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

1999 ◽  
Vol 277 (4) ◽  
pp. H1609-H1617 ◽  
Author(s):  
Hiroya Kawai ◽  
Tai-Hwang M. Fan ◽  
Erdan Dong ◽  
Rizwan A. Siddiqui ◽  
Akito Yatani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Tyrosine Hydroxylase ◽  
Nerve Terminal ◽  
Ace Inhibitors ◽  
Sympathetic Nerve ◽  
Ace Inhibition ◽  
Inotropic Response ◽  
Cardiac Sympathetic Nerve ◽  
Beneficial Effects ◽  
Sympathetic Nerve Terminal

Cardiac sympathetic nerve terminal dysfunction plays an important role in the downregulation of myocardial β-adrenoceptors in heart failure. To determine whether chronic angiotensin-converting enzyme (ACE) inhibition improved cardiac sympathetic nerve terminal function and hence increased myocardial β-adrenergic 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 β-adrenoceptor density. These changes were accompanied by decreases in right ventricular norepinephrine (NE) uptake and neuronal NE histofluorescence and tyrosine hydroxylase immunoreactive profiles. ACE inhibitors had no effect on the production of heart failure but greatly reduced the attenuation of cardiac NE uptake, neuronal NE histofluorescence, and tyrosine hydroxylase immunoreactive profiles. ACE inhibition also improved the inotropic response to isoproterenol and restored myocardial β-adrenoceptor density. The changes probably are caused by reduction of cardiac NE release by ACE inhibition and may contribute to the beneficial effects of ACE inhibitor therapy in patients with chronic heart failure.

Renin-angiotensin system inhibition on noradrenergic nerve terminal function in pacing-induced heart failure

2000 ◽  
Vol 279 (6) ◽  
pp. H3012-H3019 ◽  
Author(s):  
Hiroya Kawai ◽  
Suzanne Y. Stevens ◽  
Chang-Seng Liang
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Left Ventricular ◽  
Cardiac Sympathetic Nerve ◽  
Angiotensin System ◽  
Sympathetic Nerve Terminal

Chronic angiotensin-converting enzyme (ACE) inhibition has been shown to improve cardiac sympathetic nerve terminal function in heart failure. To determine whether similar effects could be produced by angiotensin II AT1 receptor blockade, we administered the ACE inhibitor quinapril, angiotensin II AT1 receptor blocker losartan, or both agents together, to rabbits with pacing-induced heart failure. Chronic rapid pacing produced left ventricular dilation and decline of fractional shortening, increased plasma norepinephrine (NE), and caused reductions of myocardial NE uptake activity, NE histofluorescence profile, and tyrosine hydroxylase immunostained profile. Administration of quinapril or losartan retarded the progression of left ventricular dysfunction and attenuated cardiac sympathetic nerve terminal abnormalities in heart failure. Quinapril and losartan together produced greater effects than either agent alone. The effect of renin-angiotensin system inhibition on improvement of left ventricular function and remodeling, however, was not sustained. Our results suggest that the effects of ACE inhibitors are mediated via the reduction of angiotensin II and that angiotensin II plays a pivotal role in modulating cardiac sympathetic nerve terminal function during development of heart failure. The combined effect of ACE inhibition and angiotensin II AT1 receptor blockade on cardiac sympathetic nerve terminal dysfunction may contribute to the beneficial effects on cardiac function in heart failure.

scholarly journals 809-3 Desipramine Attenuates the Cardiac Sympathetic Nerve Terminal Abnormalities in Congestive Heart Failure

1995 ◽  
Vol 25 (2) ◽  
pp. 425A-426A
Author(s):  
Akito Yatani ◽  
Suzanne Y. Felten ◽  
Yoshihiro Himura ◽  
Michihiro Kashiki ◽  
Chang-seng Liang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Terminal

scholarly journals Alterations by Norepinephrine of Cardiac Sympathetic Nerve Terminal Function and Myocardial β-Adrenergic Receptor Sensitivity in the Ferret

Circulation ◽  
2000 ◽  
Vol 102 (1) ◽  
pp. 96-103 ◽  
Author(s):  
Chang-seng Liang ◽  
Naomi Kenmotsu Rounds ◽  
Erdan Dong ◽  
Suzanne Y. Stevens ◽  
Junya Shite ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Adrenergic Receptor ◽  
Cardiac Sympathetic Nerve ◽  
Receptor Sensitivity ◽  
Sympathetic Nerve Terminal

A new, concise dialysis approach to assessment of cardiac sympathetic nerve terminal abnormalities

