Bradykinin acetate 

Bradykinin acetate is an effective endothelium-dependent vasodilator that can lower blood pressure. Bradykinin acetate can induce contraction of bronchial and intestinal non-vascular smooth muscle, increase vascular permeability, and participate in the mechanism of pain^{[1][2][3][4][5]}.

Bradykinin acetate is a potent vasodilator peptide that exerts its vasodilatory action through stimulation of specific endothelial B2 receptors, thereby causing the release of prostacyclin, NO, and EDHF^[1]. Bradykinin acetate has been reported to be involved in the progression of many types of cancer. Bradykinin acetate treatment promotes the invasion and migration of colorectal cancer cells. Bradykinin acetate treatment stimulates ERK1/2 activation and IL-6 production^[2].
Exogenous bradykinin acetate markedly inhibits TF expression in mRNA and protein level induced by LPS in a dose-dependent manner. The NO synthase antagonist L-NAME and PI3K inhibitor LY294002 dramatically abolish the inhibitory effects of bradykinin acetate on tissue factor expression^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Application of 1 μM bradykinin acetate to the ovary produces significant decreases in heart rate and mean arterial pressure. In vagotomized animals, application of 1 μM bradykinin acetate to the ovary produces bradycardia and hypotension similar to the responses evoked when vagal innervation is intact^[4].
Vascular bradykinin acetate can improve pancreatic microcirculation and hemorheology in rats with severe acute pancreatitis. The pancreatic microcirculatory blood flow volume and velocity in the vascular bradykinin acetate treatment group increase gradually after 48 h^[5].
PI3K/Akt signaling pathway activation induced by bradykinin administration reduces the activity of GSK-3β and MAPK, and reduces NF-x03BA; B level in the nucleus, thereby inhibiting TF expression. Consistent with this, intraperitoneal injection of C57/BL6 mice with bradykinin also inhibits the thrombus formation induced by ligation of inferior vena cava^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

1060.21 (free base)

C₅₂H₇₇N₁₅O₁₃.xC₂H₄O₂

6846-03-3

Solid

White to off-white

Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg

RPPGFSPFR

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Hornig B, et al. Role of bradykinin in mediating vascular effects of angiotensin-converting enzyme inhibitors inhumans. Circulation. 1997 Mar 4;95(5):1115-8.  [Content Brief]

  [2]. Wang G, et al. Bradykinin stimulates IL-6 production and cell invasion in colorectal cancer cells. Oncol Rep. 2014 Oct;32(4):1709-14.  [Content Brief]

  [3]. Dong R, et al. Exogenous Bradykinin Inhibits Tissue Factor Induction and Deep Vein Thrombosis via Activating the eNOS/Phosphoinositide 3-Kinase/Akt Signaling Pathway. Cell Physiol Biochem. 2015;37(4):1592-606.  [Content Brief]

  [4]. Uchida S, et al. Afferent fibers involved in the bradykinin-induced cardiovascular reflexes from the ovary in rats. Auton Neurosci. 2015 Dec;193:57-62.  [Content Brief]

  [5]. Liu LT, et al. Effect of vascular bradykinin on pancreatic microcirculation and hemorheology in rats with severe acute pancreatitis. Eur Rev Med Pharmacol Sci. 2015;19(14):2646-50.  [Content Brief]