Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to measure components of the renin angiotensin system in patients with type 1 diabetes mellitus, with and without nephropathy, to study the renal sensitivity to angiotensin II in uncomplicated type 1 diabetes and to investigate the short and long-term renal effects of angiotensin II reduction with angiotensin converting enzyme inhibitors in patients with diabetic nephropathy. In patients with type 1 diabetes without complications, plasma renin activity, angiotensin II and aldosterone levels were normal. In patients with diabetic nephropathy, renin levels were elevated, probably partly as a result of diuretic treatment. However, renin levels were also elevated compared to patients with other renal diseases who had similar treatment and degree of azotemia. The renal sensitivity to angiotensin II was normal in patients with uncomplicated diabetes. The reduction in glomerular filtration rate and renal plasma flow and increases in filtration fraction during A II infusion were equal to those in healthy controls. Nine days' captopril treatment in 15 patients with diabetic nephropathy induced an increase in renal plasma flow and a decrease in filtration fraction. The glomerular filtration rate remained unchanged. During 8 weeks' randomised enalapril or metoprolol treatment in 40 patients with diabetic nephropathy, enalapril treatment reduced proteinuria to half the initial value. Metoprolol treatment had no effect on proteinuria. Furosemide was also used and the dosage was adjusted to give equally effective blood-pressure control in both groups. During long-term treatment with captopril in patients with diabetic nephropathy, the rate of decline in kidney function over time was reduced to one-fourth the initial value even though the blood pressure was only slightly reduced. The renin angiotensin system appears to be functionally intact in diabetes mellitus and interruption by ACE inhibition reduces proteinuria both by blood pressure reduction and by an effect independent of systemic blood pressure. Long-term treatment might protect kidney function in diabetic nephropathy to a greater extent than would be expected from the blood-pressure-lowering effect alone.
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PMID:The renin angiotensin system in diabetes mellitus. A physiological and therapeutic study. 219 80

The pathophysiology of the nephrotic syndrome (NS), characterized by protenuria, edema, sodium retention and hyperlipidemia, is not clear. We studied the role of some systemic factors on sodium retention in an experimental model of NS. NS was induced in rats by a single subcutaneous injection of puromycin aminonucleoside (PA) (15 mg/100 g); control animals received vehicle. All rats were kept in metabolic cages for 24 days (3 days before and 21 days after PA-injection). Urine was collected daily. Blood samples were obtained every day until day 10, and then every other day up to the end of the study. The rats showed the following alterations after PA injection: a) a rise in serum angiotensin converting enzyme activity (ACEA) and plasma aldosterone (PAldo) at day 1; b) a rise in urinary aldosterone (UAaldoV), azotemia and sodium retention at day 2; c) massive proteinuria (UProt) and decrease in plasma angiotensinogen concentration (PAC) at day 4; d) increases in plasma renin activity (PRA), plasma renin concentration (PRC) and serum creatinine as well as hypoproteinemia, hypercholesterolemia, hypertriglyceridemia, ascitis and edema at day 5; e) increase in urine volume at day 6. PAldo became normal at day 7; urine sodium (UNaV), PRA and PRC at day 8; UAldoV at day 9; serum urea and ACEA at day 10; urinary volume at day 11; PAC, serum total protein and creatinine at day 12. The edema disappeared at day 11. UProt, hypercholesterolemia and hypertriglyceridemia persisted, though they decreased substantially by the end of the study (day 21). Light microscopy studies revealed normal glomerular morphology, but electron microscopy showed fusion of podocytes before proteinuria. These data suggest that: a) sodium retention was not a consequence of proteinuria or hypoproteinemia; b) sodium retention seems non-related to renin secretion, but may be partially mediated by a fall in glomerular filtration rate or by an increased tubular resabsorption secondary to other factors; c) the increase in PAldo, UAldoV and ACEA are non-related to renin secretion: all occurred before PRA rose; d) water retention, increase in PRA and PRC, hypercholesterolemia and hypertriglyceridemia are secondary to the hypoproteinemia.
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PMID:Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. I. The role of proteinuria, hypoproteinemia, and renin-angiotensin-aldosterone system on sodium retention. 223 72

CHF may activate the RAS by various mechanisms. Acute CHF is associated with high PRA, whereas chronic, stable disease is combined with normal values. The response to ACEI is affected by blood pressure, degree of activation of the RAS, salt balance and degree of possible renal failure. It may also be affected by concomitant diuretic or, e.g., digoxin therapy. ACEI improves RPF, GFR may remain normal or may increase, if it was previously impaired due to reduced RPF. Severe hypotension in combination with decreased autoregulatory capacity may decrease GFR. Generally, renal excretion of sodium and water increase. These changes in renal handling of salt and water are primarily caused by decreased AII. They are also augmented by inhibited sympathetic tone and thirst and decreased release of ADH and aldosterone. Increased synthesis of vasodilating and natriuretic PGs is probably also of some importance. Dilutional hyponatremia may be corrected by combined ACE inhibitor and furosemide treatment. Water and sodium excretion increase and sodium is redistributed from the intracellular space. Low serum sodium values increase and azotemia may be corrected, if ACE inhibitor doses are carefully titrated to avoid severe hypotension. These effects are ascribed mainly to a decrease of AII, thirst and ADH release. The effect of furosemide is improved since increased amounts of salt are delivered to the loop of Henle and access of furosemide to its site of action is facilitated by increased RPF. ACEI does not cause any obvious negative effects on renal handling of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ACE inhibition on renal regulation of salt and water. 301 59

