Hemopressin, human

USA

As a novel nonapeptide, hemopressin is vasoactive. It is derived from hemoglobin’s alpha-chain. Acting as endogenous peptide ligand for CB1 receptors, the hemoglobin fragment hemopressin dilates the rat systemic vascular bed by releasing nitric oxide. Current studies are focused on the effects of intravenous (i.v.) administration of rat hemopressin (rHP), 30-1000 microg/kg, on systemic arterial pressure (SAP), cardiac output (CO), and systemic vascular resistance (SVR) in the anesthetized rat. Bolus i.v. injections of rHP result in dose-dependent mild decreases in SAP. With an unaltered level of CO, the decreases in SAP show a relationship with SVR reduction. Unaffected by tachyphylaxis, the systemic vasodilator response to rHP is abolished by L-nitro-arginine methyl ester (L-NAME) but is not altered by meclofenamate. In addition, rHP does not have direct contractile or relaxant activity on either isolated rat aortic rings (AA) or pulmonary arterial rings (PA). Current data suggest that the mechanism of rHP dilation of the rat systemic vascular bed is through the endogenous release of nitric oxide (NO) independent of the formation of cyclooxygenase products such as prostacyclin. It is possible for rHP to act as an endogenous vasodilator substance regulating the local blood flow during clinical states of altered red cell turnover, microvascular disease and hemolysis.