Joanna Burns, David A.S.G. Mary, Alan F. Mackintosh, Stephen G. Ball, and John P. Greenwood

Department of Cardiology, Leeds Teaching Hospitals NHS Trust, Leeds, U.K.

Abstract

Essential hypertension (EHT) and sympathetic activation are recognized as independent cardiovascular risk factors. The effects of several chronic anti-hypertensive therapies on efferent sympathetic nerve activity have been studied previously. Thiazide diuretics are often recommended therapy, either first line, or in combination, although we know little of their effects in this regard. Therefore, this study was designed in patients with untreated EHT to quantify any effect of bendroflumethiazide (BFZ) therapy on muscle sympathetic nerve activity (MSNA).

We examined 11 EHT patients before and after 3 ± 0.5 months of oral BFZ therapy (EHT + BFZ) in comparison to 11 age, gender and body weight matched group of patients with mild EHT who were followed up over a similar period of time with no anti-hypertensive therapy (EHT-N). MSNA was quantified as the mean frequency of single units (s-MSNA) and as multiunit bursts (MSNA bursts) using the technique of microneurography. BFZ significantly (at least P 0.03) increased MSNA by 6.0 ± 2.3 bursts/100 cardiac beats and s-MSNA by 9.0 ± 3.2 impulses/100 cardiac beats from 57 ± 2.3 bursts/100 cardiac beats and 70 ± 3.6 impulses/100 cardiac beats respectively. The increase of indices of sympathetic nerve activity in EHT+ BFZ group amounted to at least 9.4 ± 4.6% of baseline values; in contrast, no significant changes occurred over the same time in EHT-N group.

These findings of a significant increase in central sympathetic neural drive to the periphery with bendroflumethiazide therapy have implications for the planning of anti-hypertensive therapy if the aim is to reduce the cardiovascular risk associated with sympathetic hyperactivity.

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