Effects of amlodipine on sympathetic nerve traffic and baroreflex control of circulation in heart failure

Guido Grassi, Domenico Spaziani, Gino Seravalle, Giovanni Bertinieri, Raffaella Dell'Oro, Cesare Cuspidi, Giuseppe Mancia

Research output: Contribution to journalArticle

Abstract

Short-acting calcium antagonists exert a sympathoexcitation that in heart failure further enhances an already elevated sympathetic activity. Whether this is also the case for long-acting formulations is not yet established, despite the prognostic importance of sympathetic activation in heart failure. It is also undetermined whether in this condition long-acting calcium antagonists favorably affect a mechanism potentially responsible for the sympathetic activation, ie, the baroreflex impairment. In 28 heart failure patients (NYHA functional class II) under conventional treatment we measured plasma norepinephrine and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during arterial baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were performed at baseline and after 8 weeks of daily oral amlodipine administration (10 mg/d, 14 patients) or before and after an 8-week period without calcium antagonist administration (14 patients). Amlodipine caused a small and insignificant blood pressure reduction. Heart rate, left ventricular ejection fraction, and plasma renin and aldosterone concentrations were not affected. This was the case also for plasma norepinephrine (from 2.213±0.41 to 2.50±0.34 nmol/L, mean±SEM), muscle sympathetic nerve activity (from 54.4±5.9 to 51.0±4.3 bursts/min), and arterial baroreflex responses. No change in the above- mentioned variables was seen in the control group. Thus, in mild heart failure amlodipine treatment does not adversely affect sympathetic activity and baroreflex control of the heart and sympathetic tone. This implies that in this condition long-acting calcium antagonists can be administered without untoward neurohumoral effects anytime conventional treatment needs to be complemented by drugs causing additional vasodilatation.

Original languageEnglish
Pages (from-to)671-675
Number of pages5
JournalHypertension
Volume33
Issue number2
Publication statusPublished - Feb 1999

Keywords

  • Autonomic
  • Baroreceptors
  • Calcium antagonists heart failure
  • Nervous system
  • Sympathetic

ASJC Scopus subject areas

  • Internal Medicine

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