Patients with EHT+DM2, EHT, or DM2 had central sympathetic hyperactivity, although plasma insulin levels were raised only in EHT+DM2 and DM2. The combination of EHT and DM2 resulted in the greatest sympathetic hyperactivity and level of plasma insulin, and this hyperactivity could constitute a mechanism for the increased risks of this condition.

Abstract-Hypertension is a major cardiovascular risk factor in the metabolic syndrome (MS) in which the presence of insulin resistance, glucose intolerance, abnormal lipoprotein metabolism, and central obesity all confer an increased risk. Because essential hypertension (EHT), insulinemia, and visceral fat are associated with sympathetic hyperactivity, which is itself known to increase cardiovascular risk, the aim of this study was to see if MS is a state of sympathetic nerve hyperactivity and if the additional presence of EHT intensifies this hyperactivity. In 69 closely matched subjects, comprising hypertensive MS (MSϩEHT, 18), normotensive MS (MS-EHT, 17), hypertensives without MS (EHT, 16), and normotensive controls without MS (NC, 18), we measured resting muscle sympathetic nerve activity (MSNA) as assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in MSϩEHT (76Ϯ3.1 impulses/100 beats) was greater (at least PϽ0.01) than in MS-EHT (62Ϯ3.2 impulses/100 beats) and in EHT (60Ϯ2.3 impulses/100 beats), and all these were significantly greater (at least PϽ0.01) than in NC (46Ϯ2.7 impulse/100 beats). The multi-unit MSNA followed a similar trend. These findings suggest that MS is a state of sympathetic nerve hyperactivity and that the additional presence of hypertension further intensifies this hyperactivity. The degree of sympathetic hyperactivity seen in this study could be argued at least partly to contribute to the higher cardiovascular risk and metabolic abnormalities seen in MSϩEHT patients. Key Words: sympathetic nervous system Ⅲ hypertension Ⅲ metabolism L ittle information exists on the level of sympathetic nerve activity in the metabolic syndrome (MS) and whether the presence of essential hypertension (EHT), which is itself a state of sympathetic nerve hyperactivity, 1-4 augments this activity. Sympathetic activation has already been associated with many of the individual components of the MS, such as visceral obesity, 5 insulinemia, 6 EHT, 1-4 and type 2 diabetes. 7 The majority of treated hypertensives have in addition at least one other MS component; 8 also, it is now widely recognized that MS constitutes a cluster of major cardiovascular risk factors, 9 represented mainly by insulin resistance and obesity in which hypertension as an individual component overlaps the least with the other components. 10 Hypertension is known to be one of the highest predictors of cardiovascular morbidity and mortality associated with the MS. 11,12 Furthermore, sympathetic activation in EHT is believed to contribute to cardiovascular risk. 13,14 We therefore tested the hypothesis that the level of sympathetic nerve activity would be increased in normotensive MS and that the additional presence of EHT would further amplify this sympathetic activation. Methods SubjectsA total of 72 white subjects were examined, comprising 18 subjects with hypertensive MS (MSϩEHT), 18 normotensive MS (MS-EHT), 18 hypertensives without MS (EHT), and 18 normotensive controls wi...

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Aims/hypothesis: Acute insulinaemia activates the sympathetic drive in a nonuniform manner. The extent and nature of such activation in type 2 diabetic patients who do not have neuropathy have not yet been addressed despite evidence relating sympathetic activation to cardiovascular risk. We planned to determine the magnitude and extent of the sympathetic drive and its reflex responses in patients with type 2 diabetes and fasting hyperinsulinaemia. Methods: We measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multiunit bursts and single unit muscle sympathetic nerve activity (s-MSNA) in 17 overweight patients with type 2 diabetes and two matched normal control groups comprising 17 overweight and 16 normal-weight subjects. We also tested the MSNA and s-MSNA responses to cold pressor and isometric hand-grip tests, along with the effect of sympatho-vagal balance on heart period variability. Results: Both MSNA and s-MSNA in the group with type 2 diabetes (66±3.5 bursts/100 beats and 78±4.5 impulses/100 beats) were greater (at least p<0.0001) than in the overweight control group (42±2.6 bursts/100 beats and 48±3.4 impulses/100 beats) and normal-weight control group (43±6.2 bursts/100 beats and 51±7.1 impulses/100 beats), though the three groups had similar reflex responses, baroreflex sensitivity and sympathovagal balance controlling the heart period. Conclusions/ interpretation: The patients with type 2 diabetes had no evidence of impaired reflex or autonomic control of heart period variability at a time when there was central sympathetic activation to the periphery. Furthermore, being overweight itself was not associated with sympathetic activation.

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