Background: It has been reported that administration of low-dose aspirin si
gnificantly reduces the frequency of major cardiovascular events in patient
s 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 rest
ores endothelium-dependent vasodilatation, and this study was undertaken to
prove or disprove this question in patients with hypertension.
Methods: How-mediated endothelium-dependent dilatation and glyceryl trinitr
ate-induced endothelium-independent dilatation were investigated in 18 hype
rtensive patients and 10 normotensive control subjects. In the hypertensive
patients, flow-mediated dilatation was investigated and cyclic guanosine m
onophosphate plasma (cGMP) was measured before and at 8 weeks after the adm
inistration of 162 mg of aspirin.
Results: Flow-mediated dilatation before aspirin administration was more re
duced 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 b
efore aspirin administration was similar in hypertensive patients and contr
ol subjects. Flow-mediated dilatation after aspirin administration was impr
oved 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 endot
helial function induced by administration of low-dose aspirin.