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)

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

A moderate elevation of the daily excretion of free noradrenaline and adrenalin is observed in chronic circulatory insufficiency, beginning with Stage IIA. The catecholamines metabolism is elevated, as shown by the daily excretion of normethanpherine and methanpherine and of vanillyl-mandelic acid. The activity of renin and angiotensinases was growing along with the progressing cardiac insufficiency. The blood level of angiotensinogen was decreasing, especially in patients with Stage IIB and III of decompensation. The daily excretion of aldosterone was growing along with the development of cardiac insufficiency. The functional state of the glucocorticoid function of the adrenal cortex was of a phased nature in cases of circulatory insufficiency. The study of the functional state of the epiphysis was conducted by way of determining the blood level of melatonine and of its daily excretion. In Stages I and IIA the level of this hormone was clearly elevated, in Stages IIB and III -- decreased as compared with the initial and normal levels. The plasma level of the antidiuretic hormone was distinctly growing, beginning with Stage IIB, reaching its maximal values in Stage III.
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PMID:[State of the neurohumoral regulatory system in circulatory insufficiency]. 18 17

The renin-angiotensin system is thought to maintain elevated systemic vascular resistance in heart failure. The hemodynamic effects of captopril (SQ 14225), an oral inhibitor of angiotensin-converting enzyme, were measured in 10 patients with stable congestive heart failure poorly controlled by digitalis and diuretics. At single daily doses of 25 to 150 mg, the cardiac index rose from 1.75 +/- 0.18 to 2.27 +/- 0.39 (mean +/- S.D.) liters per minute per square meter (P less than 0.001), and pulmonary-wedge pressure fell from 26.5 +/- 7.5 to 17.3 +/- 6.1 mm Hg (P less than 0.01). Systemic vascular resistance decreased from 2006 +/- 300 to 1393 +/- 238 dyne seconds per centimeter (P less than 0.001), and mean arterial pressure fell from 83.7 +/- 7.0 to 70.3 +/- 9.9 mm Hg (P less than 0.001) (mean +/- S.D.). Heart rate did not change appreciably. Hemodynamic alterations peaked at 90 minutes and persisted for three to four hours. Control plasma renin activity ranged from 1.1 to 7.3 ng per milliliter per hour and did not correlate with changes in hemodynamic values. Three patients on long-term treatment maintained clinical improvement. Although its mechanism of action has not been completely elucidated, captopril may prove useful in the treatment of chronic congestive heart failure.
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PMID:Treatment of chronic congestive heart failure with captopril, an oral inhibitor of angiotensin-converting enzyme. 22 10

Clonidine, propranolol, bethanidine and debrisoquine effectively decrease blood pressure by suppressing renin secretion or interfering with function of the sympathetic nervous system. In man these compounds exert an antihypertensive effect within several hours or days and their duration of action is sufficient to permit administration twice or thrice daily. Clonidine and propranolol are especially useful if sexual dysfunction or postural hypotension is undesirable. Although bethanidine and debrisoquine may produce these adverse effects, they are beneficial in severe hypertension and produce fewer side effects than guanethidine. Clonidine frequently causes sedation, and rebound hypertension may occur with sudden cessation of therapy. Injudicious use of propranolol may provoke heart failure or asthma in susceptible individuals. The combination of a thiazide diuretic with propranolol and one of hydralazine, bethanidine and debrisoquine may be used to treat severe or complicated hypertension.
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PMID:New drugs in hypertension. 34 94

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.
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PMID:Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. 38 61

d-3-Acetoxy-cis-2,3-dihydro-5-]2-(dimethylamino)ethyl]-2-(p-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one hydrochloride (diltiazem HCl) was orally administered to 9 patients with chronic congestive heart failure (Class IIb to III, NYHA) to examine whether the drug induces sodium retention and aggravates congestive heart failure. Renal hemodynamics and urinary electrolytes excretion were measured for 3 h after the medication in 6 out of 9 patients. Four of the rest of patients had received chronic administration of the drug for about 2 weeks. There was a significant increase in urinary sodium excretion without noticeable change in renal hemodynamics after diltiazem administration, demonstrating the presence of its direct inhibitory action on renal tubules. The increase in urinary sodium excretion was more marked in patients with heart failure than in those without. This difference in the response to diltiazem may be due to the functional constriction of renal cortical vessels in heart failure. This constriction may be related to renin-angiotensin system which diltiazem was reported to antagonize. The chronic administration of the drug did not induce sodium retention and edema. There was no deterioration of symptoms due to congestive heart failure such as dyspnea and body weight increase. It may be concluded that diltiazem does not aggravate congestive heart failure through its diuretic action and probably its systemic vasodilating action.
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PMID:The effect of diltiazem hydrochloride upon sodium diuresis and renal function in chronic congestive heart failure. 58 67

