Advances in the role of the Sympathetic Nervous System in cardiovascular medicine
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Sympathetic neural activation in nondiabetic metabolic syndrome and its further augmentation by hypertension

Huggett RJ, Burns J, Mackintosh AF, Mary David ASG



Summary

Similar results were found in nondiabetic patients with metabolic syndrome receiving antihypertensive treatment if needed. The aim of this study was to investigate whether the level of sympathetic nervous system (SNS) activity would be increased in normotensive patients with metabolic syndrome and whether the additional presence of essential hypertension would further amplify this sympathetic activation. Results showed that SNS activity was increased in metabolic syndrome to a similar extent compared with essential hypertension and potentiated when essential hypertension occurs with the metabolic syndrome. Baroreflex sensitivity was decreased in patients with essential hypertension compared with normotensive patients, indicating that essential hypertension is correlated with SNS activity. Vascular resistance is significantly increased in hypertensives with metabolic syndrome compared with those without metabolic syndrome, despite antihypertensive treatment, suggesting that SNS overactivity exerts a vasoconstrictor effect at the peripheral level, which is potentiated in the presence of metabolic syndrome. In addition, the positive and significant correlation between plasma insulin levels and the sympathetic activity observed in patients with metabolic syndrome suggests that SNS overactivity aggravates the metabolic syndrome in the long term.

Hypertension. 2004;44:847-852.


Commentary

The authors investigated whether the metabolic syndrome without diabetes is associated with SNS overactivity. They also studied whether hypertension could enhance SNS overactivity in subjects with metabolic syndrome. For this purpose, they measured muscle sympathetic nervous activity (MSNA), as well as a series of relevant hemodynamic and metabolic activities in the following groups of subjects:

  • Metabolic syndrome + hypertension
  • Metabolic syndrome, normotensives
  • Hypertensives, no metabolic syndrome
  • Control subjects, without hypertension or metabolic syndrome

As expected, the authors observed the occurrence of enhanced MSNA, reflecting enhanced SNS activity in all subjects with metabolic syndrome. Furthermore, the occurrence of hypertension appeared to further stimulate SNS overactivity in subjects with metabolic syndrome.
Accordingly, they concluded that:

  1. SNS overeractivity occurs in subjects with metabolic
    syndrome, and the presence of hypertension further
    enhances sympathetic activity.
  2. The activation of vasoconstrictor sympathetic activity appears to be stronger in subjects with hypertension + metabolic syndrome than in subjects with either hypertension or metabolic syndrome alone.
    It can therefore be concluded that the metabolic syndrome is a state of SNS overactivity, and that the presence of hypertension aggravates this condition.

The enhanced SNS activity can be expected to contribute to the elevated cardiovascular risk, in subjects with metabolic syndrome and hypertension, and even more so in patients suffering from both conditions simultaneously. These pathological changes deserve to be taken into account in the pharmacotherapeutic approach to the metabolic syndrome.

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