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

To study the effects of a novel angiotensin I converting enzyme inhibitor (ACEI) on hypertension-induced cardiac hypertrophy, benazepril hydrochloride (CGS 14824 A, CAS 86541-74-4) at the dose of 3 and 10 mg/kg/d p.o. was administered to spontaneously hypertensive rats from 4 to 16 weeks of age. In addition to suppression of developing blood pressure, benazepril hydrochloride reduced both the wet weights of whole heart and left ventricle dose-dependently and significantly. Benazepril hydrochloride had no effect on hydroxyproline concentration and content or protein concentration in the left ventricle, whereas is reduced the total protein content dose-dependently. Serum ACE activity was significantly reduced at 10 mg/kg/d of benazepril hydrochloride, but renin activity, aldosterone and noradrenaline concentration in serum were not changed. From the microscopic findings of the left ventricle, benazepril hydrochloride reduced the myocardial hypertrophy significantly. From these results, benazepril hydrochloride seems to suppress the increase in volume load by acting through the renin-angiotensin-aldosterone system, and dose not seem to cause a significant reflex of catecholamine which often occurs with peripheral vessels dilation. Thus, benazepril hydrochloride may be expected to suppress cardiac hypertrophy in patients with hypertension.
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PMID:Effect of benazepril hydrochloride on cardiac hypertrophy in spontaneously hypertensive rats. 183 66

The cardiac organ manifestation of arterial hypertension comprises the myocardium itself with left-ventricular hypertrophy, the interstitium with perivascular and interstitial fibrosis, and the coronary circulation with disease of large and small coronary arteries. The consequences of the sum and interactions of these cardiac organ manifestations have an impact on left-ventricular systolic and diastolic function, the ischemic risk, and the occurrence of arrhythmias in hypertensive patients. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive coronary microangiopathy in order to improve the coronary reserve and to reduce the ischemic risk. Regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympatholytic substances). While normal systolic function was maintained in the compensated stage of hypertensive hypertrophy and was not significantly influenced by antihypertensive therapy, diastolic function was impaired in a very early stage of arterial hypertension. Both the phase of isovolumic relaxation and the phase of early diastolic filling were imparied, while after long-term antihypertensive treatment with Ca-channel blockers of the dihydropyridine type or ACE inhibitors, only the latter one was improved. From preliminary results there is clinical evidence that hypertensive disease of small coronary arteries can be reversed after long-term antihypertensive treatment with a consequently improved coronary reserve and a reduced ischemic risk. Moreover, to what extent the prognosis of hypertensive heart disease can be improved by reversal of myocardial hypertrophy and disease of small coronary arteries is yet unknown.
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PMID:Long-term treatment in arterial hypertension for protecting hypertrophic myocardium. 183 50

Cardiac hypertrophy in hypertension is related to increased peripheral vascular resistance and reduced aortic compliance. Non-invasive measurement of pulse wave velocities and systolo-diastolic variations of the diameter of the aortic arch show that an increase in the elastic modulus of the aorta is closely related to the increase in cardiac mass. This relationship holds even after correction for mean arterial pressure. Therefore, it has been suggested that, in hypertension, the decreased aortic compliance leads to a disproportionate increase in systolic blood pressure and end systolic wall stress, predisposing to cardiac hypertrophy. The blood pressure, arterial haemodynamics of the forearm (by pulsed Doppler flow measurement) and echocardiographic parameters were studied in 16 patients with permanent essential hypertension, before and 3 months after treatment with perindopril, an ACE inhibitor. In a simple blinded study versus placebo, perindopril was shown to significantly reduce the blood pressure (p less than 0.01) while brachial blood flow increased (p less than 0.01) because of a simultaneous increase in blood flow velocity and arterial diameter. During 5 minutes' occlusion at the wrist, blood flow velocity decreased more in patients taking perindopril than those on placebo (p less than 0.01) whilst the reduction in arterial diameter was equivalent, indicating that the increase in arterial diameter with perindopril could not be explained by flow-dependent dilatation alone but by a direct effect of the drug on the artery. During the treatment phase, brachial arterial compliance increased (p less than 0.01) and pulse wave velocity decreased (p less than 0.01) and there was no change in arterial shear stress defined as the product of mean blood pressure and arterial diameter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac hypertrophy and arterial compliance after antihypertensive treatment]. 183 23

Arterial hypertension is often complicated by left ventricular hypertrophy (LVH) and by vascular structural changes resulting in decreased proximal and distal compliance. LVH is an adverse prognostic factor because it increases the incidence of sudden death and other morbid events related to ischaemic heart disease, whereas vascular alterations may induce target organ damage and contribute to the maintenance of elevated blood pressure values. Thus, antihypertensive treatment must both reduce blood pressure and halt regression of cardiovascular structural changes. A review of the literature suggests long-term use of calcium antagonists, ACE inhibitors, and beta-blockers may revert LVH. We have found that such long-term drug use not only reduces blood pressure and LVH, but also ventricular arrhythmias that are often related to cardiac hypertrophy; however, diuretics do not have this beneficial effect. As regards vascular disturbances ACE inhibitors partially revert these alterations, whereas beta-blockers do not. Further studies are needed to determine whether there are regional differences in the regression of cardiovascular structural changes or whether different antihypertensive drugs have different effects on these changes.
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PMID:Cardiovascular structural changes in hypertension: possible regression during long-term antihypertensive treatment. 183 19

