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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The remodelling of the left ventricle after myocardial infarction results from the expansion of the infarcted zone in the acute phase and the dilation of the healthy zone of the left ventricle which complicates the initial expansion. It brings about an increase in the left ventricular volume which is a major pejorative prognosis factor after myocardial infarction. The expansion, defined by the dilation and parietal stricture of the infarcted zone, complicates about 30 p. cent of the infarctions and appears in the first hours of the infarction. It is favoured by the transmural nature of the infarction, by its extent and its previous topography, and by arterial hypertension. It is accompanied by a higher mortality rate, increases the risk of parietal rupture, exposes to post-infarction aneurysm and to intraventricular thrombi, and initializes the ventricular remodelling, factor of secondary cardiac failure. The dilation of the healthy zone of the left ventricle is observed mainly in case of initial expansion. Its importance increases with the size of the infarction. It corresponds to the volume overload secondary to the increase in the telediastolic parietal constraint of the left ventricle. The remodelling of the left ventricle after infarction is limited by captopril, and possibly by the restoration of the blood flow in the artery responsible for the infarction. Captopril, administered in the first weeks following the infarction, limits the dilation of the left ventricle in man as well as in animals. This beneficial effect is due to a decrease in the post-load of the left ventricle. Captopril improves the survival after infarction in animals, but its effect on the post-infarction mortality in man is still under study.
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PMID:[Expansion and remodelling of the left ventricle after myocardial infarction]. 214 11

Diabetes-associated hypertension is accompanied by high levels of body sodium and cardiovascular hyper-reactivity to noradrenaline. Captopril, a promising drug for the treatment of hypertension in diabetics, may influence sodium metabolism and adrenergic pathways. This possibility was investigated in 11 patients with non-azotaemic diabetes mellitus and hypertension, studied after a 3-week placebo phase and after an 8-week phase of captopril treatment (50-100 mg/day). Blood pressure, exchangeable body sodium, blood volume, plasma renin activity, angiotensin II (Ang II), aldosterone, catecholamine levels and the pressor reactivity to infused Ang II or noradrenaline were measured. Compared with placebo, captopril caused a significant decrease in arterial pressure and stimulation of plasma renin activity. Exchangeable sodium, blood volume, plasma Ang II, aldosterone, noradrenaline and adrenaline levels, the pressor and aldosterone responsiveness to infused Ang II and the pressor response to infused noradrenaline (alone or combined with atropine) were not modified. These findings suggest that in hypertensive diabetics angiotensin converting enzyme inhibition causes a marked decrease in blood pressure. The mechanism of action is unrelated to changes in body sodium or noradrenergic-dependent pressor reactivity. In the stable phase of therapy, Ang II-dependent pathways are left unaltered when captopril is administered twice a day.
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PMID:Cardiovascular regulation during angiotensin converting enzyme inhibition with captopril in diabetes-associated hypertension. 216 58

The urinary albumin excretion measured by the albumin creatinine clearance ratio (Calb/Ccreat) and the mean supine arterial blood pressure (MAP) were studied before the start of ACE inhibition, at the start and during up to 1 year of ACE inhibition with Captopril or Enalapril in 35 patients with various chronic proteinuric renal disorders with or without renal failure, arterial hypertension and nephrotic syndrome. Before the start of ACE inhibition mean Calb/Ccreat, MAP, s-albumin and s-creatinine did not change. During ACE inhibition the Calb/Ccreat was reduced from 75% (p less than 0.05) in patients with minimal albuminuria to 41% (p less than 0.005) in patients with extensive albuminuria. Average reduction of albuminuria was 44% at one year's observation time. Serum albumin increased 9% (p less than 0.05), serum creatinine did not change significantly and MAP showed a slight, not uniformly significant decrease. The reduction of Calb/Ccreat was of the same order in the different renal disorders studied and was independent of the renal function, presence or absence of nephrotic syndrome and treatment with antihypertensive or immunosuppressive drugs. The decrease in Calb/Ccreat during ACE inhibition was related to the reduction in MAP at most time intervals, but Calb/Ccreat decreased also when MAP was unchanged or increased. Thus the decrease in Calb/Ccreat during ACE inhibition does not only seem to be a consequence of a decrease in the systemic arterial blood pressure but reasonably also due to changes in the intra-renal hemodynamics and most probably a decrease in the glomerular capillary pressure.
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PMID:Reduction of albuminuria after angiotensin converting enzyme inhibition in various renal disorders. 218 37

