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

Short term angiotensin converting enzyme inhibition may induce a transient salt and water retention in patients with hypertension or heart failure. To verify the glomerular and tubular effects of short term converting enzyme inhibition, thirteen patients with mild to moderate essential hypertension (WHO I-II) were treated orally either with perindopril (4 mg o.d.) or captopril (25 mg b.i.d.) for one week. Both drugs reduced supine mean blood pressure significantly (p less than 0.01) (perindopril from 126 +/- 11 to 108 +/- 7 mmHg, mean +/- SD, and captopril from 132 +/- 12 to 121 +/- 16). Plasma volume (radio-iodinated albumin space) was unchanged while mean extracellular fluid volume (inulin space) increased although not significantly (from 5.05 +/- 1.32 l/sqm to 5.71 +/- 2.21 with perindopril and from 4.96 +/- 2.6 to 5.6 +/- 1.7 with captopril). Sodium clearance decreased (from 1.4 +/- 0.6 to 1.1 +/- 0.5 ml/min 1.73 sqm with perindopril, p less than 0.05, and from 0.97 +/- 0.44 to 0.88 +/- 0.51 with captopril, n.s.). In 9 patients (6 on captopril and 3 on perindopril) extra-cellular fluid volume increased simultaneously with reduction in glomerular filtration rate and in proximal tubule sodium re-absorption as well as an increase in distal tubule sodium reabsorption. In these patients the changes in proximal and distal tubule sodium reabsorption were significantly (p = 0.05) different from those of the patients with no extra-cellular fluid expansion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Volume of the extracellular liquid and renal function during short-term administration of angiotensin converting enzyme inhibitors in essential hypertension]. 267 Jun 57

To evaluate the effects of compensated heart failure (HF) on digoxin pharmacokinetic properties in cats, 6 cats with dilated cardiomyopathy were compared with 6 clinically normal (control) cats. Digoxin tablets were administered at a dosage of 0.01 mg/kg of body weight, q 48 h for approximately 10 days, until presumed steady state was reached. Both groups were treated concomitantly with aspirin, furosemide, and a commercial low-salt diet. Retrospectively, control and HF cats were calculated to be at 95% and 97% steady state, respectively. At the time blood samples were collected, HF cats were clinically compensated. Serum digoxin concentration [( DXN]) was determined by radioimmunoassay on samples drawn immediately before and 1, 2, 4, 8, 12, 24, 34, and 48 hours after digoxin administration. Measured and calculated values (peak, 8-hour, and mean [DXN]; elimination half-life [t1/2]; oral clearance; and hours during which [DXN] was in the toxic range) were not significantly different between control and HF cats. To predict individual propensity for digoxin intoxication, serum creatinine and urea concentrations and sulfobromophthalein dye retention were measured in control and HF cats prior to the onset of treatment with digoxin. There was no statistically significant correlation between serum creatinine and urea concentrations when compared with sulfobromophthalein dye retention nor between any of these values and digoxin peak, 8-hour, and mean concentrations or t1/2, oral clearance, or hours during which [DXN] was in the toxic range. Mean serum creatinine and urea nitrogen concentrations were significantly greater (P less than 0.01) and sulfobromophthalein dye retention approached significant prolongation (P less than 0.06) in HF cats, compared with that in control cats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of compensated heart failure on digoxin pharmacokinetics in cats. 279 76

Plasma atrial natriuretic peptide levels are increased in heart failure. In rats with experimental heart failure, the elevation in plasma atrial natriuretic peptide bore a close relationship to the size of the myocardial infarct and the degree of ventricular dysfunction. Sodium retention, assessed by changes in exchangeable body sodium, could not be demonstrated in this model of cardiac dysfunction. Even rats receiving a low-sodium diet had increased plasma atrial natriuretic peptide levels following coronary artery ligation despite a significant decrease in exchangeable body sodium. This establishes that the elevated plasma atrial natriuretic peptide levels found in heart failure are a consequence of ventricular dysfunction and increased intracardiac pressures rather than a reflection of the salt and water status. Alternatively, the elevated plasma atrial natriuretic peptide may limit salt and water retention in this model. In these animals with high circulating atrial natriuretic peptide levels, "down-regulation" of renal atrial natriuretic peptide receptors could be demonstrated. This decrease in renal atrial natriuretic peptide receptor numbers may, in part, explain the blunted response to infused atrial natriuretic peptide in heart failure. However, changes in renal atrial natriuretic peptide receptors alone would appear to be insufficient to lead to salt and water retention without the activation of other sodium-retaining mechanisms that occur with the progression of cardiac failure. Nevertheless, this down-regulation of renal atrial natriuretic peptide may then contribute to the salt and water retention that occurs in congestive biventricular heart failure. The close relationship between increases in atrial natriuretic peptide and ventricular dysfunction rather than sodium balance suggests that atrial natriuretic peptide's primary role in the circulation may be to produce venodilation and increase capillary permeability. This may act rapidly to reduce cardiac preload and prevent pulmonary congestion. Vasodilation and natriuresis may then become supplementary actions to maintain cardiac output and remove the excess fluid.
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PMID:Regulation of cardiac preload by atrial natriuretic peptide in congestive cardiac failure. 285 Dec 66

