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)

The presence of alpha-hANP immunoreactive material in human heart and plasma was investigated with a specific and sensitive radioimmunoassay and immunohistochemical method. It was found that alpha-hANP immunoreactive staining of specific atrial granules was located around the nucleus of atrial cardiocytes. No immunoreactive staining was found in the ventricle. The content of immunoreactive hANP was 0.5 pmol/mg protein in the atria and 0.11 +/- 0.01 pmol/ml in the plasma of 26 normal volunteers. In 16 patients with congestive heart failure and 26 patients with essential hypertension, the plasma level of immunoreactive alpha-hANP was significantly lower than that in normal humans. The above evidence indicate that alpha-hANP is a putative hormone secreted by human atrium. A relative shortage of alpha-hANP in the circulatory system may be involved in the mechanism of heart failure and hypertension.
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PMID:Alpha-human atrial natriuretic polypeptide (alpha-hANP) in normal volunteers and patients with heart failure or hypertension. 294 May 20

Alpha-human atrial natriuretic polypeptide (alpha-hANP) was applied to 16 clinical patients, 6 patients with essential hypertension, 7 patients with congestive heart failure and 3 patients with cirrhosis. Following intravenous bolus injection of 400 micrograms of synthetic alpha-hANP, a hypotensive effect of very rapid onset was found, which was more potent in the hypertensive patients than in the normotensive cases. Cardiac functions were improved significantly with a similar time course as the depressor response in the cases of heart failure or hypertension. Hemodynamic observations showed a marked increase in cardiac output, cardiac index, stroke volume, ejection fraction and ejection rate, and a concomitant decrease of the pressure in the right side of the heart and pulmonary circulation in these subjects. In addition, the renal response to alpha-hANP induced obvious increases in urine volume, electrolytes and creatinine excretions in all the subjects. Finally, plasma levels of aldosterone, Arg-vasopressin and noradrenaline were also altered by alpha-hANP. No significant side effects were registered. The above result confirms the therapeutic actions of alpha-hANP in human subjects and opens the possibility to research alpha-hANP as a powerful pharmacological tool as well as potential new medicine for human disorders.
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PMID:Therapeutic actions of alpha-human atrial natriuretic polypeptide in 16 clinical cases. 295 43

Research on the physiological role of atrial peptides in man is limited, and the potential for these peptides, or more stable analogues, in therapeutics is uncertain. It is clear, however, that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are increased in volunteers taking a high sodium diet, and are elevated in patients with heart failure, chronic renal failure, and primary aldosteronism. There is suggestive evidence that IR-ANP levels are increased also in essential hypertension, although overlap with normotensives is considerable. Injection or infusion of atrial peptides into man results in a diuresis, an increased output of urine electrolytes, a fall in blood pressure and a rise in heart rate, suppression of aldosterone and sometimes of renin also, and stimulation of norepinephrine. In essential hypertensives, urinary effects may be greater than in normotensives. Heart failure patients show a rise in cardiac output and falls in both systemic and pulmonary arterial pressure. Over the next few years and especially if specific antagonists can be developed, the physiologic and pathophysiologic roles of atrial peptides in normal man and in clinical disorders should be clarified. It is possible that stable analogues of atrial peptides will find a place in the treatment of cardiac failure, renal failure, and perhaps hypertension.
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PMID:Atrial natriuretic peptides in man. 296 23

The human heart secretes ANP, mainly or exclusively as the 1-28-amino-acid alpha-hANP. Secretion is increased when there is hypervolemia of the central circulation, either acute or chronic, the stimulus being, it is presumed, atrial stretch. The clearance rate of alpha-hANP has been documented in healthy volunteers but not in patients with clinical disorders. Injection or infusion of atrial peptides into normal humans has clear-cut hemodynamic, renal, and hormone effects. However, the doses used have been high and the results do not allow extrapolation to the realms of physiology. Patients with essential hypertension appear to have exaggerated renal responses to administered alpha-hANP, although the number of subjects studied is small and matching with normotensive controls was imperfect. By contrast, cardiac failure is characterized by impaired renal responses to atrial peptides. The place of atrial peptides in human physiology and pathophysiology is not clear and will require very low-dose infusion studies under exacting experimental conditions or the development of a specific inhibitor of circulating ANP. In theory, atrial peptides might find a place in therapeutics, most likely in cardiac failure or renal failure, but also essential hypertension if an orally active agonist can be developed.
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PMID:Human studies with atrial natriuretic factor. 296 67

