Background-Cardiovagal autonomic control declines with age in adult subjects, which is related in part to increasing stiffness of the barosensory vessel wall. It is not known, however, whether autonomic function changes with age in children. Methods and Results-We studied 137 healthy subjects divided into 4 age groups: group 1, 7 to 14 years; group 2, 11 to 14 years; group 3, 15 to 18 years; and group 4, 19 to 22 years. Brachial artery pressure was measured by sphygmomanometry and continuous radial artery pressure and carotid artery pulse pressure (⌬P) by applanation tonometry. The R-R interval was derived from the ECG. Autonomic function was assessed by spontaneous sequence and frequency-domain indices, which indicate the extent of coupling between fluctuations in heart rate and systolic pressure. Carotid artery diastolic diameter (DD) and pulsatile distension (⌬D) were measured by echo wall tracking; carotid compliance coefficient (CC) was defined as ⌬D/⌬P and distensibility coefficient as 2⌬D/DD · ⌬P. , with no significant changes afterward. CC and DC were inversely proportional to age (rϭϪ0.49 and Ϫ0.62, respectively, PϽ0.001). The efficiency of neural integrative mechanisms, estimated as the ratio of spontaneous indices and CC, more than doubled from group 1 to group 3. Spontaneous indices were linearly related to measures of cardiac vagal activity. Conclusions-The increase in spontaneous indices from early childhood to adolescence, despite gradual stiffening of the carotid artery, may indicate improved cardiovagal autonomic function, which is most likely a result of maturation of neural mechanisms, attaining peak level at adolescence.

According to conventional wisdom, hysteresis in cardiac vagal baroreflex function exhibits a specific pattern: pressure falls are associated with longer heart periods and a smaller linear gain. A similar pattern occurs in the pressure-diameter relationship of barosensory vessels, and therefore it has been suggested that baroreflex hysteresis derives solely from vascular behaviour. However, we hypothesized that mechanical and neural baroreflex components contribute equally to baroreflex hysteresis. Blood pressure, carotid diameter and the electrocardiogram were recorded continuously during two trials of sequential bolus injections of nitroprusside and phenylephrine in 14 young healthy subjects. Baroreflex gain and its mechanical and neural components were estimated for falls and rises in pressure and diameter. The position or set point of the relations was quantified at the mean pressure and mean diameter. Gains were determined via piecewise linear regression. Set points and gains for falls versus rises in pressure and diameter were compared with the Chow test. Hysteresis was observed in all individuals, but not in every trial. In most, but not all, trials pressure falls were associated with longer heart periods and smaller linear gain, as conventional wisdom would predict. However, the pattern of hysteresis derived from the interaction of both mechanical and neural components. The two components most often acted in opposition to determine differences in set point, but in conjunction to determine differences in baroreflex gain. Therefore, we conclude that hysteresis is not solely determined by barosensory vessel behaviour but by the complex interaction of mechanical and neural aspects of the arterial baroreflex.

In the current study we explored (1) if there were differences in sympathetic activity and baroreflex function by age, sex, or physical activity status, (2) if any aspect of baroreflex function related to differences in resting sympathetic activity, and (3) if mechanical and/or neural baroreflex components related to differences in integrated baroreflex gain. Electrocardiogram, blood pressure, carotid diameter and muscle sympathetic nerve activity were recorded continuously at rest and during sequential bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 older sedentary and 10 older trained individuals. Analyses of co-variance were used to examine age, sex and training status differences and to explore the explanatory power of integrated baroreflex gain and its mechanical and neural components. Training status and sex influenced neither resting sympathetic outflow nor sympathetic baroreflex gain components. Older subjects had a smaller mechanical component and a strong tendency towards a greater neural component of the sympathetic baroreflex during both pressure falls and pressure rises. Opposing age-related changes in mechanical and neural components resulted in a smaller integrated gain during pressure falls, but a greater integrated gain during pressure rises in older subjects. Thus, in older individuals, compromised sympathetic activation to pressure falls was owing to the stiffening of barosensory vessels, whereas the more sensitive sympathoinhibition to pressure rise was due to an increased neural control. Enhanced neural control with age, however, did not contribute the increased resting sympathetic outflow, which indicates that these two changes are probably driven by distinct neural mechanisms.