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

The effect of a single oral dose (50 mg) of captopril was studied in 12 hypertensive patients divided into 2 groups: 6 had a normal hemodynamic profile; the other 6 had NYHA class III or IV heart failure. Medical history and clinical and laboratory investigation showed that the heart failure was due exclusively to arterial hypertension. Mean arterial pressure (MAP), aldosterone, plasma renin activity (PRA) and atrial natriuretic factor (ANF) were followed for 4 hours after administration of captopril. MAP values showed a similar decrease in the 2 groups but the variations in the 3 hormones were much greater in the second group. This group showed higher basal levels of PRA, aldosterone and ANF; after stimulation PRA increased sharply preceded by a substantial decrease in aldosterone and ANF. To explain this phenomenon, the Authors propose that the liver of the patients with heart failure is unable to rapidly compensate the reduction in synthesis of angiotensin II caused by the drug with a corresponding increase in angiotensinogen production; the consequent sharp drop in plasma aldosterone would lead to a rise in renin production by the kidney. The arteriolar and venous vasodilatation induced by the ACE-inhibitor, would explain the drop in intra-atrial pressure with reduced plasma levels of ANF. The decrease in ANF could also be caused by the inhibition of the renin-angiotensin system of the heart leading to improved blood supply and hence myocardial contractility.
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PMID:[Captopril and hypertensive cardiopathy : therapeutic effects and hormonal changes]. 215 Mar 43

The cardiovascular reflexes have the key role in the rapid adjustments of the circulatory system in response to daily stresses such as standing and muscular exercise. Arterial and cardiopulmonary mechanoreceptors continuously signal to the cardiovascular centers in the brain the moment to moment pressure changes in the larger arteries, atria and ventricles and exert a tonic restraint on the sympathetic noradrenergic outflow. Depending on the stress, the vasomotor centers adjust this outflow, both qualitatively and quantitatively, to the heart and to the different vascular beds to maintain an appropriate arterial blood pressure. In addition, the sympathetic nerves modulate renin release from the juxtaglomerular cells and receptors at the veno-atrial junctions regulate vasopressin release from the posterior pituitary. Congestive heart failure is characterized by excessive neuro-humoral excitation as evidenced by direct recordings of sympathetic activity and by increased plasma levels of catecholamines, renin, angiotensin II and arginine vasopressin. The evidence indicates that this is a consequence of the reduced ability of the arterial and cardiopulmonary mechanoreceptors to inhibit the vasomotor centers. The cause(s) of this diminished circulatory control requires further studies. The cardiac glycosides, which normally cause vasoconstriction, cause vasodilatation in patients with heart failure. This is attributed to sensitization of the mechanoreceptors. The term atrial natriuretic factor refers to a family of peptide hormones released when the atrial myocytes are stimulated by an increase in transmural pressure. They cause diuresis, natriuresis and vasorelaxation. In severe congestive heart failure, the plasma levels are increased and this helps to compensate for the increased neurohumoral activation by inhibiting the renin-angiotensin system and enhancing sodium and water excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart failure: role of cardiovascular reflexes. 215 12

The alpha-adrenergic component of the sympathetic nervous system plays a major role in the pathophysiology, clinical manifestations, and natural history of human congestive heart failure. While the augmentation of alpha-adrenergic tone (through the neuronal release of norepinephrine) is a valuable mechanism to maintain adequate systemic blood pressure and perfusion of vital organs in states of circulatory collapse, stimulation of alpha-adrenergic receptors produces detrimental hemodynamic effects in congestive heart failure. These undesirable effects result from alpha-mediated vasoconstriction and consist of excessive elevation of right and left ventricular filling pressures and pulmonary and systemic vascular resistances. The enhancement of alpha-adrenergic tone preferentially reduces blood flow to the hepatosplanchnic circulation. Many of the hemodynamic responses that are seen after activation of the renin-angiotensin system are related to the ability of angiotensin II to amplify the actions of the alpha-adrenergic system. Stimulation of myocardial alpha-adrenergic receptors in most species elicits a modest positive inotropic effect, but the presence and importance of this property in the human heart remains controversial. Chronic stimulation of myocardial alpha-adrenergic receptors may result in the hypertrophy of cardiomyocytes and may also contribute to the development of catecholamine-induced cardiomyopathy. Acute blockade of the heightened alpha-adrenergic tone in congestive heart failure (e.g., with first doses of prazosin) results in favorable hemodynamic effects, but repeated dosing leads to pharmacological tolerance. Consequently, the long-term administration of alpha-adrenergic blocking agents in human heart failure has not been accompanied by an improvement in clinical status, exercise capacity, or survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha-adrenergic component of the sympathetic nervous system in congestive heart failure. 216 97

