Urotensin-2

Also known as: Urotensin II, UTS2, O95399

Urotensin-2 (U-II) is a cyclic undecapeptide that acts as one of the most potent endogenous vasoconstrictors identified to date, with potency up to 10–100 times greater than endothelin-1 in certain vascular beds. Its mechanism of action is mediated through binding to the G-protein-coupled receptor GPR14 (UTS2R), which activates phospholipase C, leading to intracellular calcium mobilization and smooth muscle contraction. U-II also exerts pleiotropic effects, including modulation of cardiac contractility, vascular smooth muscle cell proliferation, and pro-inflammatory signaling, depending on tissue context and species. Key research findings indicate that U-II and its receptor are widely expressed in the cardiovascular, renal, and central nervous systems. Elevated plasma U-II levels have been observed in conditions such as hypertension, heart failure, atherosclerosis, and chronic kidney disease, suggesting a role in disease pathophysiology. Experimental studies in animal models have demonstrated that U-II contributes to myocardial fibrosis, endothelial dysfunction, and renal injury, while UTS2R antagonists have shown potential in attenuating these effects. However, translational outcomes remain inconsistent, and the precise physiological role of U-II in humans is still under investigation. Clinically, U-II is considered an experimental target for cardiovascular and renal disorders, though no UTS2R-targeted therapies have been approved. Its complex, context-dependent actions—including paradoxical vasodilatory effects in some vascular beds—pose challenges for therapeutic development. Ongoing research aims to clarify its biomarker potential and the utility of receptor modulation in disease management. For research purposes only — not medical advice.

Key data

Mechanism of action

Highly potent vasoconstrictor

Research & studies

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