In 28 patients with chronic angina pectoris grade II-III (NYHA) the authors investigated the antianginous effect of captopril. All patients had a normal blood pressure and the diagnosis was confirmed by coronary angiography. The investigation was made in three sub-groups as a simple crossover experiment with a randomized onset. In 10 patients without dysfunction (group A) and eight with severe left ventricular dysfunction (group C) a short-term comparative study of captopril and placebo was made; 10 patients of group B took first for 7 days diltiazem, 3 X 60 mg, and then during subsequent weeks the action of diltiazem with placebo was compared and the action of diltiazem combined with captopril 3 X 25 mg per day. Captopril significantly reduced the blood pressure and Robinson's index at rest and during activity. It protracted significantly the time before the development of stenocardia in patients with left ventricular dysfunction and in the group treated with diltiazem where it reduced even further the incidence of stenocardias. ACE inhibitors may apparently enhance the effectiveness of diltiazem in normotensive patients with angina pectoris and it may be assumed that it will have an even more potent effect in concurrent hypertension or left ventricular dysfunction.
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PMID:[Captopril in the therapy of stable angina pectoris]. 218 38

The chemistry, pharmacology, pharmacokinetics, adverse effects, and dosages of the three currently available angiotensin-converting enzyme (ACE) inhibitors are reviewed. This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. The ACE inhibitors, therefore, are capable of lowering blood pressure primarily by promoting vasodilatation and reducing intravascular fluid volume. Captopril, the first orally active, commercially available ACE inhibitor, is a sulfhydryl-containing compound. Captopril was followed by the introduction of enalapril and lisinopril, two non-sulfhydryl ACE inhibitors. The pharmacokinetic profiles of these three ACE inhibitors differ. Captopril has rapid onset with relatively short duration of action, whereas enalapril and lisinopril have slower onset and relatively long duration of action. Captopril is an active ACE inhibitor in its orally absorbable parent form. In contrast, enalapril must be deesterified in the liver to the metabolite enalaprilat in order to inhibit the converting enzyme; this accounts for its delayed onset of action. Lisinopril does not require metabolic activation to be effective; however, a slow and incomplete absorption pattern explains the delay in onset of activity. Captopril and its disulfide metabolites are primarily excreted in the urine with minor elimination in the feces. Approximately two-thirds of an administered enalapril dose is excreted in the urine as both the parent drug and the metabolite enalaprilat; the remainder of these two substances are excreted in the feces. Lisinopril does not undergo measurable metabolism and approximately one-third is excreted unchanged in the urine with the remaining parent drug being excreted in the feces. The ACE inhibitors lower systemic vascular resistance with a resultant decrease in blood pressure. Their efficacy is comparable to diuretics and beta-blockers in treating patients with mild, moderate, or severe essential and renovascular hypertension. In those patients with severe congestive heart failure (CHF) the ACE inhibitors produce a reduction in systemic vascular resistance, blood pressure, pulmonary capillary wedge pressure, and pulmonary artery pressure. These drugs may produce improvement in cardiac output and stroke volume and, with chronic administration, may promote regression of left ventricular hypertrophy. The antihypertensive effects of the ACE inhibitors are enhanced when these agents are combined with a diuretic. Captopril and enalapril have been shown to be of particular benefits as adjunctive therapy in patients with congestive heart failure, both in terms of subjective improvement of patient symptoms, and in improving overall hemodynamic status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors: a comparative review. 218 39

