Objectives: Whether muscle sympathetic nerve activity (MSNA) is increased in young subjects with mild essential hypertension has not been firmly established, and the potential haemodynamic correlates of any such increase have not been specifically investigated. The objectives of this study were to quantitate MSNA from the peroneal nerve of young subjects with mild hypertension, to determine the haemodynamic and neurohumoral correlates of sympathetic vasoconstrictor nerve traffic in such subjects, and to document the stability of these observations.
Design: Twelve young untrained subjects with mild essential hypertension (mean age 31 years, average clinic blood pressure 151/95 mmHg) and 11 age- and weight-matched normotensive subjects were studied on two sessions, at least 1 month apart, at the same time of day and under identical laboratory conditions.
Methods: Blood pressure (non-invasive), microneurography (MSNA; peroneal nerve), cardiac output and calculated total peripheral resistance (echocardiography and continuous-wave Doppler) and calf blood flow and resistance (plethysmography) were recorded during supine rest and assessed for condition and study order effects by two-way analysis of variance. Reproducibility of MSNA was quantified by the standard deviation of the mean difference (SDD) between the values obtained on the two study days.
Results: Muscle sympathetic nerve burst frequency and incidence, calf vascular resistance and cardiac output and index were significantly higher in hypertensive subjects, whereas heart rate, total peripheral resistance, plasma noradrenaline and plasma atrial natriuretic factor concentrations were similar in the two groups. There was no study order effect, in either group, on mean values for MSNA or these haemodynamic variables, but the SDD (day 1-day 2 variation) in muscle sympathetic burst frequency was significantly greater in hypertensive subjects.
Conclusions: Mild essential hypertension in young subjects can be characterized by augmented MSNA as measured from the peroneal nerve, greater between-session variation in sympathetic burst frequency (but no study order effect), and increased calf vascular resistance and cardiac output. These sympathoneural and haemodynamic alterations are potential mechanisms of primary hypertension.