A clinical study on the role of the renin-angiotensin-aldosterone system and catecholamines in chronic congestive heart failure.

Nishioka, Akinori; Kubo, Shinichiro; Hirota, Yuzo; Kawamura, Keishiro; Takatsu, T

doi:10.1536/ihj.23.527

Cited by 7 publications

(3 citation statements)

References 40 publications

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“…It has been shown clinically in complicated acute myocardial infarction [22] and in chronic congestive heart failure [5,9,12,14,24]. Our results demonstrate that such activation also takes place in an acute form of experimental failure in dog.…”

Section: Discussionsupporting

confidence: 71%

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Hall

Karlberg

1986

Res. Exp. Med.

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Acute left ventricular failure was induced in anesthetized dogs by left coronary embolization. Treatment with the converting enzyme inhibitor enalaprilat (MK-422) was then given. Hemodynamic registrations confirmed the development of left ventricular failure. Plasma concentrations of angiotensin II and aldosterone rose significantly. Treatment with enalaprilat was accompanied by significant reductions in heart preload and afterload and in plasma hormone concentrations.

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Section: Discussionsupporting

confidence: 71%

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Hall

Karlberg

1986

Res. Exp. Med.

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“…After one week of prazosin, resting plasma noradrenaline was increased by 371 pg/ml (+ 41, + 702) (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) nmol/l: + 0 24, + 4-14) (p = 0 02), but after one month resting and exercise values were similar to control values.…”

Section: Renin-angiotensin-aldosterone Systemmentioning

confidence: 87%

Vasodilatation with captopril and prazosin in chronic heart failure: double blind study at rest and on exercise.

Bayliss¹,

Canepa‐Anson²,

Norell³

et al. 1986

Heart

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SUMMARY A double blind cross over study was performed to compare the long term hormonal, haemodynamic, and clinical responses to specific inhibition of the renin-angiotensin-aldosterone system (captopril) and of the oa adrenoceptors of the sympathetic system (prazosin) both at rest and during upright exercise in patients with chronic heart failure. Sixteen patients completed one month's treatment with each drug.During conventional diuretic treatment (control) plasma renin activity, aldosterone, and noradrenaline were increased at rest and on exercise. Control left ventricular filling pressures were raised, and correlated significantly with plasma renin activity both at rest and on exercise. Systemic vascular resistance was increased at rest, and its reduction during exercise correlated inversely with the increase in plasma renin activity and plasma noradrenaline.After one month's treatment with captopril there were reductions in plasma aldosterone, weight, left ventricular filling pressure, and systemic vascular resistance at rest and on exercise. Dyspnoea was relieved and exercise capacity increased. The greater fall in systemic vascular resistance on exercise no longer correlated with the increase in plasma renin activity. During treatment with prazosin there were increases in plasma noradrenaline and, transiently, in plasma aldosterone. Fluid retention occurred, and left ventricular filling pressure was unchanged. Compared with control values systemic vascular resistance was reduced at rest but not on exercise. Dyspnoea and exercise capacity did not improve.In chronic heart failure, vasodilatation by inhibition of the a adrenergic system with prazosin causes compensatory stimulation of the renin-angiotensin-aldosterone system and does not result in clinical benefit. Inhibition of the renin-angiotensin-aldosterone system with captopril causes secondary vasodilatation at rest and on exercise and results in improvement in symptoms and exercise capacity.The haemodynamic abnormalities that occur at rest reduced, and there is arteriolar and venous conand during exercise in chronic heart failure have striction with abnormal distribution of blood flow. been well documented"2 At rest ventricular filling These abnormalities are accentuated during exercise pressures are usually raised, cardiac output is and this results in breathlessness and fatigue. Treatment with directly acting vasodilating drugs usuallyRequests for reprints to Dr G C Sutton, Hillingdon Hospital, produces acute haemodynamic changes, but the long Uxbridge, Middlesex UB8 3NN. term clinical response is often disappointing.

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“…9) Activation of the renin-angiotensin-aldosterone system (RAAS) has been shown to trigger the exacerbation of congestive heart failure and cardiac sympathetic nerve activity. 10,11) In addition, CTGF was reported to be produced by the stimulation of angiotensin II. 12,13) Therefore, we assumed that the plasma CTGF level is correlated with cardiac sympathetic nerve activity evaluated by 123 I-MIBG scintigraphy in patients with dilated cardiomyopathy.…”

Section: 2) 123mentioning

confidence: 99%

Relation Between Connective Tissue Growth Factor and Cardiac Sympathetic Nerve Activity in Heart Failure in DCM Patients

et al. 2012

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SummaryCardiac fibrosis is an important process of myocardial remodeling. Connective tissue growth factor (CTGF) is a cytokine that plays a key role in the occurrence of progressive fibrosis and excessive scarring. CTGF levels are increased in the failing heart. In addition, sympathetic nerve activity is enhanced in the failing heart, and exacerbates heart failure. To clarify the relation between cardiac sympathetic nerve activity and CTGF, we studied 35 (M/F = 28/7 patients) aged 57 ± 15 years with dilated cardiomyopathy (DCM). Cardiac sympathetic nerve activity was estimated from the total defect score (TDS) and from the H/M ratio and washout rate (WR) on I-123-MIBG imaging. Cardiac symptoms (NYHA class), exercise capacity (specific activity scale: SAS), brain natriuretic peptide (BNP), hemodynamics, and CTGF were assessed. There was a significant correlation between the CTGF and WR on I-123-MIBG (r = 0.45, P = 0.008). Also, a higher plasma CTGF level was associated with a lower SAS score (r = 0.51, P = 0.002), but not the TDS, H/M ratio, or BNP concentration. Moreover, a higher NYHA class and pulmonary artery wedge pressure were associated with a higher plasma CTGF level. The plasma CTGF level can be strongly related with cardiac sympathetic nerve activity in heart failure in DCM patients. (Int Heart J 2012; 53: 282-286)

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A clinical study on the role of the renin-angiotensin-aldosterone system and catecholamines in chronic congestive heart failure.

Cited by 7 publications

References 40 publications

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Vasodilatation with captopril and prazosin in chronic heart failure: double blind study at rest and on exercise.

Relation Between Connective Tissue Growth Factor and Cardiac Sympathetic Nerve Activity in Heart Failure in DCM Patients

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