Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In patients with congestive heart failure, both the sympathetic nervous system and renin-angiotensin system are often stimulated. In order to assess the contribution of the renin-angiotensin system to limb vascular resistance, the forearm haemodynamic response to captopril was studied in 13 patients with heart failure. 2. Seven subjects were studied while supine and during 60 degrees head-up tilt. To eliminate alpha-adrenergic effects, six additional patients with heart failure were pretreated with intra-arterial phentolamine and then given captopril. Venous occlusion plethysmography was used to determine forearm blood flow and forearm vascular resistance. 3. Tilt did not significantly increase pretreatment plasma renin activity or plasma noradrenaline concentration, nor did it decrease forearm blood flow. Furthermore, captopril did not alter forearm vascular resistance during supine or upright posture. During the phentolamine infusion, however, captopril reduced forearm vascular resistance by 19% (P < 0.05). 4. Despite increased plasma renin activity, captopril did not cause forearm vasodilatation during supine or upright posture in these patients with heart failure. When the contribution of the sympathetic nervous system was eliminated, captopril decreased forearm vascular resistance. Therefore, in patients with congestive heart failure, the sympathetic nervous system is important in limb vasoregulation, and the contribution of the renin-angiotensin system is apparent only after alpha-adrenergic blockade.
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PMID:The contribution of the renin-angiotensin system to limb vasoregulation in patients with heart failure: observations during orthostasis and alpha-adrenergic blockade. 248 67

The diuretic and natriuretic effects of r-alpha-ANP (99-126) were investigated in rats with chronic ischaemic heart failure (IHF) produced by left coronary artery ligation. The plasma concentration of immunoreactive ANP (IrANP) was significantly higher, 91.8 +/- 16.0 pm in the IHF rats compared to 31.0 +/- 4.9 pm in sham-operated controls. In the control rats, ANP infusion (0.25-1.0 micrograms kg 1 mm 1) increased urine flow rate (V) and urinary sodium (UNa V) excretion. At the highest dose level, both V and UNa V were increased approximately fivefold. The diuresis and natriuresis seen in the control group after the infusion of ANP were blunted in the IHF rats. A bilateral surgical renal denervation in the IHF rats did not alter the renal dopamine levels, but induced a significant decrease in renal noradrenaline content, and almost completely restored the renal responsiveness to the ANP infusions. We conclude that renal denervation reversed the blunted renal excretory response to ANP in IHF rats. Thus, in experimental IHF, there seems to be a functional antagonism between efferent renal sympathetic nerve activity and ANP.
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PMID:Renal interaction between sympathetic activity and ANP in rats with chronic ischaemic heart failure. 252 11

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33

The noradrenaline (NA) that has diffused from sympathetic synapses into plasma can be assayed accurately and reliably in plasma, as it is the best index of sympathetic activity. A considerable advance has been achieved by using infusions of tritium-labelled exogenous NA, such infusions being devoid of functional effect. By measuring simultaneously blood NA levels and circulating tritiated NA levels the amplitude of synaptic spillover and therefore of sympathetic activity can be evaluated and the metabolic NA clearance can be measured. Synaptic NA spillover and NA metabolic clearance were measured in 24 physiological, pathological and pharmacological situations, providing an accurate definition of the sympathetic states explored. By combining these techniques with selective vascular catheterization, the sympathetic activity of the organs explored can be assessed, and regional sympathetic activities are currently being mapped. Such regional studies are of great value to understand the mechanisms involved in heart failure, cirrhosis or arterial hypertension. Sympathetic system regulations result from a central influence and from peripheral adjustments that are potentially specific to each organ.
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PMID:[Plasma noradrenaline. Significance and practical value of its determination]. 253 59

