Ucn2 increases left ventricular function independent of the β-adrenergic receptor but dependent on the binding of Ucn2 to CFR2.
[1] The ability of Ucn2 to produce PKA and alter calcium flux has led to the hypothesis that administration of Ucn2 may increase the risk of arrhythmias.
[3] Infusion of Ucn2 in healthy humans has shown a dose dependent increase in cardiac output, heart rate and left ventricle ejection fraction and a decrease in systemic vascular resistance.
[2] The production of PKA results in the phosphorylation of phospholamban and inhibition of its block on the sarcoendoplasmic reticulum calcium ATPase (SERCA).
[7][8][9] In rat coronary vessels, PKA mediates inhibition of calcium-independent phospholipase A and calcium influx which results in relaxation of the vasculature.
[10] This suggests Ucn2 may be beneficial in improving blood but these findings have less biological applicability to human medicine as they were completed on rats.