Captopril, an orally active angiotensin I-converting inhibitor, is an effective drug in the treatment of hypertension in adults and children. The use in newborn infants has been, nevertheless, short. We report five cases of hypertension in newborn infants poorly responsive to large doses of other potent antihypertensive agents: furosemide, propanolol and hydralazine. We have got a reduction in mean blood pressure in three cases, with doses of 0.1-0.2 mg/kg/day for a time lesser than a month. Another patient had a reduction with high doses (5 mg/kg), showing increase in mean serum urea, creatinin, potassium and phosphorus levels. This effect disappeared after captopril was discontinued. We suggest the use of captopril in hypertension non-responsive to other antihypertensive agents, mainly in those of renovascular cause.
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PMID:[Captopril treatment of neonatal arterial hypertension]. 218 32

A study was undertaken on the role of brainstem renin-angiotensin system in maintenance of hypertension in chronic renovascular hypertensive rats. Hypertension was induced by unilateral renal artery clamping, while the contralateral kidney was left intact (2 KIC). Blood pressure (BP), plasma renin activity (PRA) and brainstem angiotensin (ang-I) levels were measured after 24 days, in hypertensive and sham-operated animals. In separate subgroups of these animals, the effect of intracerebroventricular administration of captopril on the parameters listed was studied. The results showed high ang-I levels in 2 KIC rats as compared to controls (P less than 0.05). Captopril administration (500 micrograms/50 microliters icv) caused a fall in BP and increase in brainstem ang-I levels (P less than 0.01). In control animals, however, captopril produced a rise in BP without any significant change in brainstem ang-I levels. Peripheral plasma renin activity was normal, despite significant sodium retention in 2 KIC rats. The results are suggestive of activation of brainstem renin-angiotensin system (RAS) in chronic 2 KIC hypertension.
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PMID:Increased brainstem angiotensin-I levels in chronic 2 KIC hypertensive rats. 218 30

Hypertensive patients prescribed captopril while attending a hospital hypertension clinic were studied, to identify the benefits of the drug, its adverse effects and factors predisposing to them. One hundred and eighty two patients were followed for a mean of 18 months; 24 received captopril alone, and 158 combinations of captopril and other antihypertensive drugs, especially loop diuretics (91/158), or thiazide diuretics (57/158), or other vasodilators (57/158). The mean final dose of captopril was 67 mg/day. Blood pressure (BP) was effectively controlled in 73% of patients (mean fall in systolic BP 29 mmHg, CI 24 to 34, P less than or equal to 0.001; mean fall in diastolic BP 18 mmHg, CI 16 to 20, P less than or equal to 0.001). Blood urea and creatinine rose slightly in all patients (urea by 0.9 mmol/l [13%], CI 0.5-1.3, P less than or equal to 0.001 and creatinine by 9 mumols/l [8%], CI 4-13, P less than or equal to 0.001). Twenty six patients were withdrawn from captopril therapy: 6 because of poor control of their blood pressure, two because it was no longer necessary and 12 (7.7%) because of extrarenal adverse effects--10 for rashes, one each for gastric upset and impotence. Captopril was withdrawn in a further 6 patients, because of deteriorating renal function. Factors discriminating those at risk of renal dysfunction were high doses of captopril, concomitant high dose diuretic therapy and undiagnosed renovascular disease.
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PMID:Adverse effects of captopril in hospital outpatients with hypertension. 219 Feb 1

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.
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PMID:Effect of captopril on plasma prolactin in patients with essential hypertension. 219 85

In four children the role of captopril-radionuclide nephrography in the diagnosis of renovascular hypertension was studied. Captopril (0.5-1.0 mg/kg orally) did not affect Iodine-123 Hippuran nephrography in two children with mild renal artery stenosis, but induced an accumulation of the tracer within the kidneys in two children with hemodynamically significant renal artery stenosis. As in adults Iodine 123 Hippuran nephrography appears to be a useful tool to identify patients with significant renal artery stenosis.
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PMID:[The diagnostic value of captopril radionuclide nephrography for renovascular hypertension in childhood]. 219 62


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