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 guanosine 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.
- Cyclic guanosine monophosphate plasma
- Endothelial function
- Nitric oxide
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine