Aim To investigate the correlation between serum homocysteine (Hcy) level and high density lipoprotein (HDL) subclasses in patients with H-type hypertension, and to study the function of HDL subclasses on the anti-inflammatory capacity of endothelial cells. Methods 76 patients with isolated hypertension, 85 patients with H-type hypertension and 133 healthy adults were included in our study. The concentration of fasting blood glucose (FBG), serum creatine(SCr), uric acid (UA), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDLC), high density lipoprotein cholesterol (HDLC), HDL2, HDL3 and Hcy were measured for each participants. Furthermore, HDL subclasses were isolated and purified from plasma of 6 participants for each group by fast protein liquid chromatography (FPLC). Large HDL (L-HDL) anti-inflammatory capacity was determined as its ability to suppress tumor necrosis factor alpha (TNF-α)-induced vascular cell adhesion molecule-1 (VCAM-1) expression in human umbilical vein endothelium (HUVEC) in vitro. Results There were no significant differences of FBG, UA, TC, LDLC level between health control, isolated hypertension and H-type hypertension(P＞0.05). Compared with health control and isolated hypertension, patients with H-type hypertension had significantly lower level of HDL2 and HDLC and higher level of HDL3(P＜0.001). Correlation analysis indicated that plasma Hcy level was negatively related with HDLC(r＝－0.532,P＜0.01) and HDL2 level (r＝－0.626, P＜0.01). There was no significant relationship between plasma Hcy level and HDL3 (r＝0.10,P＝0.083). The L-HDL from health controls and patients with isolated hypertension significantly decreased TNF-α-induced VCAM-1 expression in HUVEC (P＜0.05). However, the L-HDL from patients with H-type hypertension indicated no effect on decreasing TNF-α-induced VCAM-1 expression in HUVEC (P＞0.05). Conclusion Patients with H-type hypertension had abnormal HDL subclasses distribution and decreased function of L-HDL on anti-inflammatory capacity of HUVEC.