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Background: We aimed to investigate the effects and dose dependency of aspirin on endothelial functions and prevalence of aspirin resistance in newly diagnosed hypertensive patients without previous drug therapy and development of cardiac complications. Hypothesis: Acetylsalicyclic acid improves endothelial function. Methods: Fifty-eight hypertensive patients and 61 healthy subjects in the control group were included in the study. Endothelial functions of the patient and control groups were evaluated with brachial artery examination. Patient and control groups were divided into 2 groups. A total of 100 mg and 300 mg of aspirin were given to the separate groups for 1 week. After 1 week, endothelial functions were reevaluated and aspirin resistance examined with a platelet function analyzer (PFA-100; Dade Behring, Marbourg, Germany). Results: Baseline flow-mediated dilatation (FMD) change percent in hypertensive patients was 9.8%, and it was significantly lower than in the control group (12%) (P < 0.001). Frequency of acetylsalicylic acid (ASA) resistance was 20% and 26% in control and hypertensive patient groups, respectively (P = not significant). ASA resistance was 28% and 24% in 100 mg and 300 mg in hypertensive patients, respectively (P = not significant). FMD change percent increased both in the control and hypertensive groups after ASA treatment from 12.4% to 13.3% and 9.8 % to 11.9 %, respectively. FMD percentage change was significantly increased in hypertensive patients irrespective of ASA resistance (P = 0.02, for ASA resistance [+]; P < 0.012, for ASA resistance [−]). Conclusions: Endothelial functions were impaired more in hypertensive patients compared to the control group. Endothelial functions were improved with all ASA doses in hypertensive patients irrespective of ASA resistance. IntroductionThe vascular endothelium regulates cardiovascular homeostasis and blood pressure (BP) through the release of nitric oxide (NO).1,2 NO is an anti-inflammatory, antithrombotic, and antiproliferative agent that limits expression of adhesion molecules and chemotactic factors on endothelium, and inhibits platelet aggregation and proliferation of smooth muscle cells.