Abstract T P249: Upregulation of Relaxin After Experimental Subarachnoid Hemorrhage

Abstract

Background and Purpose: Relaxin is a pregnancy hormone which exerts vasodilatory effects by activating nitric oxide synthase and matrix metalloproteinases through receptor (RXFP1). Recently, this vasodilatory effect has been considered useful as a potential therapeutic target in acute heart failure. However, the role of relaxin in the cerebral artery has not been fully explored. In this study, we investigated the role of relaxin in rabbit basilar artery (BA) after subarachnoid hemorrhage (SAH). Methods: Basilar arteries were collected from a rabbit SAH model on days 3, 5, and 7 after SAH. Total RNA was extracted from the BA and a cDNA microarray containing 43,623 genes was performed. The expression of relaxin and RXFP1 mRNA was investigated by quantitative RT-PCR. Serum and cerebrospinal fluid (CSF) relaxin concentrations were measured by ELISA. Perfusion fixation was performed on days 0, 3, 5 and 7, and the localization of RXFP-1 in the BA was examined using immunohistochemistry. Results: The expression of relaxin mRNA was significantly up-regulated on days 5 and 7 compared to the control sample. The expression of RXFP1 mRNA was significantly down-regulated on day 3 and sustained on day 7. The serum relaxin concentration in the rabbit SAH model was not significantly changed after SAH, whereas the CSF relaxin concentration was significantly elevated on days 5 and 7. Immunohistochemistry revealed strong RXFP1 staining in media of the BA on day 0, and showed weak staining on days 3, 5 and 7. Conclusions: Relaxin expression in the BA and relaxin concentration in the CSF increase after SAH, and considerably, relaxin expression is negatively correlated with the RXFP1 expression in the rabbit BA after SAH.