The effects of angiotensin-converting enzyme (ACE) inhibitors on renal hemodynamics vary widely depending on the preexisting physiologic and pathologic state of the kidneys. Although some studies of ACE inhibitors in primary essential hypertension have demonstrated increases in glomerular filtration rate (GFR) and effective renal plasma flow in patients with renal impairment, other studies have not shown these same beneficial results. The difference may involve the choice of ACE inhibitor used in the investigations, but controlled comparison trials are needed to determine whether this is the case. The use of ACE inhibitors in renovascular hypertension remains controversial. ACE inhibition can interfere with the autoregulation of GFR mediated by angiotensin II and may lead to deterioration of renal function, especially in patients with bilateral renal artery stenosis or stenosis of a solitary kidney. Additionally, ACE inhibitors have been shown to cause a decline in GFR in the kidney affected by the stenosis, whether or not clinically apparent renal insufficiency occurs. Although the functional impairment associated with ACE inhibitors in renal artery stenosis has generally been reversible following removal of the drug, the consequences of a long-term reduction in GFR are unknown. Treatment of stable congestive heart failure (CHF) with ACE inhibitors can result in enhancement of GFR and reduction of sodium and fluid retention, thus improving the clinical state. However, in patients with decompensated cardiac failure, renal perfusion pressures may already be at or near the autoregulatory breakpoint and ACE inhibition may cause deterioration of renal function. In general, ACE inhibitors can be used safely in CHF if they are initiated cautiously, with adjustment of ACE inhibitor and diuretic dosages to avoid systemic hypotension and sodium and fluid depletion. In studies comparing the agents, enalapril and lisinopril have both been shown to cause higher incidences of renal function deterioration than has captopril. These findings suggest that the more complete or sustained ACE inhibition seen with the longer-acting agents may be detrimental to renal function in patients with CHF. The use of ACE inhibitors in the treatment of proteinuria is the newest area of research with these agents. At present it appears that ACE inhibitors reduce urinary protein excretion the most effectively in diabetic patients with mild proteinuria and in hypertensive patients with renal insufficiency and proteinuria due to glomerular disorders. More study is needed to determine whether these agents can reduce the rate of renal failure progression and to define the patient populations expected to benefit most.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors and renal function. 218 38

The syndrome of heart failure results from inappropriate sodium and water retention by the kidneys which results, at least in part, from changes in renal haemodynamics. Renal blood flow at rest in heart failure is reduced in proportion to the reduction in cardiac output and falls dramatically during exercise as the cardiac output is redistributed to the exercising muscles. Both these phenomena are associated with a rise in plasma noradrenaline concentration. Afferent arteriolar tone is partly controlled by alpha-adrenoceptor stimulation while stimulation of beta 2-receptors will stimulate renal release of renin; through the elaboration of angiotensin II, profound effects on extra- and intra-renal vascular tone can occur. Although alpha-adrenoceptor stimulation can result in coronary vasoconstriction and a fall in coronary blood flow in patients with heart failure due to underlying atheromatous coronary heart disease, increased myocardial oxygen demand as the result of beta 1 (and cardiac beta 2) simulation may be more relevant. The control of limb blood flow is of great importance symptomatically. The systemic vasoconstriction that typifies the severe heart failure state has been a target for many vasodilatory interventions including alpha 1-receptor blockade and beta 2-receptor stimulation. Unfortunately, there is little evidence that such treatment leads to any specific increase in muscle blood flow either at rest or during exercise. In severe heart failure, sympathetic activity is increased at rest leading to vasoconstriction in several vascular beds, while in milder heart failure, excessive sympathetic stimulation is evident only during exercise. In either circumstance, however, it is evident that certain advantages may accrue from modulation of this excessive sympathetic activity.
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PMID:Sympathetic activity and regional blood flow in heart failure. 218 37

The renin-angiotensin-aldosterone system (RAAS) has been implicated in the pathogenesis of congestive heart failure (CHF). Abnormal activation of the RAAS adversely affects cardiac performance and impairs functional status, increasing both afterload and preload through direct and indirect mechanisms. Conventional first-line therapy for CHF consists of diuretics and/or digitalis. Diuretics offer rapid relief of symptoms, effective volume control, and ease of administration, but are associated with a number of disadvantages, including further activation of neurohormonal systems resulting in augmented vasoconstriction. Angiotensin-converting enzyme (ACE) inhibitors, which block the RAAS by inhibiting production of angiotensin II from angiotensin I, are emerging as the vasodilators of choice in combination with diuretics with or without concomitant digitalis. Direct comparative studies have shown that ACE inhibitors provide acute and long-term symptomatic, hemodynamic, and exercise-related benefits as well as improved functional class and, possibly, slowed progression of disease with enhanced survival in specific subgroups. Captopril was the first orally effective ACE inhibitor associated with improved exercise tolerance and functional class in large multicenter trials of patients with severe heart failure and mild to moderate heart failure. Enalapril reduced the probability of death in patients with severe heart failure in the CONSENSUS trial. The new ACE inhibitor quinapril has been shown to improve hemodynamic status both acutely and chronically and to produce dose-related improvements in exercise tolerance. ACE inhibitors have a favorable safety profile, although hypotension can occur with initial doses, particularly in volume-depleted patients or at times when excessive initial doses are administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACE inhibitors in the treatment of heart failure. 218 19