Alterations in the vasopressor system found in cardiac failure are part of compensatory measures that may modify pharmacologic-therapeutic response. Therefore, in 64 patients with dilated cardiomyopathy, we investigated its enhanced activity in different clinical stages of the disease as compared to normal controls. Patients in NYHA class II (n = 20) demonstrated increased activity of the sympathico-adrenal, renin-angiotensin-aldosterone, vasopressin, and atrial natriuretic factor systems, while maximum values were found in patients of NYHA class IV (n = 24). In these patients, noradrenaline was enhanced by a factor of 7, adrenaline by a factor of 2, plasma-renin-activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 as compared to normal controls. Clinical NYHA classes correlated to a certain degree with the various plasma hormones. Patients treated with an aldosterone inhibitor in addition to digitalis and diuretics revealed significantly higher values for aldosterone, vasopressin, and angiotensin II as compared to those who received digitalis and diuretics alone. The addition of ACE-inhibitor therapy resulted in a decrease of angiotensin II, aldosterone, and vasopressin. Plasma catecholamines and ANF, however, did not change under the influence of cardiac medication. Diuretic treatment in NYHA class II patients reduced plasma volumes (p less than 0.01). Plasma volume in NYHA class IV patients only was found to be higher than in normal controls. Thus, analysis of the neurohumoral system can aid both in the identification of the clinical degree of dilated cardiomyopathy and in its optimal therapy.
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PMID:The vasopressor system in patients with heart failure due to idiopathic dilated cardiomyopathy--influence of the clinical stage of disease and of chronic drug treatment. 253 2

The effects of the angiotensin converting enzyme inhibitor enalapril on myocardial sympathetic tone, as represented by noradrenaline overflow, were studied in 14 men with congestive heart failure (mean ejection fraction 20%) in a double blind crossover comparison with placebo. Arterial and coronary sinus catecholamine concentrations and oxygen content, and coronary sinus blood flow, were measured at rest and during peak symptom limited upright exercise on a bicycle ergometer. There were no significant changes four hours after the first dose of enalapril, but after six weeks of treatment (10-20 mg/day) enalapril reduced myocardial overflow of noradrenaline at peak exercise. The external workload (exercise duration) increased from baseline values after both placebo and enalapril, and there was no difference between placebo and enalapril at six weeks. Heart work, however, was lower after enalapril: stroke work index was reduced at rest and the double product was lower at peak exercise. The reduction in maximal myocardial oxygen consumption after enalapril did not reach statistical significance. Coronary sinus adrenaline concentrations after enalapril and after placebo were not significantly different. The long term reduction of myocardial sympathetic activity on exercise may represent a significant benefit from angiotensin converting enzyme inhibition in heart failure and may reflect a reduced cardiac workload.
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PMID:Effects of enalapril on myocardial noradrenaline overflow during exercise in patients with chronic heart failure. 253 95

The interactions between yohimbine (selective alpha 2-antagonist) with noradrenaline (mixed agonist) and phenylephrine (selective alpha 1-agonist) were studied in the canine dorsal pedal artery in an attempt to characterize the peripheral vascular response to adrenergic agents before and after the development of congestive heart failure in the dog. The contractile responses of the dorsal pedal artery to potassium chloride were also examined. Both noradrenaline and phenylephrine contracted the dorsal pedal artery in a concentration-dependent manner before and at peak heart failure, the responses to the agonists being enhanced at heart failure. The responses of the artery to potassium were not modified by congestive heart failure. Yohimbine caused concentration-dependent antagonism of noradrenaline, without altering the magnitude of the maximum response, providing pA2 values ranging from 8.26 to 7.06 against low and high concentrations of noradrenaline, respectively, before heart failure development. Following heart failure, the pA2 values for yohimbine against noradrenaline remained unchanged, but slopes from the Arunlakshana-Schild plots were significantly different from unity, implying a noncompetitive antagonism. The pA2 values of yohimbine against phenylephrine were at least 10 orders of magnitude lower than those against noradrenaline. After congestive heart failure, yohimbine was even less effective against high concentrations of phenylephrine. These findings suggest that enhanced vasoconstriction during heart failure results, in part, from increased alpha 1-adrenoceptor mechanisms in peripheral arterial smooth muscle.
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PMID:Alpha 1-adrenoceptor activity in arterial smooth muscle following congestive heart failure. 254 Aug 94

