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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ibopamine (IP) is a novel dopamine analogue for which beneficial effects have been shown in chronic heart failure. Hemodynamic effects of the substance include an increase in cardiac output and a decrease in the peripheral resistance. Aside from these hemodynamic effects, changes in renal (increased diuresis) and neurohumoral parameters (decreased plasma renin activity, aldosterone, norepinephrine, increased ANF and cGMP) have been found. The renal effects may originate from three independent mechanisms: 1) direct impact of improved hemodynamic parameters on the renal perfusion; 2) the improved cardiac performance results in a reduction of compensatory hormonal adaptations, such as the activation of the renin-angiotensin-aldosterone-axis or the sympathetic system; 3) direct effects on the intrarenal hemodynamic and glomerular/tubular functions induced by stimulation of renal dopaminergic receptors. The continued decrease of the plasma renin activity by 35% results in a reduction of the plasma levels of angiotensin II and aldosterone. Additionally, an increase in plasma atrial natriuretic factor (ANF) and its second messenger cyclic guanosine monophosphate (cGMP) was observed after ibopamine, which could contribute to the diuretic action of the drug. These findings underline the importance of extrarenal effects of a drug in the treatment of heart failure, this may essentially contribute to the improvement of cardiac performance, independent of positive inotropy.
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PMID:[Ibopamine--acute hemodynamic, renal and neurohumoral effects]. 168 94

The prognosis for clinical congestive heart failure remains poor even with modern treatment as severe ventricular dysfunction is often present at the time of clinical presentation. A substantial improvement in prognosis might be achieved through earlier intervention and a preventive approach to treatment following myocardial infarction to delay progressive ventricular dilation and the occurrence of clinical heart failure. The rationale for treatment of left ventricular dysfunction following myocardial infarction is further supported by the prognostic importance of ventricular dilation and by experimental animal studies that demonstrate that converting enzyme inhibition can improve ventricular function and survival following myocardial infarction. Similarly, clinical studies have demonstrated that converting enzyme inhibition can improve ventricular function during the year following transmural myocardial infarction. Possible mechanisms of action that require further understanding include ventricular afterload reduction and direct coronary and tissue effects of angiotensin II blockade. The further benefit to be obtained from very early intervention following myocardial infarction is currently being addressed in several studies. Large-scale studies also in progress should determine the mortality benefit of such treatment. Further questions that remain include the optimal timing of intervention, comparison with other treatments such as nitrates and beta-blockade, and also the use of appropriate combination treatments.
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PMID:Angiotensin-converting enzyme inhibitors in heart failure: a role after myocardial infarction. 172 54

The effects of inhibition of the renin angiotensin aldosterone system on the natriuretic and diuretic actions of an intravenous dose of frusemide 40 mg in patients with chronic cardiac failure maintained on oral diuretics were studied in the supine and erect positions. In the patients studied in the supine position the total 4 hour diuresis was decreased from 995 (92) ml to 668 (66) ml and the total 4 hour natriuresis fell from 105 (14) mmol to 67 (14) mmol following the administration of captopril. Creatinine clearance fell from 87 (8) ml/minute to 52 (15) ml/minute. In the patients studied in the erect position the total 4 hour diuresis was 596 (87) ml without captopril and 562 (83) ml with captopril. Total 4 hour natriuresis was 71 (13) mmol without captopril and 65 (9) mmol with captopril. Creatinine clearance was reduced by captopril from 82 (7) ml/minute to 47 (12) ml/minute. The reduction in the diuretic and natriuretic response to frusemide caused by captopril in the supine position is mediated through a fall in glomerular filtration rate. However, in the erect position, which is associated with even further increases in activity of the renin angiotensin aldosterone system, the reduction in diuresis and natriuresis that a fall in glomerular filtration rate would cause is offset by abolition of the rise in sodium retaining hormones, angiotensin II and aldosterone that mediate the antinatriuretic effect of the erect position.
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PMID:Posture determines the nature of the interaction between angiotensin converting enzyme inhibitors and loop diuretics in patients with chronic cardiac failure. 176 31

