Aim: Raynaud’s phenomenon (RP) commonly co‐exists with systemic lupus erythematosus (SLE). The obvious pathophysiological mechanism in RP is vasoconstriction. Although the roles of certain vasoconstrictor substances, like endothelin‐1, have been identified in RP, underlying mechanisms remain unclear.
Methods: In this pilot study, we researched a relatively recently identified, very potent vasoconstrictor peptide, urotensin‐II (U‐II), in SLE patients versus those without RP. In addition to its vasoconstrictor effect, U‐II has been implicated in cardiovascular events and atherosclerosis. Increased frequencies of atherosclerosis and cardiovascular events comprise another issue in SLE patients. To address these effects, we included 15 Raynaud’s (+) and 15 Raynaud’s (−) SLE patients and compared both cohorts against age and sex‐matched controls.
Results: We found significantly elevated U‐II activity in both RP (+) and RP (−) SLE patients, relative to controls (P < 0.0001); however, the difference among RP (+) SLE patients was more prominent. U‐II was significantly elevated in RP (+) SLE patients when compared to RP (−) SLE patients (P < 0.001).
Conclusions: The results of our study suggest that, either as a cause or by‐product, U‐II may have some role in Raynaud’s‐related vasoconstriction. It also might contribute to atherosclerosis and cardiovascular diseases in SLE patients. Further studies clearly are warranted.