The two major causes of death in congestive heart failure (CHF) are progressive heart failure (approximately 60% of cases) and sudden death (30%). Sudden death in CHF is caused primarily by malignant ventricular arrhythmias. The underlying mechanism has yet to be established, but myocardial metabolic factors are probably involved. Although there is a clear association between complex ventricular arrhythmias and left ventricular function, it has not been shown convincingly that antiarrhythmic agents can reduce sudden death in CHF. Progressive deterioration of myocardial function is associated with altered myocardial energy production. Notably, the physiological effects of neuroendocrine activation in chronic CHF may be deleterious to myocardial function. The CONSENSUS study was carried out to evaluate the association between neuroendocrine activation and deterioration of myocardial function using ACE inhibitors. A marked reduction in mortality rate occurred in the enalapril-treated group, where the one-year mortality was reduced by 31%. The reduction in mortality was solely among patients with progressive CHF (a reduction of 50%); there was no difference in the incidence of sudden death. Analysis of blood samples drawn at baseline in the placebo group showed a significant positive correlation between mortality and plasma angiotensin II (P less than 0.05), aldosterone (P = 0.003), noradrenaline (P less than 0.001), adrenal levels (P less than 0.001), and atrial natriuretic peptide (P = 0.003). This was not observed in enalapril-treated patients. The significant reduction in mortality in the enalapril group was found consistently among patients with baseline hormone levels above the median value. In CHF, the underlying disease may induce serious arrhythmias and/or progressive failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms for improved survival in heart failure. 255 Jun 46

There can be no doubt that in human heart in addition to beta 1-adrenoceptors, functional beta 2-adrenoceptors exist. Their (patho)physiological role in regulating heart rate and/or contractility, however, is still an open question. Under normal physiological conditions cardiac beta 2-adrenoceptors may not be of functional importance, since heart rate and contractility seem to be under the control of noradrenaline that in the human heart acts nearly exclusively at beta 1-adrenoceptors. However, in situations of stress when large amounts of adrenaline are released from the adrenal medulla additional stimulation of cardiac beta 2-adrenoceptors may contribute to increases in heart rate and/or contractility. Moreover, in endstage congestive cardiomyopathy where cardiac beta 1-adrenoceptors are selectively down-regulated, cardiac beta 2-adrenoceptors may substitute for the loss of beta 1-adrenoceptors to maintain (at least partially) contractility; under these conditions beta 2-adrenoceptor agonists, like dopexamine, may be of beneficial therapeutic effect. While a decrease in cardiac beta-adrenoceptor function appears to be a general phenomenon in all kinds of heart failure, it is not always due to a selective reduction in cardiac beta 1-adrenoceptors: in mitral valve disease both cardiac beta 1- and beta 2-adrenoceptors decline concomitantly in relation to the degree of heart failure. It is, therefore, doubtful whether under these conditions beta 2-adrenoceptor agonists may also be useful to support the failing heart.
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PMID:Do human cardiac beta-2 adrenoceptors play a (patho)physiological role in regulation of heart rate and/or contractility? 255 71

We measured increments of peripheral venous pressure induced by dynamic leg exercise (delta VP) in 10 healthy subjects (Group C) and 70 patients with heart diseases which primarily affect the left-side of the heart. None of the subjects showed apparent symptoms of left- or right-sided heart failure. The patients were divided into 2 groups on the basis of delta VP, namely, Group N (delta VP less than 35 mmH2O, n = 30, normal reaction) and Group H (delta VP greater than or equal to 35 mmH2O, n = 40, abnormal reaction). We measured the increments of plasma concentrations of noradrenaline (delta NAPH) and adrenaline (delta APH) with infusion of phentolamine (PH). Parallel studies with nitroglycerin and prazosin supplied strong evidence that delta NAPH was brought about mainly by the blockade of alpha 2-receptors at the sympathetic nerve terminals. Thus, we estimated the degree of sympathetic nerve activity from the central nervous system by opening using PH the negative feed-back loop for noradrenaline (NA) release at the sympathetic nerve terminals, and this degree of sympathetic nerve activity was compared with the degree of delta VP. The results obtained were 1) there was a rough overall correlation between delta VP and delta NAPH in the subjects of Groups C, N and H, and 2) delta NAPH was significantly higher in Group H than in Groups C and N. These results suggest that much reliance can be placed on the measured increment of plasma NA concentration in response to the administration of PH in assessing the degree of enhanced sympathetic nerve activity in the patients with "latent" left-sided heart failure.
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PMID:Increase in plasma noradrenaline concentration after the administration of phentolamine in the patients with "latent" left-sided heart failure. 256 Nov 61


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