM)-treated PV cardiomyocytes were smaller than those in the control by 67%. Argipressin (Vasopressin)(1 μM)-treated PV cardiomyocytes had greater Ca2+ leak than the control, which was attenuated by the presence of KN-93 (1 μM).

Animal models

Rats

Dosage form

1.0 or 5.0 ug/kg; s.c.

Preparation method

Rats were injected with a single subcutaneous dose of either saline, argipressin (vasopressin) (1.0 or 5.0 ug/kg), or an argipressin (vasopressin) analog with only weak endocrinological activity, des-gly-argipressin vasopressin ( 1.0, 5.0 or 10.0 ug/kg). Additional extinction trials were conducted at 2, 4, 6 and 8 h post-injection.

Applications

Argipressin (Vasopressin) potentiated this radial maze extinction behavior while DG-AVP produced behavioral results directionally opposite to those predicted by a memory facilitation hypothesis. In a subsequent experiment, vasopressin had no effects on unconditioned locomotor activity measured 2 and 4 h post-injection.

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.