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

Five children with high-renin hypertension unresponsive to conventional medications were effectively treated with the angiotensin I-converting enzyme inhibitor, captopril, for six to 26 months. Age groups included children 6 to 13 years old and a 33-week gestation preterm infant with hypertension related to umbilical artery catheterization. Significant adverse reactions were limited to transient renal insufficiency in the preterm infant and increased azotemia in an older child with chronic renal failure.
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PMID:Captopril. Long-term treatment of hypertension in a preterm infant and in older children. 633 72

Twenty-four cats with spontaneous systemic hypertension were retrospectively studied. Blood pressure (BP) was measured indirectly by the Doppler technique in 17 cats (mean systolic 219.4 +/- 43.2 mm Hg) and directly by femoral arterial puncture in 15 cats (mean systolic/diastolic 233.2 +/- 40.9/148.1 +/- 28.7 mm Hg). All cats had bilateral retinal hemorrhages and/or detachments. Twenty cats presented because of blindness. Other presenting signs included polyuria/polydipsia, weight loss, neurological signs, and/or epistaxis. Diagnostic tests were performed to determine the presence and the cause of any secondary organ damage. Common findings included retinal hemorrhages/detachments, low-grade systolic murmurs, cardiomegaly with left ventricular hypertrophy (LVH), small kidneys, mild azotemia, and urine specific gravity < or = 1.020. Only 3 cats had hyperthyroidism. One cat was transiently diabetic. Necropsies on 2 cats with neurological signs showed nephrosclerosis, arteriosclerosis, and multifocal cerebral hemorrhages. Twenty cats were treated with diuretics, beta-adrenergic antagonists, and/or an angiotensin converting enzyme (ACE) inhibitor. One cat was treated with methimazole only, and 1 was treated with insulin transiently. The median survival of the 24 cats was 18 months. Response to therapy did not appear to have an impact on survival time.
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PMID:Spontaneous systemic hypertension in 24 cats. 804 80

Renal crisis occurs in systemic sclerosis patients with rapidly progressive diffuse cutaneous thickening early in their disease course. SRC is characterized by malignant hypertension, hyperreninemia, azotemia, and microangiopathic hemolytic anemia. This complication was almost uniformly fatal but can now be treated successfully in most cases with ACE inhibitors. The result has been improved survival, reduced requirement for dialysis, and even discontinuation of dialysis after 6 to 18 months of treatment. Prompt diagnosis and early aggressive treatment of SRC with ACE inhibitors will result in the most optimal outcome.
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PMID:Renal involvement in systemic sclerosis. 807 63

Management of congestive heart failure in the past has focused on sodium and fluid restriction, rest, and digitalis glycosides. Now, significant new evidence justifies early and aggressive ACE inhibitor therapy in patients with asymptomatic or mildly symptomatic LV dysfunction. ACE inhibitors reduce the likelihood of symptomatic heart failure in asymptomatic patients with reduced ejection fraction. Patients with reduced LV function following acute MI who receive ACE inhibitors have a decreased risk of death, a lower probability of developing systematic heart failure, and fewer MI recurrences. Hypotension and azotemia can be avoided by reducing the concomitant dose of diuretics and carefully titrating the ACE inhibitor dosage to target levels.
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PMID:Mild heart failure: why the switch to ACE inhibitors? 822 26

Despite advances in the pharmacological management of cardiac failure, some patients remain refractory to this therapy. However, improved understanding of the physiology and technique of peritoneal dialysis has recently allowed ambulatory peritoneal ultrafiltration to be applied to the treatment of patients with intractable heart failure. We report the management of three such patients with New York Heart Association (NYHA) class IV cardiac failure, each with a left ventricular ejection fraction < 20%. They had become unresponsive to maximum pharmacological management with inotropes, diuretics and ACE inhibitors. All patients had biochemical evidence of pre-renal azotemia. Initially, patients received aggressive ultrafiltration by continuous veno-venous haemofiltration (CVVH) or one- to two-hourly peritoneal dialysis exchanges until they achieved an optimal dry body weight. Once stabilized, they were converted to an intermittent ambulatory peritoneal ultrafiltration (IAPU) regimen of one to three exchanges per 24 h according to their individual needs. During an 18 +/- 10-month follow-up, their duration of hospital confinement was reduced by 85% and all three patients improved from class IV to class II cardiac failure. IAPU may have a useful role in the long-term management of intractable heart failure in a selected group of patients.
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PMID:Long-term successful management of refractory congestive cardiac failure by intermittent ambulatory peritoneal ultrafiltration. 891 42

Renal crisis occurs in systemic sclerosis patients with rapidly progressive diffuse cutaneous thickening early in their disease. SRC is characterized by malignant hypertension, hyperreninemia, azotemia, microangiopathic hemolytic anemia, and renal failure. This complication, which in the past has been almost uniformly fatal, is now successfully treated in most cases with ACE inhibitors. This therapy has improved survival, reduced requirement for dialysis, and in those on dialysis has often allowed discontinuation of this procedure 6 to 18 months later. Prompt diagnosis and early, aggressive initiation of therapy with ACE inhibitors will result in the most optimal outcome. Chronic nonrenal crisis renal insufficiency is unusual and rarely progresses to significant renal dysfunction.
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PMID:Scleroderma renal crisis. 892


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