Dose‐dependent inhibition of the hemodynamic response to dipyridamole by caffeine

We investigated the effects of the adenosine antagonist caffeine on the hemodynamic response to dipyridamole infusion (0.4 mg/kg for 4 minutes). According to a randomized, placebo‐controlled double‐blind protocol, eight normotensive volunteers each participated in five tests: placebo after placebo, dipyridamole after placebo, and dipyridamole after 1, 2, and 4 mg/kg caffeine. Infusion of caffeine alone (4 mg/kg) induced an increase in mean arterial pressure of 6.1 ± 0.5 mm Hg versus 1.5 ± 0.9 mm Hg after placebo ( p < 0.05). Infusion of dipyridamole alone exerted a characteristic hemodynamic response with an increase in systolic blood pressure (+ 8.4 ± 2.4 mm Hg), pulse pressure (+ 7.0 ± 2.4 mm Hg), heart rate (+ 25.7 ± 3.8 beats/min) and calculated rate‐pressure product (+ 3419 mm Hg × beats per minute), all being significantly different from the changes induced by placebo. Caffeine induced a dose‐dependent attenuation of the response to dipyridamole, with a significant negative correlation between the dose of caffeine on the one hand (0, 1, 2, and 4 mg/kg) and the dipyridamole‐induced increments in systolic blood pressure ( r = −0.53), pulse pressure ( r = −0.50), heart rate ( r = −0.95), and rate‐pressure product ( r = −0.93) on the other hand. We conclude that caffeine attenuates the hemodynamic response to dipyridamole infusion in humans in a dose‐dependent fashion. Because of the widespread use of caffeine, this pharmacologic interaction may be of clinical importance, for example, in the diagnostic use of dipyridamole in thallium‐201 myocardial imaging. Clinical Pharmacology and Therapeutics (1991) 50, 529–537; doi: 10.1038/clpt.1991.178