摘要
Background Some studies have shown that serum resistin levels increase in hypertensive patients. Whether the increase of resistin is related to inflammatory or vascular endothelial function is still unknown. We investigated the relationship of increased resistin levels to inflammatory factors and circulating biomarkers of vascular endothelial function in hypertensive patients. Methods One hundred and forty-four nondiabetic patients with new onset, hypertension were recruited. Blood pressure, blood glucose, insulin, resistin, tumour necrosis factor-a （TNF-a）, interleukin-6 （IL-6）, von Willebrand factor （vWF）, endothelin-1 （ET-1） and nitric oxide （NO） were measured. The homeostasis model assessment, insulin resistance index （HOMA-IR） was calculated. Patients were divided into two groups according to the median level of resistin. Cytokine levels and indicators of vascular endothelial function were compared. Multiple linear regression was used to determine factors influencing resistin. Results Serum resistin ranged from 2.57 ng/ml to 20.18 ng/ml in hypertensive patients. High resistin group （〉8.36 ng/ml） had higher levels of TNF-a, IL-6, vWF and ET-1 but lower level of NO compared with low resistin group （P 〈0.01）. Resistin was positively correlated with body mass index, systolic blood pressure, HOMA-IR, low-density lipoprotein cholesterol, TNF-a and ET-1 but negatively correlated with NO （all P 〈0.05）. Multiple linear regression analysis revealed that HOMA-IR, TNF-a, NO and ET-1 are independent predictors of resistin with standardized regression coefficients of 0.625, 0.368, -0.260 and 0.222, respectively （all P 〈0.01）. Conclusions We conclude that higher resistin levels are associated with inflammatory activation and endothelial dysfunction, because patients with essential hypertension have increased TNF-a, IL-6, vWF and ET-1 and decreased NO. Moreover, the statistical association of resistin with TNF-a, NO and ET-1 suggests involvement of resistin in the progression of hypertension by influencing inflammation and endothelial function.
Background Some studies have shown that serum resistin levels increase in hypertensive patients. Whether the increase of resistin is related to inflammatory or vascular endothelial function is still unknown. We investigated the relationship of increased resistin levels to inflammatory factors and circulating biomarkers of vascular endothelial function in hypertensive patients. Methods One hundred and forty-four nondiabetic patients with new onset, hypertension were recruited. Blood pressure, blood glucose, insulin, resistin, tumour necrosis factor-a （TNF-a）, interleukin-6 （IL-6）, von Willebrand factor （vWF）, endothelin-1 （ET-1） and nitric oxide （NO） were measured. The homeostasis model assessment, insulin resistance index （HOMA-IR） was calculated. Patients were divided into two groups according to the median level of resistin. Cytokine levels and indicators of vascular endothelial function were compared. Multiple linear regression was used to determine factors influencing resistin. Results Serum resistin ranged from 2.57 ng/ml to 20.18 ng/ml in hypertensive patients. High resistin group （〉8.36 ng/ml） had higher levels of TNF-a, IL-6, vWF and ET-1 but lower level of NO compared with low resistin group （P 〈0.01）. Resistin was positively correlated with body mass index, systolic blood pressure, HOMA-IR, low-density lipoprotein cholesterol, TNF-a and ET-1 but negatively correlated with NO （all P 〈0.05）. Multiple linear regression analysis revealed that HOMA-IR, TNF-a, NO and ET-1 are independent predictors of resistin with standardized regression coefficients of 0.625, 0.368, -0.260 and 0.222, respectively （all P 〈0.01）. Conclusions We conclude that higher resistin levels are associated with inflammatory activation and endothelial dysfunction, because patients with essential hypertension have increased TNF-a, IL-6, vWF and ET-1 and decreased NO. Moreover, the statistical association of resistin with TNF-a, NO and ET-1 suggests involvement of resistin in the progression of hypertension by influencing inflammation and endothelial function.