The treatment of hypertension must be based on pathophysiologic grounds. The drugs that have been used in the classic stepped-care approach are still useful, but the rationale for their usage should not be based on the presumption that all hypertension is mediated by salt and water. Thus, the adolescent obtains greater benefits from a beta-adrenergic blocking drug or a centrally acting antihypertensive. The individual with heart failure may benefit more from a converting enzyme inhibitor than a vasodilator. In cerebrovascular disease with hypertension, dosage must be reduced owing to the enhanced sensitivity of response. New drugs are discussed, and their place in the armamentarium is evaluated.
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PMID:Hypertension update for the 1980s. 285 24

In chronic cardiac failure, various neurohumoral mechanisms are activated to sustain blood volume, blood pressure, and organ perfusion. Using the coronary artery ligation model of heart failure in the rat, we have measured changes in vasoactive hormone secretion and related these changes to salt and water status during a 1-month period. When compared with controls, rats with infarction had a marked rise in plasma atrial natriuretic peptide (294 +/- 59 vs. 79 +/- 10 pg/ml, p less than 0.001) although there was no increase in total exchangeable body sodium. Plasma renin activity and plasma aldosterone concentrations were the same for both rats with infarction and controls. Similarly, there were no significant differences in plasma arginine vasopressin, plasma osmolality, or plasma sodium concentration in rats with infarction. Ventricular norepinephrine levels were reduced in animals with infarction (p less than 0.01). Plasma atrial natriuretic peptide levels were raised in this model of chronic left ventricular failure. However, there was no salt retention and little stimulation of the renin-angiotensin-aldosterone system or vasopressin. The results suggest that high circulating atrial natriuretic peptide levels may prevent or limit salt and water retention, either directly or indirectly, by inhibiting the renin-angiotensin-aldosterone system.
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PMID:Neurohumoral responses to chronic myocardial infarction in rats. 289 63

The diuretic effect of the supine position was evaluated in six patients with cirrhosis and ascites and six with congestive cardiac failure. All patients received 1 mg bumethanide intravenously and were randomly assigned to either bed rest in the supine position or normal daily activity in the upright position for the next six hours. The diuretic response was similar in patients with heart failure and cirrhosis, and was significantly greater in the supine than in the upright position: mean 1,133 v 626 ml/6 h (p less than 0.01). The natriuresis was similarly greater during recumbency: mean sodium 96 v 45 mmol (mEq)/6 h (p less than 0.01), and the excreted potassium in six hours was similar in both postures. The glomerular filtration rate was 100 and 66 ml/min (p less than 0.01) and the heart rate 76 and 83 beats/min (p less than 0.05) in the supine and upright positions, respectively. Plasma concentrations of noradrenaline, renin, and aldosterone rose significantly during the upright position. The results suggest that the attenuated response to intravenous bumethanide in the upright position and during normal daily activity may be due to the activation of several, homoeostatic mechanisms which may reduce the excretion of water and salt.
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PMID:[Effect of posture on the diuretic treatment of decompensated cirrhosis and heart failure]. 291 77

