Baroreflex sensitivity and the blood pressure response to beta-blockade

The objective of this analysis was to determine whether changes in barorefl ex sensitivity (BRS) within 35 hypertensive patients (25 M, 10 F, mean age 47 years) treated with beta-blockade as monotherapy relate to reductions in ambulatory blood pressure (BP) or its variability. BP was recorded intra-a rterially directly from the brachial artery before and during submaximal ex ercise. BRS was determined by the phenylephrine injection technique. MAP an d its variability were determined for the awake period of 24-h BP monitorin g. Subjects were randomised to one of atenolol, metoprolol, pindolol, or pr opranolol, and restudied after a mean of 5 months. B-blockade increased BRS in 24 patients and decreased BRS in 11. BRS increased from 6.53 +/- 4.94 t o 9.40 +/- 8.62 ms/mm Hg (mean +/- s.d.) (P < 0.01). Waking ambulatory MAP decreased from 125.8 +/- 15.8 to 106.4 +/- 16.2 mm Hg (P < 0.0001), but its variability did not change. Higher BRS after chronic beta-blockade was ass ociated with a decrease in waking ambulatory MAP (r = -0.55, P < 0.001), bu t not with its variability (r = - 0.08). beta-blockade attenuated the press er response to exercise, but there was a positive relationship between the effect of beta-blockade on BRS, and on the rise in systolic BP during bicyc ling (r = 0.63; P < 0.001). Any dampening effect of beta-blockade on BP var iability at rest in hypertensive patients with the greatest increase in BRS may be offset by increased presser responses to physical activity such as exercise. consequently, BP variability is unaffected, even though reduction s in ambulatory BP during chronic beta-blockade are inversely related to ch anges in BRS. BP responses to beta-blockade may be a function of the action of this class of drugs on BRS. However, there is considerable variation, b etween subjects, in their effect on BRS. This may have implications for oth er conditions, such as dilated cardiomyopathy, or following myocardial infa rction, in which improvement in BRS is one mechanism by which beta-adrenoce ptor blockade could improve survival.