In this study plasma levels of atrial natriuretic peptide and of the catecholamines epinephrine and norepinephrine were investigated in hypertensive patients (HT) (n = 30). 22 normotensive patients (NT) served as controls. Hypertensives showed an elevated ANP-level in comparison with controls (46.8 +/- 3.3 vs. 36.8 +/- 3.3 pg/ml, M +/- SEM, p less than 0.01). When patients with myocardial infarction or with reduced ejection fraction were excluded, the same relation was demonstrated (49.3 +/- 3.2 vs. 33.6 +/- 2.0 pg/ml, p less than 0.01). Plasma norepinephrine was 230.8 +/- 52.3 pg/ml in HT compared with 138.0 +/- 19.6 pg/ml in NT (p less than 0.05). Epinephrine was 70.8 +/- 10.5 vs. 54.8 +/- 9.7 pg/ml in HT and NT. To exclude an increased left ventricular enddiastolic - and hence left atrial - pressure as the cause for the elevation of ANP and norepinephrine, HT and NT were matched for the same levels of enddiastolic pressure (LVEDP) (n = 18). For each level of LVEDP ANP was higher in HT than in NT (p less than 0.01). The same held true for norepinephrine (p less than 0.05) and to a lesser extent for epinephrine (p = 0.09). Our results demonstrate that patients with essential hypertension exhibit markedly elevated levels for ANP and catecholamines which is not due to myocardial failure. We propose that the increased secretion of the vasodilatory hormone ANP serves as counterregulation against the vasoconstrictor norepinephrine. The endocrine function of the heart may play a pivotal role in the modulation of sympathetic activity.
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PMID:[Elevated levels of atrial natriuretic peptide and plasma catecholamines in arterial hypertension--indications for an interaction]. 297 96

Left-ventricular functions were assessed by means of mechanocardiography in patients with essential hypertension in the absence of signs of heart failure. A significant prolongation of the isovolumic relaxation phase, rapid filling phase, and an increase in the amplitude of apex-cardiographic "a" wave were found in hypertensive patients showing no ventricular hypertrophy. Similar but more pronounced disorders were observed in patients with ventricular hypertrophy where, in addition, the pre-ejection period was prolonged and there were signs of asynergic contraction. The findings testify to diastolic dysfunction of the left ventricle as a result of its impaired compliance, already present in the early phases of essential hypertension. Mechanocardiography is a suitable method for the detection of cardiac dysfunction in essential hypertension.
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PMID:[Non-invasive evaluation of left-ventricular function in hypertension]. 297 14

Angiotensin-converting enzyme (ACE) inhibitors are a new class of drugs, whose main indications are the treatment of hypertension and of heart failure. Data obtained with captopril, the first orally active ACE inhibitor, affords an understanding of the rationale of their therapeutic use based on the knowledge of their mechanisms of action, efficacy, contraindications and precautions, dosage and frequency of administration, side-effects, interactions and advantages. ACE inhibitors appear to exert their haemodynamic effect mainly by inhibiting the renin-angiotensin-aldosterone system, but also by modulating sympathetic nervous system activity and by increasing prostaglandin synthesis. Therefore they act both on vasoconstrictor and volume factors, since they cause vasodilation (the main effect) and mild natriuresis without affecting the heart rate and contractility and, probably, favourably influencing renal, coronary and cerebral circulation. So far it appears that ACE inhibitors can be usefully employed in the treatment of heart failure, in which they reduce both pre- and after-load, and mainly of hypertension. In the past captopril has been used to treat only severe and or resistant hypertension and some secondary forms, like renal parenchymal and renovascular hypertension, but now it seems that captopril is useful also to treat mild to moderate essential hypertension. Their efficacy in reducing blood pressure is similar to that of thiazide diuretics and of beta-blockers, the two drugs now considered of first choice and they exert their hypotensive action without the development of pseudotolerance or tolerance. ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. It is now established that captopril has a flat dose response curve and that it must be given (twice daily) at a dose not exceeding 150 mg/day. The same pharmacological approach must be used with future ACE inhibitors in order to establish the right posology and the frequency of administration. In this respect enalapril seems to be a promising ACE inhibitor with a prolonged action (at least 24 hours). The exact posology of ACE inhibitors might be crucial, since it has been shown that the side-effects of captopril (skin rashes, fever, taste disturbances, proteinuria and neutropenia) are dose dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors in hypertension: a review. 300 82

The effects of the rapid infusion of large doses of dibutyryl cyclic AMP (DBcAMP) were studied to clarify the clinical usefulness of its vasodilating action in 32 middle-aged patients, who underwent various types of surgery and developed systolic hypertension of over 160 mmHg during general anaesthesia. DBcAMP was given i.v. with an infusion pump at a rate of 0.6 mg kg-1 min-1 for 20 min. In all patients just after the infusion, systolic arterial pressure decreased from 174.0 +/- 20.7 to 129.0 +/- 23.9 mmHg, diastolic pressure decreased from 93.1 +/- 13.4 to 64.8 +/- 13.3 mmHg, heart rate increased from 81.2 +/- 15.7 to 91.5 +/- 19.5 beats min-1, and urine volume increased from 69.4 +/- 54.8 to 182.7 +/- 143.5 ml h-1. In three patients, cardiac index increased from 3.44 to 4.24 l min-1 m-2. In seven patients, tachycardia exceeding 120 beats min-1 developed. DBcAMP was also effective in patients with a history of hypertension. The strongest antihypertensive effect was observed in patients anaesthetized with nitrous oxide-oxygen and enflurane. We speculate that DBcAMP is useful to control hypertension and may be particularly indicated in patients with cardiac failure, renal disorders and essential hypertension.
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PMID:The control of hypertension with dibutyryl cyclic AMP. 303 96

