Presynaptic modulation of evoked NE release contributes to sympathetic activation after pressure overload

Wendell S. Akers, Lisa A. Cassis

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Activation of the sympathetic nervous system is well documented in heart failure. Our previous studies demonstrated an increase in evoked norepinephrine (NE) release from left ventricle (LV) slices at 10 days of pressure overload. The purpose of this study was to test the hypothesis that presynaptic modulation of NE release contributes to sympathetic activation after pressure overload. We examined the functional status of the presynaptic α 2- and β2-receptors and ANG II subtype 1 (AT 1) receptors in LV slices from 10-day aortic constricted (AC) and sham-operated (SO) rats. Evoked 3H overflow from LV slices preloaded with [3H]NE was increased in AC rats. The α 2-agonist UK-14,304 decreased evoked 3H overflow with no differences between groups. The β2-agonist salbutamol increased evoked 3H overflow with greater sensitivity in slices from AC rats. The β-antagonist propranolol decreased evoked 3H overflow from LV slices of AC rats but not controls. ANG II increased evoked 3H overflow with greater sensitivity in slices from AC rats. These data support the hypothesis that aberrant presynaptic modulation of catecholamine release contributes to sympathetic activation after pressure overload.

Original languageEnglish
Pages (from-to)H2151-H2158
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume286
Issue number6 55-6
DOIs
StatePublished - Jun 2004

Keywords

  • Angiotensin II
  • Heart
  • Norepinephrine
  • α-autoreceptor
  • β -receptor

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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