Attempts at treating idiopathic cardiomyopathy have been made both clinically and experimentally using the cardiomyopathic Syrian hamster. In recent years, the angiotensin converting enzyme (ACE) inhibitor has attracted considerable attention as an agent to treat heart failure. We administered the ACE inhibitor captopril to the cardiomyopathic hamster. In this study, 15 mg/kg body weight of captopril was administered to the cardiomyopathic hamster J2N at 5 weeks of age for 10 weeks; age matched J2N hamsters were used as non-treated control animals. At the end of captopril administration, blood was collected from the ventral aorta. Serum malondialdehyde (MDA), serum CPK, aldolase and LDH were determined, and myosin isoenzyme patterns of the extirpated myocardium were compared. Additionally, ECGs were compared and the fibrotic ratio of both ventricles determined. Serum MDA, CPK, and aldolase increased significantly in the cardiomyopathic hamster, whereas these indices were significantly inhibited in the hamster treated with captopril. The pathological ECG findings and the ventricular V3 predominant myosin isoenzyme patterns of the J2N were also much improved in the captopril group. However, the improvement in these parameters by enalapril administration was less than that seen with captopril. These results suggested that the effect of captopril is not only due to decrease of the angiotensin II level, but also due to increase in tissue kinin and vasodilatory prostaglandin which play an important role in the beneficial effect of captopril.
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PMID:Protective effect of ACE- and kininase-inhibitor on the onset of cardiomyopathy. 178 64

Seventy four patients aged 35-74 years who had mitral valvular disease were examined for renin, angiotensin II, aldosterone, and vasopressin, of whom 49 patients were diagnosed as having a mitral valve defect with prevalent stenosis, 25 presented with a mitral valve defect with prevalent heart failure. Circulatory disorders, Stages I-II, were found in 41 patients, Stage IIB in 23, and Stage III in 10 patients. There were no significant differences in the parameters of the renin-angiotensin-aldosterone system (RAAS) and vasopressin in untreated adult and elderly patients with mitral valvular disease at rest. As circulatory disorders progressed, the RAAS parameters significantly increased in all the groups. However, the patients with prevalent stenosis showed higher blood renin levels than did those with prevalent heart failure, irrespective of its severity. In refractory heart failure, the significant differences remained to a greater extent only for renin. The treatment with peripheral vasodilators (isosorbide dinitrate and corinfar) resulted in compensatory activation of the neurohumoral vasoconstrictive system, thereafter the RAAS parameters significantly increased after the drugs.
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PMID:[Renin-angiotensin-aldosterone system and vasopressin in adult and aged patients with acquired mitral valve defects]. 179 80

Left ventricular hypertrophy (LVH) is the major risk factor associated with myocardial failure. An explanation for why a presumptive adaptation such as LVH would prove pathological has been elusive. Insights into the impairment in contractility of the hypertrophied myocardium have been sought in the biochemistry of cardiac myocyte contraction. Equally compelling is a consideration of abnormalities in myocardial structure that impair organ contractile function while preserving myocyte contractility. For example, in the LVH that accompanies hypertension, the extracellular space is frequently the site of an abnormal accumulation of fibrillar collagen. This reactive and progressive interstitial and perivascular fibrosis accounts for abnormal myocardial stiffness and ultimately ventricular dysfunction and is likely a result of cardiac fibroblast growth and enhanced collagen synthesis. The disproportionate involvement of this nonmyocyte cell, however, is not a uniform accompaniment to myocyte hypertrophy and LVH, suggesting that the growth of myocyte and nonmyocyte cells is independent of each other. This has now been demonstrated in in vivo studies of experimental hypertension in which the abnormal fibrous tissue response was found in the hypertensive, hypertrophied left ventricle as well as in the normotensive, nonhypertrophied right ventricle. These findings further suggest that a circulating substance that gained access to the common coronary circulation of the ventricles was involved. This hypothesis has been tested in various animal models in which plasma concentrations of angiotensin II and aldosterone were varied. Based on morphometric and morphological findings, it can be concluded that arterial hypertension (i.e., an elevation in coronary perfusion pressure) together with elevated circulating aldosterone are associated with cardiac fibroblast involvement and the resultant heterogeneity in tissue structure. Nonmyocyte cells of the cardiac interstitium represent an important determinant of pathological LVH. The mechanisms that invoke short- (e.g., collagen metabolism) and long-term (e.g., mitosis) responses of cardiac fibroblasts require further investigation and integration of in vitro with in vivo studies. The stage is set, however, to prevent pathological LVH resulting from myocardial fibrosis as well as to reverse it.
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PMID:Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system. 182 92

The potent diuretic and natriuretic properties of atrial natriuretic factor (ANF) suggest that atrial hormones may participate to the regulation of salt and water excretion under physiological conditions. ANF, via the increase of its intracellular second messenger cGMP, has been recently shown to inhibit the apical sodium channel of the inner medullary collecting tubule (IMCD). In addition, ANF inhibits renin and aldosterone synthesis and antagonizes the antinatriuretic effects of angiotensin II. ANF may also contribute to the excretion of free water by inhibiting both the secretion of vasopressin and its antidiuretic action. ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. All these factors could explain the lack of significant natriuretic effect of both endogenous and exogenous ANF in some pathological conditions such as heart failure or liver cirrhosis. ANF may also been concerned in water homeostasis. In addition to the well-known osmoregulatory pathways of water metabolism, we recently found that ANF could be involved in the volume adjustment to acute water intake in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor and the endocrine control of electrolyte homeostasis. 183 42