The effects of renin inhibition have not previously been documented in established heart failure (HF). Accordingly, we investigated the acute hemodynamic and hormonal effects of a renin inhibitor (EMD 52297) in an ovine model of HF induced by rapid ventricular pacing (LVP). In seven sheep, recordings were made for 1 h before, during a 2-h infusion of renin inhibitor (RI) or vehicle, and after each infusion on the 5th and 6th day after commencing LVP. The RI (20 micrograms.kg-1.min-1) or vehicle was given in random order. RI infusion induced a rapid fall in plasma renin activity (PRA) and angiotensin II, reaching a nadir at 20 min. The vasodilator response was characterized by a 16% fall in mean arterial pressure (MAP), which was related to the fall in PRA (r = 0.78, P less than 0.05). MAP and PRA remained suppressed throughout the infusion period, and both returned to preinfusion levels within 10 min of terminating infusions. Left atrial pressure and plasma aldosterone were not significantly altered, while renal function was preserved despite the fall in perfusion pressure. RI has significant hemodynamic actions in a model of established HF.
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PMID:Hemodynamic and hormonal effects of renin inhibition in ovine heart failure. 219 44

Challenge to a new therapeutic principle to treat heart failure is to ameliorate or eliminate symptoms, decelerate progression of the disease and reduce mortality. However, to begin, one would request improvement of objective hemodynamic parameters. Angiotensin converting enzyme (ACE) inhibitors may have acute and chronic, global and regional effects. ACE inhibitors acutely and chronically reduce pre- and afterload without reflex tachycardia. They lower myocardial oxygen consumption and improve the relation of coronary blood flow to myocardial oxygen consumption. Cerebral and renal blood flow generally are beneficially influenced if the blood pressure is not lowered too much. Left ventricular dilatation following extensive myocardial infarction which is prognostically unfavourable, may be retarded or prevented by ACE-inhibitors. It is not yet clear whether mortality may thus be reduced as in patients with severe heart failure. Large multicenter studies currently address this question. It is unclear as well whether the effects of ACE-inhibitors are exclusively due to a reduction of circulating angiotensin II. Most likely, interference is of major importance with local renin-angiotensin systems, other hormone systems and the central and peripheral nervous system.
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PMID:[Modification of hemodynamics by angiotensin converting enzyme inhibitors in heart failure]. 219 16

The four major diagnostic criteria for the syndrome of congestive heart failure are left ventricular dysfunction, exercise intolerance, pulmonary congestion or edema and ventricular arrhythmias. Activation of norepinephrine, angiotensin II, vasopressin and atrial natriuretic peptide may be a key factor in the vasoconstriction and increased impedance to left ventricular ejection in heart failure. Interventions that interfere with these vasoconstrictor mechanisms should have a salutary effect on left ventricular performance. Treatment with angiotensin-converting enzyme (ACE) inhibitors, alpha-adrenoceptor blockers and vasopressin antagonists has resulted in hemodynamic benefits, but it has been more difficult to demonstrate long-term clinical effectiveness. Reductions in mortality have been demonstrated in patients with heart failure treated with vasodilators and ACE inhibitors. Improvement in the quality of life and prolongation of life are the only two appropriate goals in the management of heart failure. Further understanding of the role of angiotensin II and its interference by ACE inhibition in the tissue processes of heart failure is needed.
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PMID:Mechanisms in heart failure and the role of angiotensin-converting enzyme inhibition. 222 Jun 1

The circulating renin-angiotensin system (RAS) plays an important role in the maintenance of cardiovascular homeostasis. It has recently been demonstrated that endogenous RAS exist in target tissues that are important in cardiovascular regulation. This article reviews the multiple effects of angiotensin II in target tissues, the evidence for the presence of functional tissue RAS and the data that suggest a role for these tissue RAS in the pathophysiology of heart failure. Activation of circulating neurohormones is predictive of worsened survival in heart failure; however, cardiac and renal tissue RAS activities are also increased in the compensated stage of heart failure, when plasma renin-angiotensin activity is normal. It is hypothesized that the plasma RAS maintains circulatory homeostasis during acute cardiac decompensation, while changes in tissue RAS contribute to homeostatic responses during chronic sustained cardiac impairment. This concept of different functions of circulating and tissue RAS in the pathophysiology of heart failure may have important pharmacologic implications.
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PMID:Potential role of the tissue renin-angiotensin system in the pathophysiology of congestive heart failure. 222 Jun 2


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