Captopril is an orally active inhibitor of angiotensin-converting enzyme (ACE) and has been widely studied in the treatment of patients with mild to moderate essential hypertension, severe hypertension not responsive to conventional diuretic/beta-adrenoceptor blocker/vasodilator regimens, and patients with chronic congestive heart failure refractory to treatment with a diuretic and digitalis. In patients with mild or moderate essential hypertension, titrated low doses of captopril used alone or in conjunction with a diuretic are similar in efficacy to usual doses of hydrochlorothiazide, chlorthalidone, or beta-adrenoceptor blocking drugs, as well as to the other ACE inhibitors. In addition, captopril improved well-being to a greater extent than methyldopa or propranolol in a study designed specifically to determine the effect of treatment on the quality of life of patients with mild or moderate essential hypertension. The earlier demonstrated efficacy of captopril, used with a diuretic and often also with a beta-adrenoceptor blocking drug, in the treatment of severe hypertension refractory to conventional 'triple therapy' has been confirmed in more recent trials which illustrate the generally marked antihypertensive effect of captopril-containing regimens in such patients. Results of initial trials in patients with scleroderma are promising, with control of hypertension and stabilization of renal function in these patients when treated at an early stage of the disease. Several comparative and long term trials of captopril in patients with chronic congestive heart failure refractory to treatment with a diuretic/digitalis regimen clearly demonstrate that initial haemodynamic improvement is maintained and correlates with clinical benefit. A tendency for overall clinical response to captopril to be better than the response to prazosin, hydralazine, nisoldipine or enalapril has been reported. Results of a multicentre comparison with digoxin and placebo indicate that captopril is a suitable alternative to digoxin in patients with mild to moderate heart failure who are receiving maintenance diuretic therapy. The tolerability of captopril has now been studied in many thousands of patients involved in formalized trials and the early impression of poor tolerability can no longer be justified. The use of generally lower dosages of captopril in patients with normal or slightly impaired renal function has resulted in a generally low incidence of rash (0.5 to 4%), dysgeusia (0.1 to 3%), proteinuria (0.5%), neutropenia (0.3% during first 3 months) and symptomatic hypotension (0.1 to 3%). Cough is an infrequent but troublesome effect resulting from ACE inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Captopril. An update of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension and congestive heart failure. 306 99

Novel approaches to managing refractory arterial hypertension (AH) have been tested in 130 patients aged 28 to 59 years with severe or malignant hypertension. Hemosorption was performed in 70 patients in whom AH was caused by chronic diffuse glomerulonephritis (49 cases) or chronic pyelonephritis (21 cases) accompanied by the appearance of chronic renal failure. In all patients, blood pressure after hemosorption decreased by 15% to 16% on the average, resulting in progressively improved renal function and a nearly 2.0-fold reduction in plasma aldosterone concentration (PAC), and allowing the doses of antihypertensive drugs to be reduced. Plasmapheresis was performed in 31 patients with refractory severe or malignant AH due to essential hypertension or parenchymatous diseases of the kidneys. After two to four plasmapheresis sessions with up to 2 L of plasma exchanged, blood pressure dropped by 24% compared to baseline while the doses of antihypertensive drugs were diminished and some were discontinued completely in several cases. Analysis of the sensitivity to antihypertensive drugs after plasmapheresis using the rosette technique revealed a significant decrease in the number of rosette-forming cells. The level of angiotensin II and urinary excretion of aldosterone-18-glucuronide declined progressively by nearly 50% after plasmapheresis, correlating with the antihypertensive effect of plasmapheresis. In 32 patients with severe AH complicated by refractory cardiac failure, isolated ultrafiltration was used. After one to eight sessions and the removal of 1.0 L to 35.8 L of fluid, the signs of cardiac failure diminished, the blood pressure level responded to drug therapy, and the PAC level decreased significantly. Although the mechanisms of the antihypertensive actions of hemosorption, plasmapheresis, and isolated ultracentrifugation are still not completely elucidated, these data suggest that hemosorption may act by removing nitrogenous residues from the body and reducing PAC, plasmapheresis by deblocking receptors for antihypertensive drugs and reducing the concentration of angiotensin II and the synthesis of aldosterone in the body, and isolated ultrafiltration by eliminating hyperhydration and edema of the parenchymatous organs.
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PMID:Extracorporeal methods in the management of severe and malignant arterial hypertension. 324 17


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