The purpose of this investigation was to compare the chronic effects of converting enzyme inhibition with captopril to direct blockade of angiotensin II (AII) with DuP 753 in the rat model of heart failure. Rats with chronic heart failure postinfarction were treated for 2 weeks with either captopril (2 g/L, N = 9) in their drinking water or with DuP 753 (40 mg/kg/day for two weeks by gastric gavage, N = 10), or placebo (N = 9). At this dose, DuP 753 shifted the log dose-pressor response curve to AII parallel to the right by two orders of magnitude in both chronically treated normal and heart failure rats. In rats with heart failure, DuP 753 and captopril reduced left ventricular end-diastolic pressure from 26.7 +/- 1.5 to 14.2 +/- 3.0 (P less than .01) and 15.8 +/- 2.2 mm Hg (P less than .05), respectively, left ventricular end-diastolic volume index from 2.71 +/- 0.10 to 2.03 +/- 0.17 (P less than .05) and 2.18 +/- 0.15 (P less than .05), respectively; venous compliance increased from 2.27 +/- 0.06 to 2.80 +/- 0.18 (P less than .05) and 3.02 +/- 0.21 mL/mm Hg/kg (P less than .01), respectively. There were no significant changes in left ventricular weight/body weight ratio, mean aortic pressure, heart rate, or right atrial pressure. There was a trend, but not significant, for a reduction in total blood volume from 65.8 +/- 1.1 to 59.4 +/- 3.0 and 64.9 +/- 3.9 mL/kg, respectively. Thus, direct blockade of AII with DuP 753 or with converting enzyme inhibition with captopril produces similar hemodynamic changes in rats with heart failure after myocardial infarction.
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PMID:Hemodynamic effects of direct angiotensin II blockade compared to converting enzyme inhibition in rat model of heart failure. 185 61

If ACE-inhibitors are considered for therapy in patients with heart failure, the actual renal function has to be taken into account. In patients with reduced intravascular volume, e.g. during therapy with diuretics, the renin-angiotensin system is activated. In this situation, the renin-angiotensin-system contributes to the maintenance of arterial blood pressure and glomerular filtration rate by angiotensin II mediated vasoconstriction in vas efferens and systemic circulation. A sudden complete inhibition of the renin-angiotensin system therefore may cause a pronounced decrease in blood pressure and a reduction in glomerular filtration rate (impaired renal excretory function). In patients with heart failure concomitant chronic renal failure, the use of ACE-inhibitors is without major risk; however, the clinical efficacy may be limited. This does not apply to patients with diabetes, where the risk for impairment of renal function is increased. The potential advantage of short acting ACE-inhibitors such as captopril may clinically be relevant only in patients with very advanced severe heart failure and low arterial pressure. In any case, it is recommended to start ACE-inhibitors with a low dose and withdraw diuretics one or two days before in order to restore the intravascular volume.
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PMID:[ACE inhibition in heart failure and compromised kidney function]. 186 34

Modification of the renin-angiotensin system, part of a powerful feedback system for long-term control of arterial pressure and volume homeostasis, through use of angiotensin-converting enzyme (ACE) inhibitors, offers a powerful means of reducing blood pressure in many hypertensive patients. There is considerable evidence to suggest that the chronic renal and blood pressure actions of ACE inhibitors are mediated mainly by blockade of angiotensin II formation, rather than by other effects such as increased levels of kinins or prostaglandins. The long-term actions of angiotensin II and aldosterone on blood pressure are closely intertwined with their effects on volume homeostasis and the renal pressure natriuresis mechanism. In most instances, changes in angiotensin II and aldosterone act to amplify the effectiveness of pressure natriuresis and minimize changes in blood pressure needed to maintain sodium balance. When angiotensin II or aldosterone levels are inappropriately elevated, the antinatriuretic effects of these hormones shift pressure natriuresis to higher levels, thereby necessitating increased blood pressure to maintain sodium balance. Control of renal excretory function and modulation of pressure natriuresis by angiotensin II is mediated by intrarenal and extrarenal effects, including stimulation of aldosterone secretion. Current evidence indicates that the intrarenal effects of angiotensin II are quantitatively more important than changes in aldosterone in regulating renal excretion and arterial pressure. The intrarenal actions of angiotensin II include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles, which increases reabsorption by altering peritubular capillary forces. The constrictor effect of angiotensin II on efferent arterioles also helps to stabilize glomerular filtration rate and therefore excretion of metabolic waste products, an action that may be particularly important when renal perfusion is impaired (e.g., in renal artery stenosis or heart failure).
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PMID:Control of blood pressure by the renin-angiotensin-aldosterone system. 189 44


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