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 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.

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

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.

Chronic administration of angiotensin II receptor antagonist, TCV-116, in cardiomyopathic hamsters

1994 ◽  
Vol 267 (6) ◽  
pp. H2297-H2304 ◽  
Author(s):  
F. Nakamura ◽  
M. Nagano ◽  
R. Kobayashi ◽  
J. Higaki ◽  
H. Mikami ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Cardiac Dysfunction ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Lv Function ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
At1 Antagonist

We examined whether specific blockade of the renin-angiotensin system is beneficial for the treatment of cardiac dysfunction in heart failure. The angiotensin II type-1 (AT1) receptor antagonist TCV-116 (10 mg.kg-1.day-1) or its vehicle was given orally to UM-X 7.1 cardiomyopathic (CM) and normal Golden Syrian (GS) hamsters for 8 wk. Plasma and cardiac angiotensin II levels were significantly higher in CM than in GS hamsters. The CM heart showed a smaller response of left ventricular (LV) pressure and first derivative of maximal LV pressure (+dP/dtmax) to the elevation of perfusion pressure (from 60 to 120 cmH2O) in Langendorff-perfused than in GS heart. Treatment with TCV-116 did not affect LV function in GS but significantly improved cardiac contractility in CM hamsters. These results suggest that the renin-angiotensin system plays an important role in the development of cardiac dysfunction due to cardiomyopathy. Blockade of this system by the AT1 antagonist TCV-116 appears to be useful in the prevention of heart failure.

A Review of Angiotensin Receptor Blocker-based Therapies at all Levels of Cardiovascular Risk

2011 ◽  
Vol 7 (4) ◽  
pp. 254 ◽  
Author(s):  
Giuliano Tocci ◽  
Lorenzo Castello ◽  
Massimo Volpe ◽  
◽  
◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Clinical Settings ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Receptor Blockers ◽  
Artery Disease

The renin–angiotensin system (RAS) has a key role in the maintenance of cardiovascular homeostasis, and water and electrolyte metabolism in healthy subjects, as well as in several diseases including hypertension, left ventricular hypertrophy and dysfunction, coronary artery disease, renal disease and congestive heart failure. These conditions are all characterised by abnormal production and activity of angiotensin II, which represents the final effector of the RAS. Over the last few decades, accumulating evidence has demonstrated that antihypertensive therapy based on angiotensin II receptor blockers (ARBs) has a major role in the selective antagonism of the main pathological activities of angiotensin II. Significant efforts have been made to demonstrate that blocking the angiotensin II receptor type 1 (AT1) subtype receptors through ARB-based therapy results in proven benefits in different clinical settings. In this review, we discuss the main benefits of antihypertensive strategies based on ARBs in terms of their efficacy, safety and tolerability.

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
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