Search for a command to run...
Blood pressure and heart rate variabilities were studied in 89 ambulant normotensive or essential hypertensive subjects in whom blood pressure was recorded intra-arterially for 24 hours (Oxford method) under standardized living conditions. Data were analyzed beat to beat by a computer to provide mean values of the 48 half hours of the 24-hour period. Variabilities were assessed by the standard deviation and variation coefficients separately obtained for each half hour, as well as by the standard deviations and variation coefficients obtained by averaging the 48 mean values. In each subject, blood pressure and heart rate varied markedly either among or within half hours, indicating the existence of relatively long- and short-term variabilities during the 24 hours. When averaged for all subjects, the long-term variabilities showed only one systematic component, i.e., the marked reduction occurring during sleep. Sleep was further responsible for a marked reduction in the short-term blood pressure and heart rate variabilities. These variabilities showed marked (though nonsystematic) modifications, even outside sleep, which were positively related to the blood pressure and heart rate means. Modifications in blood pressure and heart rate means and short-term variabilities were also positively related to each other. All these features were common to normotensives and hypertensives. In hypertensives, the absolute long- and short-term blood pressure variabilities were greater than in normotensives, but the percent blood pressure variabilities were similar. Heart rate variabilities (both absolute and percent) were similar in normotensive and hypertensive subjects. Heart rate variabilities were also similar whether the subjects had impaired or preserved baroreflex control of heart rate (vasoactive drug technique). These findings uncover a number of factors that are associated with and responsible for blood pressure and heart rate variabilities in human beings. The nature of these factors suggests a primary role of central nervous mechanisms in the production of these phenomena and in the overall cardiovascular modulation, with no substantial difference between conditions of normal and chronically elevated blood pressure.