Expression and mechanism of endogenous relaxin in hypertensive patients

Objective This study aimed to investigate the role of endogenous relaxin in the development of hypertension by examining its expression in hypertensive patients and various hypertensive rat models. Methods In this study, 61 hypertensive patients and 31 matched healthy individuals in the control group were included. Plasma samples from all participants were analyzed for biochemical markers, including relaxin-2, relaxin-3, triglycerides, fasting blood glucose, total cholesterol, and high-density lipoprotein cholesterol (HDL-C). Additionally, we examined the expression levels of relaxin-2 and relaxin-3 in both the heart and kidneys of rat models, specifically those with abdominal aortic coarctation and salt-sensitive hypertension. This allowed us to investigate the role of relaxin in these hypertensive conditions. Results There were no significant differences in age or gender between the control and hypertensive groups. However, the expression level of relaxin-2 in the hypertensive group was significantly lower compared to the control group. Specifically, the median plasma concentration of relaxin-2 in hypertensive patients was 7.61 pg/mL, while it was 9.34 pg/mL in the control group (P = 0.014). In contrast, relaxin-3 levels showed no significant difference between the hypertensive and control groups (P = 0.872). Correlation analysis indicated that relaxin-2 levels were associated with total cholesterol, red blood cell count, and white blood cell count, while relaxin-3 was only correlated with total cholesterol. In the kidney tissues of rats in the abdominal aortic coarctation model, relaxin-1, relaxin-3, and relaxin receptor 3 were significantly reduced compared to the control group (P < 0.05). In the salt-sensitive rat model, mRNA expression of relaxin-1 was increased, while relaxin receptor 1 mRNA was decreased compared to the control group. Conclusion The plasma level of relaxin-2 is decreased in hypertensive patients and shows correlations with total cholesterol, red blood cell count, and white blood cell count. These findings suggest that endogenous relaxin may play a role in the development of hypertension, potentially through specific signaling pathways in the kidneys.