Townend et al18 showed that single doses of indomethacin attenuated the increase in cardiac output and renal blood flow in response to captopril therapy, but did not attenuate the increase in forearm or calf blood flow. Hall et al19 noted that a single dose of ASA, 350 mg, attenuated the decrease in systemic vascular resistance, left ventricular filling pressure, and total pulmonary resistance as well as the increase in cardiac output elicited by enalapril maleate therapy. Nashimura et al20 showed that indomethacin therapy attenuated the peripheral hemodynamic effects of captopril therapy in patients with heart failure. These findings were not confirmed by studies of van Wijngaarden et al,21 who found that even though the combination of ASA and captopril reduced the levels of prostaglandins, there was no discernible difference in the hemodynamic effects of captopril therapy alone or with ASA. The fact that a lower dose of ASA (<300 mg) was used in this study might explain the discrepancy, as other authors who used low doses of ASA (<300 mg) also did not find a significant hemodynamic interaction.22,23 Low doses of ASA have been shown to inhibit thromboxane synthesis, but higher doses of ASA (>325 mg) are required to inhibit synthesis of vasodilating prostaglandins.24 Therefore, a higher dose of ASA would be necessary to inhibit the presumed vasodilating prostaglandin-mediated hemodynamic effect of ACE inhibitors. Thus, prostaglandin synthesis would not be inhibited by lower doses of ASA (80-100 mg), which would still exert the intended antiplatelet action through blockade of thromboxane synthesis.