In 15 patients with severe chronic left ventricular failure, plasma renin activity (PRA) ranged widely, from 0.2--39 ng/ml/hr. The level of PRA was unrelated to cardiac output (CO) or pulmonary artery wedge pressure (PWP), but was slightly negatively correlated with mean arterial pressure (MAP) (r = -0.45) and systemic vascular resistance (SVR) (r = -0.40). After infusion of the angiotensin converting enzyme inhibitor teprotide (SQ 20,881) PWP fell from 26.3 +/- 1.3 (SEM) to 20.3 +/- 1.4 mm Hg (P less than 0.001), CO rose from 3.94 +/- 0.23 to 4.75 +/- 0.31 l/min (P less than 0.001), MAP fell from 87.5 +/- 3.8 to 77.9 +/- 4.1 mm Hg (P less than 0.001) and SVR from 1619 +/- 148 to 1252 +/- 137 dyne-sec-cm-5 (P less than 0.001). The fall in MAP and in SVR was significantly correlated with control PRA (r = 0.68 and r = 0.58, respectively). When subjects were divided on the basis of control PRA the hemodynamic response to teprotide was greatest in the high renin group. PRA rose after teprotide (8.7 +/- 3.4 to 37.9 +/- 7.7 ng/ml/hr, P less than 0.05) but plasma norepinephrine fell (619.1 +/- 103.6 to 449.7 +/- 75.7, P less than 0.05). The renin-angiotensin system thus appears to have an important role in the elevated SVR in some patients with heart failure. Chronic inhibition of converting enzyme should be explored as a possible therapeutic approach.
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PMID:Role of the renin-angiotensin system in the systemic vasoconstriction of chronic congestive heart failure. 69 45

The renin-aldosterone system was studied in cardiomyopathic hamsters (CMH) before and after the onset of untreated clinical congestive heart failure. Age-matched random-bred hamsters (RB) served as controls. Before heart failure, there were no differences in body weight accretion, sodium balance, plasma renin activity or in vitro aldosterone production. After the onset of heart failure in CMH, body weight increased at a greater rate than in RB and positive sodium balance was nearly twice control levels. Although plasma renin activity was greater (P less than 0.005) in CMH than in RB (23.4+/-4.2 (mean+/-SEM) vs. 3.8+/-1.8 ng/ml/h), aldosterone production (101+/-15 vs. 95+/-16 ng/h) did not differ. Plasma aldosterone was low or undetectable in RB and in CMH in heart failure. In response to angiotensin stimulation, aldosterone production increased in both strains and did not differ. No difference in muscle potassium content, potassium balance or excretion was detected. Thus, in CMH, congestive heart failure is attended by increased plasma renin activity without a significant increase in aldosterone production, a dissociation which does not appear to be due to adrenal unresponsiveness to angiotensin II or to potassium depletion.
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PMID:Renin and aldosterone in the cardiomyopathic hamster in congestive heart failure. 88 11

The renin-angiotensin-aldosterone system and electrolyte levels in 11 patients with heart failure controlled on digoxin and frusemide were investigated after separate periods of Slow K, spironolactone, and amiloride therapy. When spironolactone or amiloride replaced Slow K, distinct parallel increments in the levels of renin, angiotensin II, and aldosterone resulted. Though plasma potassium was generally higher after spironolactone and amiloride than after Slow K, exchangeable potassium was similar with the three regimens. There was no significant relation between plasma potassium and concurrent exchangeable potassium.
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PMID:Effect of potassium-sparing diuretics on the renin-angiotensin-aldosterone system and potassium retention in heart failure. 97 76

1. Pindolol lowers blood pressure both, immediately after administration by a reduction of cardiac output and heart rate and after long-term administration by reducing peripheral resistance. Cardiac index, initially decreased, reached the control value after 8 weeks of treatment. 2. The persistent reduction in heart rate and increase of the cardiac index during exercise after prolonged treatment together with the increase of right and left heart filling pressures seems to be due to augmentation of the Starling mechanism. The increase of the stroke volume at rest and during exercise diminished the blood-pressure lowering effect of the drug. 4. The exercise-induced increase of noradrenalin was abolished by acute administration of pindolol. After long-term treatment, however, we found a consistent and significant elevation of the plasma-catecholamines. This may reflect the development of heart failure [1], a tyramin- or cocain-like action of pindolol [2] or an indirect sympathicomimetic effect of this drug at low doses (10--15 mg/day orally ) [3]. 5. The elevation of plasma-noradrenalin reflects increased sympathetic tone and may be responsible for the increase in stroke volume and plasma renin activity observed by several authors. 6. Since there was no evidence for a hemodynamic mode of action, the lowering of blood rpessure by pindolol may be a central effect.
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PMID:[Hemodynamic long-term effects of a beta-receptor blockader (Pindolol) in primary essential hypertension]. 103 73


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