Beta blockers modify cardiovascular neural regulation, which may contribute to their protective effect against sudden cardiac death. To evaluate the effects of beta blockade on cardiovascular autonomic reactions caused by acute coronary occlusion in humans, heart rate (HR) variability was analyzed in the time and frequency domains immediately before and during balloon occlusion of a coronary artery in 116 patients randomly assigned to either chronic beta-blocker therapy (beta-blocker group) or no beta blockade (control group) during elective 1-vessel coronary angioplasty. Coronary occlusion (mean 112 seconds) caused a significant increase in both the high- and low-frequency components of HR variability in the control group (n = 58), from 2.7 +/- 1.6 to 3.4 +/- 1.7 (logarithmic units, p < 0.001) and from 4.3 +/- 1.3 to 4.8 +/- 1.5 (p < 0.01), respectively, whereas in the beta-blocker group (n = 58), the high-frequency power did not change during occlusion, but the low-frequency power increased from 3.9 +/- 1.4 to 4.4 +/- 1.4 (p = 0.01). Changes in high- and low-frequency components and HR were related to the change in systolic blood pressure during occlusion in the beta-blocker group (r = 0.53, p < 0.001; r = 0.34, p < 0.05; and r = -0.41, p < 0.01, respectively), but not in the control group (r = -0.17, r = -0.14, and r = 0.24, respectively). Thus, beta blockade attenuates the initial vagal activation associated with acute coronary occlusion and seems to maintain baroreflex-mediated cardiovascular control. The maintained integrity of baroreflex regulation and the alleviation of extreme autonomic reactions during beta blockade may modify the clinical outcome of acute coronary occlusion in a beneficial way.