Aim: To investigate the relationships of clinical or ambulatory pulse pressure (cPP or aPP), systolic blood pressure(SBP), diastolic blood pressure(DBP), and mean arterial pressure(MAP) with endothelial dysfunction and left ventricular hypertrophy(LVH) in patients with essential hypertension(EH), so as to study the possible mechanism of LVH and endothelial damage after EH. Methods: Totally 555 patients with mild to moderate EH were selected from the Hypertension Clinic, Department of Cardiology, Xuanwu Hospital, Capital University of Medical Sciences from June 1998 to November 2002, they were all diagnosed for the first time or had stopped all antihypertensive drugs for more than 2 weeks. According to the levels of cPP and 24-hour aPP, the 555 cases were divided into PP ≤ 40 mm Hg(1 mm Hg = 0.133 kPa) group, 40 mm Hg < PP ≤50 mm Hg group, 50 mm Hg < PP ≤ 60 mm Hg group, PP > 60 mm Hg group; According to their left ventricular mass index (LVMI), they were divided into LVH group(n = 237, LVMI > 134 g/m2 in males and > 110 g/m2 in females) and non-LVH group(n = 318). Results: With the increase of 24-hour aPP, plasma endothelin(ET) level was increased(P < 0.01), nitric oxide (NO) level was decreased (P < 0.05), and the ratio of ET to NO(ET/NO) was increased(P < 0.05). The 24-hour aPP, day PP, night PP and cPP had significant positive correlations with ET level and ET/NO(r = 0.171 to 0.377, P < 0.01), while had remarkable negative correlation with plasma No level(r = -0.269, -0.259, -0.167, P < 0.01; r = -0.141, P < 0.05). PP and 24-hour aPP had more obvious correlation with ET and NO than SBP and cPP respectively; while DBP and MAP had no correlation with ET and NO levels. SBP and PP in the LVP group were remarkably increased as compared with those in the non-LVP group(P < 0.001), while there was unobvious difference in DBP, and the main reason for the increased PP was the increase of SBP. Taking ET and NO as the dependent variables, and cPP or ambulatory SBP, DBP, PP and MAP as the independent variables, only cPP or aPP were involved in the regression equation[Results of clinical blood pressure (BP) indexes: ET = 0.497 × cPP + 44.613 (R2 = 0.029, P < 0.01); NO = -0.398 × cPP + 100.454. Results of 24-hour BP indexes: ET = 1.269 × 24-hour PP + 12.536(R2 = 0.090, P < 0.01); NO = -0.15 × 24-hour aPP + 130.266(R2 = 0.072, P < 0.01)]. Taking LVMI as the dependent variable, and cPP or 24-hour SBP, DBP, PP and MAP as independent variables, only cPP or 24-hour SBP were involved in the regression equation[Results of clinical BP indexes: LVMI = 0.405 × clinical SBP + 37.769 (R2 = 0.072, P < 0.01); Results of 24-hour HP indexes: LVMI = 0.611 × 24-hour SBP + 19.821 (R2 = 0.174, P < 0.01)]. Conclusion: Increases of both PP and SBP can lead to LVP, endothelial dysfunction and diastolic hypofunction in EH patients; Increased PP is the main decisive factor that results in the endothelial dysfunction of EH patients, with the increase of PP, vascular endothelial dysfunction is aggregated; Increased SBP is the main decisive factor that leads to LVP of EH patients; Increased DBP and MAP have no obvious influence on LVP and vascular endothelial dysfunction.