ACE inhibition improves cardiac NE uptake and attenuates sympathetic nerve terminal abnormalities in heart failure

and Chang-seng Liang. ACE inhibition improves cardiac NE uptake and attenuates sympathetic nerve terminal abnor-malities in heart failure. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1609–H1617, 1999.—Cardiac sympathetic nerve terminal dysfunction plays an important role in the downregulation of myocardial b-adrenoceptors in heart fail-ure. To determine whether chronic angiotensin-converting enzyme (ACE) inhibition improved cardiac sympathetic nerve terminal function and hence increased myocardial b-adrener-gic responsiveness, we administered ACE inhibitors to dogs with chronic right-sided heart failure (RHF) produced by tricuspid avulsion and pulmonary artery constriction. The RHF animals exhibited fluid retention, elevated right heart filling pressures, blunted inotropic response to isoproterenol, and reduced b-adrenoceptor density. These changes wer