1997 ◽  
Vol 272 (3) ◽  
pp. H1182-H1187 ◽  
Author(s):  
T. Yamazaki ◽  
T. Akiyama ◽  
H. Kitagawa ◽  
Y. Takauchi ◽  
T. Kawada ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Storage Capacity ◽  
Left Ventricular ◽  
Neuronal Uptake ◽  
Local Administration ◽  
Nerve Terminals ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Terminal ◽  
And Storage

We applied a dialysis technique to the hearts of anesthetized cats and examined whether the concentration of dialysate norepinephrine (NE) reflected NE disposition at the cardiac sympathetic nerve terminals. Dialysis probes were implanted in the left ventricular wall, and dialysate NE concentrations were measured as an index of myocardial interstitial NE levels. Stimulation of stellate ganglia significantly increased dialysate NE responses that were suppressed by local administration of an NE-releasing inhibitor (omega-conotoxin GVIA, 10 microM). Increments in basal dialysate NE levels were correlated with concentrations of a locally administered neuronal uptake blocker (desipramine; 1, 10, and 100 microM). Desipramine (100 microM) augmented stimulation-induced dialysate NE responses. Local administration of a neuronal vesicle uptake blocker (reserpine, 1 and 10 microM) did not alter dialysate NE levels but increased dialysate dihydroxyphenylglycol levels. An NE-releasing amine (tyramine, 100 microg/ml) was locally administered to examine NE storage capacity at the nerve terminal. The tyramine-induced NE-releasing response was completely abolished by pretreatment with reserpine (1 mg/kg i.p.). Thus cardiac dialysis with local administration of a pharmacological tool offers a new, concise approach to assessment of neuronal NE release, uptake, vesicle uptake, and storage capacity by cardiac sympathetic nerve terminals.

ω-Conotoxin GVIA and desipramine insensitive norepinephrine efflux from cardiac sympathetic nerve terminal

1997 ◽  
Vol 761 (2) ◽  
pp. 329-332 ◽  
Author(s):  
Toji Yamazaki ◽  
Toru Kawada ◽  
Tsuyoshi Akiyama ◽  
Hirotoshi Kitagawa ◽  
Yuji Takauchi ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Terminal

Long-term serial changes of cardiac sympathetic nerve dysfunction in acute decompensated heart failure patients with reduced, mid-range and preserved left ventricular ejection fraction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Seo ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
Y Furukawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sympathetic Nerve ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Left Ventricular Ejection ◽  
Mibg Imaging ◽  
Cardiac Sympathetic Nerve ◽  
Heart Failure Hospitalization ◽  
Nerve Dysfunction

Abstract Background Cardiac sympathetic nerve dysfunction, which is assessed by I-123 metaiodobenzylguanidine (MIBG) imaging, is associated with the poor outcomes in patients with chronic heart failure (CHF). Serial evaluation of cardiac MIBG imaging was shown to be useful for predicting adverse outcome in CHF. However, there was no information available on long-term serial changes of cardiac sympathetic nerve dysfunction after discharge of acute decompensated heart failure (ADHF) hospitalization. Purpose We aimed to clarify the serial change of cardiac MIBG imaging parameter in long-term after discharge of heart failure hospitalization, especially relating to HFrEF (LVEF<40%), HFmrEF (40%≤LVEF<50%) and HFpEF (LVEF≥50%). Methods We studied 112 patients (HFrEF; n=44, HFmrEF; n=23 and HFpEF; n=45) who were admitted for ADHF, discharged with survival and without heart failure hospitalization during follow-up period. All patients underwent cardiac MIBG imaging at the timing of discharge, in 6–12 months and in 18–24 months after discharge. The cardiac MIBG heart to mediastinum ratio (H/M) was calculated on the early image and the delayed image (late H/M). The cardiac MIBG washout rate (WR) was calculated from the early and delayed planar images after taking radioactive decay of I-123 into consideration. Results In HFrEF patients, late H/M was significantly improved from discharge to 6–12 months data (1.60±0.24 vs 1.75±0.31, p<0.0001). Late H/M of HFmrEF patients was also significantly improved from discharge to 18–24 months data (1.71±0.27 vs 1.84±0.29 p=0.043). On the other hand, late H/M of HFpEF patients was not significantly changed. As for WR, WR in HFrEF and HFmrEF patients was significantly improved from discharge to 18–24 months data, although WR of HFpEF was not significantly changed. Conclusion The improvement in cardiac sympathetic nerve dysfunction was observed in patients with HFrEF and HFmrEF, not in HFpEF, after the discharge of acute heart failure hospitalization. Funding Acknowledgement Type of funding source: None

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