SYMPATHETIC, BAROREFLEX AND METABOLIC ABNORMALITIES IN THE OPTIMAL, NORMAL AND HIGH-NORMAL BLOOD PRESSURE STATE: 9C.02

Objective: Essential hypertension is characterized by a marked sympathetic activation, which is coupled with an impairment of baroreceptor-heart rate control. Whether the behaviour of sympathetic and baroreceptor function is peculiar of the established hypertensive state or it does also characterize the so-called high-normal blood pressure (BP) state is unknown, however. Design and Methods: In 12 subjects with optimal BP (O, age: 38.1 ± 2.1 years, mean ± SEM), 10 with normal BP (N) and 9 with high-normal BP (HN, ESH guidelines classification), all age-matched with O, we measured beat-to-beat arterial BP (Finapres), heart rate (HR, EKG), plasma norepinephrine (NE, venous sample, HPLC) and muscle sympathetic nerve traffic (MSNA, microneurography peroneal nerve) at rest and during baroreceptor stimulation and deactivation (vasoactive drug infusion technique). Measurements also included anthropometric as well as metabolic parameters, such as HOMA index. Results: Body mass index,waist circumference and HOMA index were slightly, although not significantly, greater in HN than in the other 2 groups. The progressive and significant increase in BP values seen from O to N and HN was paralleled by an elevation in MSNA values, which achieved statistical significance in HN(47.4 ± 2.2 vs 37.1 ± 1.9 and 40.9 ± 2.1 bursts/100 heart beats in O and N respectively, P < 0.05). NE values were also significantly increased in HN (324.4 ± 31 vs 182.4 ± 22 and 195.6 ± 30 pg/ml, P < 0.05). In HN, baroreceptor-HR control was displaced toward elevated BP values and impaired compared with N and O (average reduction, 21.5%). In contrast, the sympathoinhibitory and sympathoexcitatory responses to baroreceptor stimulation and deactivation were displaced toward elevated BP values but similar in all the 3 groups. Conclusions: These data provide the first evidence that high-normal BP is already characterized by a sympathetic activation coupled with a baroreflex-HR impairment. The sympathetic overdrive, which is dependent on central and/or metabolic factors (i.e. insulin resistance) but not on baroreflex mechanisms, is likely to contribute to the increased cardiovascular risk seen in HN.