Vasonatrin peptide (VNP) is a chimera of atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) with potent venodilating and natriuretic activity.
Vasonatrin peptide binds with both natriuretic peptide receptor A and B, but with a preference for B. VNP-stimulated cGMP is 11-fold greater in NPRB than NPRA[1].
The high-fat diet-fed streptozotocin-induced diabetic Sprague-Dawley rats are subjected to ischemia-reperfusion operation. VNP treatment (100 g/kg iv, 10 min before reperfusion) significantly improved the instantaneous first derivation of left ventricle pressure (LV dP/dtmax) and LV systolic pressure and reduced LV end-diastolic pressure, apoptosis index, caspase-3 activity, plasma creatine kinase (CK), and lactate dehydrogenase (LDH) activities[2]. Treatment hypoxia-induced pulmonary hypertension (HPH) with Vasonatrin peptide for 1 week significantly reduceS mean pulmonary arterial pressure, pulmonary vascular resistance, RVH and muscularization of the pulmonary arteries. Acute intravenous administration of 50 microg/kg Vasonatrin peptide significantly ameliorates pulmonary haemodynamics in HPH rats[3].
[1]. Jiang YS, et al. Vasonatrin peptide stimulates both of the natriuretic peptide receptors, NPRA and NPRB. Biochem Biophys Res Commun. 2014 Apr 18;446(4):1276-80. [2]. Shi Z, et al. Vasonatrin peptide attenuates myocardial ischemia-reperfusion injury in diabetic rats and underlying mechanisms. Am J Physiol Heart Circ Physiol. 2015 Feb 15;308(4):H281-90. [3]. Yu J, et al. Protective effects of vasonatrin peptide against hypobaric hypoxia-induced pulmonary hypertension in rats. Clin Exp Pharmacol Physiol. 2010 Jan;37(1):69-74.