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Am J Physiol Heart Circ Physiol 286: H2151-H2158, 2004. First published February 5, 2004; doi:10.1152/ajpheart.00887.2003
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Presynaptic modulation of evoked NE release contributes to sympathetic activation after pressure overload

Wendell S. Akers1 and Lisa A. Cassis2,3

1Pharmacy Practice and Science and 2Pharmaceutical Sciences, College of Pharmacy, and 3Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky 40536-0082

Submitted 13 September 2003 ; accepted in final form 26 January 2004

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 {alpha}2- and {beta}2-receptors and ANG II subtype 1 (AT1) 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 {alpha}2-agonist UK-14,304 decreased evoked 3H overflow with no differences between groups. The {beta}2-agonist salbutamol increased evoked 3H overflow with greater sensitivity in slices from AC rats. The {beta}-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.

heart; angiotensin II; {alpha}2-autoreceptor; {beta}2-receptor; norepinephrine


Address for reprint requests and other correspondence: W. S. Akers, Div. of Pharmacy Practice and Science, 800 Rose St., Rm. 231B, College of Pharmacy, Univ. of Kentucky, Lexington, KY 40536-0082 (E-mail: wcaker0{at}uky.edu).






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