Several studies have reported that, at variance with clinic blood pressure, ambulatory blood pressure is not reduced by treatment with placebo. However, this evidence has usually been obtained in small groups of subjects and no data are available from a larger sample of patients. To address this issue we have analyzed data from 116 outpatients involved in placebo-controlled studies on antihypertensive treatment. The patients were studied before and at the end of a 6- to 8-week period of placebo. In all patients, blood pressure was measured by sphygmomanometry and over the 24 h by automatic ambulatory monitoring. Administration of placebo was accompanied by a significant reduction in systolic and diastolic clinic blood pressure (-5.3 +/- 1.1 and -4.4 +/- 0.6 mm Hg, respectively; P < .01), but not in 24-h, daytime and nighttime blood pressure. Hourly systolic and diastolic blood pressure profiles were virtually superimposable in the two different periods, except for the first 4 h, in which systolic blood pressure was slightly but significantly lower during than before placebo (149.5 +/- 1.2 v 146.4 +/- 1.2 mm Hg; P < .05). These results provide a large database indicating that 24-h average blood pressure is not reduced by placebo, thus it is not necessary to include a placebo control group in antihypertensive drug studies in which ambulatory blood pressure monitoring is employed. A small placebo effect occurs, however, in the first hours of ambulatory monitoring. This may lead to a slight overestimation of the peak blood pressure effect of a drug and an underestimation of its trough-to-peak ratio if placebo correction of the data is not made or if the first part of ambulatory blood pressure monitoring is not excluded from data analysis.

Aims of our study were i) to compare in a large number of hypertensive subjects the relative effect of antihypertensive treatment on clinic (C) blood pressure (BP) and various ambulatory (A) BP components, and ii) to determine whether antihypertensive treatment affects BP variability. In 266 mild essential hypertensive outpatients (age: 18-78 years) CBP (trough measurements) and ABP (Spacelabs 90202 or 90207) were measured after 3 to 4 weeks of wash-out and after 4 to 8 weeks of treatment with an ACE-inhibitor (n = 135) or a calcium-antagonist (n = 131). ABP recordings were analyzed to obtain average 24 h, day-time (6 a.m. to midnight) and night-time (midnight to 6 a.m.) systolic and diastolic BP values and standard deviations (BP variabilities). Treatment reduced both CBP and ABP. Treatment-induced changes in CBP showed a poor correlation with those in 24h, day- and night-time BP (r never > 0.23) and the correlation was poor also when trough ABP (mean of last 2 h) was considered. Twenty-four hour, day- and night-time BP were similarly reduced by treatment with a direct relationship between the initial BP values and the subsequent BP falls. BP standard deviations were also reduced by treatment in relation to the pretreatment values but the overall reduction was small, limited to the day-time and proportional or less than proportional to the reduction in mean values, with no changes or an increase in variation coefficients. The effects of ACE-inhibitor and calcium-antagonist treatments were superimposable. Our results from a large data base show that antihypertensive treatment effectively reduces all ABP components. The reduction cannot be predicted by the concomitant fall in CBP but it relates to the initial ABP values. Treatment has a limited effect on BP variability, this being the case both for ACE-inhibitors and calcium-antagonists.

Subjects with a family history of parental hypertension are reported to have a slightly higher office blood pressure in the prehypertensive stage. Whether this reflects a hyperreactivity to blood pressure measurement or a more permanent blood pressure elevation, however, is not known. In the present study, blood pressure was measured in 15 normotensive subjects whose parents are both hypertensive (FH++), 15 normotensive subjects with one hypertensive parent (FH(+)-), and 15 normotensive subjects whose parents are not hypertensive (FH--); among the three groups, subjects were matched for age, sex, and body mass index. The measurements were made in the office during a variety of laboratory stressors and during a prolonged resting period, and for a 24-hour period (ambulatory blood pressure monitoring). Office blood pressure was higher in the FH++ group than in the FH-- group (p less than 0.05). The pressor responses to laboratory stressors were similar in the two groups, but the FH++ group had higher prolonged resting and 24-hour blood pressure than the FH-- group; the difference was always significant (p less than 0.05) for systolic blood pressure. The FH++ group also had a greater left ventricular mass index (on echocardiographic examination) than the FH-- group (p less than 0.01). The blood pressure values and echocardiographic values of the FH(+)- group tended to be between those of the other two groups. Thus, the higher blood pressure shown by individuals in the prehypertensive stage with a family history of parental hypertension does not reflect a hyperreactivity to stress but an early permanent blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)