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Sympathoinhibition by atorvastatin in hypertensive patients

Marc E Gomes1, Cees J Tack, Freek W Verheugt

  • 1Department of Internal Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.

Circulation Journal : Official Journal of the Japanese Circulation Society
|October 19, 2010
PubMed

Insights

Atorvastatin, a statin drug, was found to reduce sympathetic nervous system activity in patients with hypertension. This study supports the role of HMG-CoA reductase in regulating sympathetic activity.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Hypertension Management

Background:

  • Experimental data suggest HMG-CoA reductase inhibitors (statins) may decrease sympathetic activity in hypertension.
  • This hypothesis has not been previously tested in human patients with primary hypertension.

Purpose of the Study:

  • To investigate the effect of atorvastatin on sympathetic nervous system activity in patients with primary hypertension.
  • To test the hypothesis that HMG-CoA reductase plays a role in sympathetic nervous system regulation.

Main Methods:

  • A randomized, placebo-controlled, double-blind, cross-over trial involving 13 patients with mild to moderate primary hypertension.
  • Treatment involved 3 weeks of atorvastatin (80mg/day) or placebo, followed by a crossover.
  • Sympathetic nervous system activity was measured using microneurography (muscle sympathetic nerve activity: MSNA).
  • Additional measurements included heart rate variability (HRV), plasma norepinephrine, blood pressure (BP), and heart rate (HR).

Main Results:

  • Atorvastatin significantly reduced postganglionic MSNA compared to placebo (35.0±2.0 vs 39.2±1.5 bursts/min, P=0.008).
  • Heart rate-corrected MSNA was also significantly reduced by atorvastatin (58.5±2.0 vs 64.7±3.0 bursts/100 beats, P=0.02).
  • No significant effects of atorvastatin were observed on plasma norepinephrine, HRV, BP, or HR.

Conclusions:

  • Atorvastatin effectively reduces sympathetic nervous system activity (MSNA) in patients with mild to moderate hypertension.
  • These findings support the role of HMG-CoA reductase in the regulation of sympathetic activity.
  • Further research may explore the clinical implications of statin-induced sympathetic modulation in hypertensive patients.
Abstract

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