| Abstract: | Background: It has been reported that administration of low‐dose aspirin significantly reduces the frequency of major cardiovascular events in patients with hypertension and coronary artery disease. It is generally considered that the preventative effects of long‐term aspirin administration on major cardiovascular events are due to the inhibition of platelet aggregation. Hypothesis: It is not known whether administration of low‐dose aspirin restores endothelium‐dependent vasodilatation, and this study was undertaken to prove or disprove this question in patients with hypertension. Methods: Flow‐mediated endothelium‐dependent dilatation and glyceryl trinitrate‐induced endothelium‐independent dilatation were investigated in 18 hypertensive patients and 10 normotensive control subjects. In the hypertensive patients, flow‐mediated dilatation was investigated and cyclic guano‐sine monophosphate plasma (cGMP) was measured before and at 8 weeks after the administration of 162 mg of aspirin. Results: Flow‐mediated dilatation before aspirin administration was more reduced in the hypertensive patients than in the control subjects (6.4 ± 2.0% vs. 11.3 ± 2.3%, p< 0.0001). Glyceryl trinitrate‐induced dilatation before aspirin administration was similar in hypertensive patients and control subjects. Flow‐mediated dilatation after aspirin administration was improved compared with that before aspirin administration (10.4 ± 3.5% vs. 6.4 ± 2.0%, p<0.0004). The cGMP product after aspirin administration was significantly higher than that before aspirin administration. Conclusions: Administration of low‐dose aspirin may restore the endothelium‐dependent vasodilatation in hypertensive patients. Furthermore, increased nitric oxide production may play a partial role in the improvement in endothelial function induced by administration of low‐dose aspirin. |