Overactivity of the renin-angiotensin-aldosterone system occurs in the syndrome of congestive cardiac failure. Aldosterone overactivity is crucially involved in maintaining the oedematous state as evidenced by its often complete correction by adrenalectomy, or by aldosterone antagonists, in both experimental and clinical heart failure. The hyperaldosteronism of heart failure can also be attacked by angiotensin-converting enzyme (ACE) inhibition, which not only blocks the angiotensin drive to aldosterone, but also unloads the heart by blocking renin-angiotensin-mediated vasoconstriction. Accordingly, ACE inhibition alone, if continued in full dosage, can often reduce or obviate the need for daily thiazide diuretic therapy. This specific, two-pronged therapy with fewer side effects emerges as a primary strategy for the treatment of congestive heart failure. To learn more about why and how the renin system becomes involved in heart failure, the renal functional abnormalities have been re-examined. The effects of sodium administration on central haemodynamics and on the activity of the renin system have als been studied. This research has led to a consideration of the role of atrial natriuretic hormone in this pathophysiological interplay. The study recharacterized renal haemodynamic patterns and indicated that in congestive heart failure there is a disproportionate diversion of blood away from the kidneys because of afferent vasoconstriction. However, the glomerular filtration rate is maintained by concurrent efferent arteriolar constriction, expressed by a rising filtration fraction. As heart failure advances, the filtration fraction can no longer rise. At this point, the glomerular filtration rate becomes flow-dependent and falls commensurately with the declining cardiac output. These intrarenal patterns may be mediated in part by increased intrarenal renin activity resulting from heart failure and diuretic therapy. A further study of the abnormal renin system activity operating in heart failure has shown it to be very sensitive to dietary salt intake. Thus, consuming modest amounts of salt (100 mEq/day) was sufficient to markedly suppress renin and aldosterone values. However, since peripheral resistance was not changed, another non-renin, sodium-related mechanism must take over to sustain increased arterial constriction. The fact that captopril challenge evoked no response before and a large response after sodium depletion supports this concept. preliminary data suggest that atrial natriuretic hormone may also be important in congestive heart failure by opposing renin system activity at 4 sites.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endocrine mechanisms in congestive cardiac failure. Renin, aldosterone and atrial natriuretic hormone. 295 86

The control of sodium balance plays a vital role in the regulation of both intravascular and extravascular fluid volume. The discovery and synthesis of the atrial natriuretic peptides has led to the suggestion that they may be an important hormone in the control of sodium and water balance. Studies in man have confirmed that, when injected, they are natriuretic and that the plasma level, as measured by radioimmunoassay, changes with physiological changes in extracellular volume particularly those that occur with alteration of salt intake, the levels of atrial peptide rising as salt intake is increased. A recent study with a low dose infusion of atrial peptides has shown an increase in sodium excretion at the same plasma levels as those found with saline infusion, confirming that the atrial peptides are a natriuretic hormone in man. These findings allow a better interpretation of the raised levels that are already being described in patients with heart failure, renal failure and high blood pressure.
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PMID:Are the atrial peptides a natriuretic hormone? 295 5

Congestive cardiac failure causes activation of various neurohumoral responses that increase total peripheral resistance and promote salt and water retention. These effects increase blood pressure and organ perfusion in the short term, but ultimately cause further cardiac decompensation by increasing ventricular afterload and cardiac work. The role of the renin-angiotensin-aldosterone system and the catecholamines is partially understood, and blockade of these systems as a treatment of heart failure is now established. The role of vasopressin in heart failure is more controversial, but there is now compelling evidence that vasopressin may have important vasoconstrictor actions in addition to its fluid retaining properties. Atrial natriuretic factor is a newly described cardiac hormone released from the atrium. Atrial natriuretic factor causes natriuresis, diuresis, vasodilatation, suppression of thirst, and suppression of both renin and aldosterone. These actions largely counteract the effects of the renin-angiotensin system and vasopressin. Plasma atrial natriuretic factor has been reported to be markedly elevated in human and experimental heart failure, and may act to limit the neurohumoral response to reduced cardiac output. This review summarizes our understanding of the vasoactive hormones and reports experimental evidence supporting a pathophysiological role for vasopressin and atrial natriuretic factor in congestive cardiac failure.
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PMID:Responses of vasoactive hormones in congestive cardiac failure. 296 25

1. The relationship between plasma atrial natriuretic peptide (ANP) and body sodium was determined in rats 1 month after myocardial infarction induced by coronary artery ligation. After operation rats received a normal or a low salt diet, and total exchangeable body sodium was measured sequentially. 2. Rats with infarction receiving a normal salt intake did not retain sodium when compared with sham-operated controls. Rats receiving a low salt diet had a 10% decrease in body sodium (P less than 0.01). The decrease was the same in rats with infarction as in controls. 3. Plasma ANP was similar in control rats irrespective of salt status. Plasma ANP levels were markedly elevated in rats with infarction irrespective of salt status (P less than 0.01). 4. The rise in plasma ANP was correlated with cardiac hypertrophy and infarct size in animals fed both normal and low salt diets. However, there was no relationship between plasma ANP and exchangeable body sodium. 5. These results suggest that in this model of heart failure plasma ANP is raised by increased left atrial stretch in proportion to the severity of left ventricular dysfunction. In contrast, plasma ANP concentrations do not appear to be elevated as a consequence of increased right atrial pressure caused by sodium retention and expanded extracellular volume.
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PMID:Atrial natriuretic peptide and total exchangeable body sodium: relationships in rats with chronic myocardial infarction. 296 19


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