Acute hemodynamic and hormonal effects of central versus peripheral sympathetic inhibition in patients with congestive heart failure

Maria Teresa Olivari, T. Barry Levine, Jay N. Cohn

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13 Scopus citations

Abstract

Indoramin, an α1 antagonist, and guanabenz, an α2 agonist, were given to 10 patients with severe congestive heart failure to compare the hemodynamic and hormonal effects of a reduction in sympathetic tone obtained through inhibition of postsynaptic α1 receptors versus the decrease in sympathetic activity achieved by stimulating central or presynaptic peripheral α2 adrenoceptors. Both drugs produced similar reduction in systemic arterial pressure. However, only indoramin significantly decreased systemic and pulmonary vascular resistances from 1529 ± 526 to 1071 ± 356 and from 721 ± 422 to 412 ± 257 dynes ± 5 ± cm-5, respectively, and increased stroke index from 26.6 ± 9.5 to 33.3 ± 9.5 ml/m2 (all p < 0.01). Heart rate fell significantly only after guanabenz. Plasma norepinephrine, unchanged after indoramin, fell in each patient after guanabenz: The mean value decreased from 746 ± 332 to 461 ± 255 pg/ml (p < 0.01). Plasma renin activity increased only after indoramin. The data demonstrate: (a) a decrease in sympathetic activity due to blockade of α1 adrenoreceptors produces marked peripheral and pulmonary vasodilation; (b) noradrenergic transmitter release in heart failure is regulated by α2 receptors; (c) an α2-mediated decrease in sympathetic activity and in plasma norepinephrine has a bradycardic effect but does not produce a vasodilator effect. Although the acute hemodynamic effects of indoramin were more prominent than those of guanabenz, the more favorable neurohumoral effects of guanabenz suggest the possibility of long-term benefit in the treatment of heart failure.

Original languageEnglish (US)
Pages (from-to)973-977
Number of pages5
JournalJournal of Cardiovascular Pharmacology
Volume8
Issue number5
DOIs
StatePublished - Sep 1986

Keywords

  • Plasma norepinephrine
  • Plasma renin activity
  • α agonist
  • α antagonist

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