The role of endothelial dysfunction and inflammation in young-onset hypertension

Abstract

Young-onset hypertension is defined as hypertension seen in patients under 40 years of age. The relationship between hypertension and inflammation has been identified. In hypertensive patients, YKL-40 has been shown to be increased by endothelial dysfunction as a local secreted mediator. Vaspin, an adipokine, is derived from adipose tissue and irreversibly inhibits serine proteases. It has been reported that vaspin may act as an anti-inflammatory agent and increases endothelial-dependent relaxation, also has a positive effect on nitric oxide bioavailability, which is important in the etiology of endothelial dysfunction. In clinical practice, some indirect and practical methods may help to evaluate endothelial functions, including flow-mediated dilatation (FMD), which is considered to be the most practical and effective method. The present study was performed to determine the circulating YKL-40 and vaspin levels in young-onset hypertensive patients and healthy subjects and to reveal their relationships with vascular function evaluated by FMD.We enrolled 24 patients diagnosed with young-onset hypertension and 22 volunteers without hypertension. The plasma levels of YKL-40 and vaspin were determined using an enzyme-linked immunosorbent assay and quantitative enzyme-linked immunoassay, respectively. FMD was measured using a Doppler ultrasound device. Compared with those in normotensive controls, the plasma levels of YKL-40 were significantly higher, and FMD values were significantly lower in patients with young-onset hypertension (P<0.05). The plasma levels of YKL-40 were also negatively correlated with FMD. However, no statistically significant difference was noted in the levels of vaspin between the two groups (P=0.531). In this study, decreased FMD and increased levels of YKL-40 were associated with endothelial dysfunction and inflammation in patients with young-onset hypertension, suggesting the role of these factors in the etiology of hypertension.