Activity of serum angiotensin converting enzyme (SACE) was measured in serum of 33 pregnant women with normal blood pressure or pregnancy induced hypertension (PIH), using sensitive Hippurate colorimetric micromethod. The mean level of SACE activity in 17 PIH patients (73.25 +/- 18.81 U/ml) was significantly higher than that in normotensive pregnant women (16 cases) ( 52.36 +/- 9.91 U/ml) (P less than 0.01). The mean arterial blood pressure showed a positive correlation with the level of SACE activity in all pregnant women (Y = 69.089 + 0.494x, r = 0.562, P less than 0.01). In PIH patients, the gestosis index and degree of edema also had statistically significant correlation with the level of SACE activity (Y = -0.560 + 0.056x, r = 0.549, P less than 0.01) (Y = -1.760 + 0.043x, r = 0.629, P less than 0.05). The amount of 24h urinary protein was independent of the level of SACE activity. It suggests that disturbance in regulation of ACE activity may be one of the factors responsible for the development of PIH.
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PMID:[Activity of serum angiotensin converting enzyme in pregnancy-induced hypertension]. 184

We report a patient presenting rapid deterioration of renal function due to primary cholesterol atheroembolism. The patient was 75-year-old hypertensive male and was admitted to a hospital because of rt. hemiplegia which developed 2 weeks earlier. On admission, his blood pressure was 200/100 mmHg and serum creatinine level was 2.9 mg/dl with urinalysis 1+ both for protein and hematuria. 2 weeks later, an angiotensin converting enzyme inhibitor (ACE inhibitor, delapril 15 mg/day) was given to control high blood pressure. Immediately after this medication, his renal failure rapidly progressed with a fall in blood pressure (110/60 mmHg) and oliguria (100 ml/day). Although he was transferred to our hospital and was treated with hemodialysis, he died of an attack of acute myocardial infarction in a week. At post-mortem examination, microscopic findings of the kidney disclosed numerous occlusions of medium-sized artery by cholesterol emboli. These emboli were also observed in other organs, but not so prominent as in the kidney. The coronary arteries exhibited severe sclerosis. In this presented case, acute deterioration of renal function was caused by ACE-inhibitor, although which was administered in a volume depleted condition. Therefore, further study would be necessary whether or not ACE-inhibitors predispose the patients with this disease to acute renal failure.
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PMID:[A case of renal failure due to primary cholesterol atheroembolism]. 187 61

The RAS is part of an extremely powerful feedback system for long-term control of blood pressure and volume homeostasis. Disturbances that tend to lower blood pressure, such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due, in large part, to the combined actions of ANGII and reduced arterial pressure. In response to increased sodium intake, decreased ANGII formation greatly amplifies the effectiveness of pressure natriuresis, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium retaining effects of ANGII necessitate increased blood pressure to maintain sodium balance via pressure natriuresis. Because the RAS is so powerful in regulating blood pressure, blockade of the system with ACE inhibitors offers a powerful therapeutic tool in diseases such as hypertension and congestive heart failure. The control of sodium excretion and blood pressure by ANGII is exerted through multiple intrarenal as well as extrarenal effects, including stimulation of aldosterone secretion, which can influence renal excretion. Current evidence suggests that the intrarenal effects of ANGII are quantitatively more important than those mediated by aldosterone in controlling blood pressure and renal excretion. The most important intrarenal effects of ANGII include efferent arteriolar constriction as well as direct effects on sodium transport. The constrictor effect on efferent arterioles also is important in preventing reductions in GFR in circumstances associated with impaired renal perfusion. Therefore blockade of ANGII formation in circumstances such as renal artery stenosis may caused marked reductions in GFR. However, in many patients efferent arteriolar vasodilation caused by ANGII blockade may not lower GFR markedly because of other autoregulatory mechanisms that compensate by causing parallel reductions in afferent arteriolar resistance. In these individuals, chronic ACE inhibition may prove to be beneficial in slowing the progression of renal disease because a reduction in glomerular hydrostatic pressure may help to prevent glomerular damage.
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PMID:The renin-angiotensin system: renal actions and blood pressure regulation. 187 29

The discovery and clinical availability of ACE inhibitor drugs is a triumph of rational drug development and a land-mark in biochemical pharmacology and hypertension research. The clinical pharmacological properties and haemodynamics of the clinically available drugs, captopril and enalapril, are reviewed, as is their therapeutic efficacy in African patients with essential and renal hypertension and chronic congestive heart failure. ACE inhibitors act as balanced arteriolar vasodilators and venular dilators and do not excite a reflex tachycardia in contrast to other vasodilator drugs. Their efficacy is, at least in part, dependent on plasma renin activity, which is low in Blacks and in Africans. Consistent with this, is the poor response to ACE inhibitor monotherapy of essential hypertension in controlled studies in Africans. However, the compensatory neuroendocrine activation which occurs in malignant hypertension, renal failure and congestive heart failure and concurrent diuretic therapy appears to enhance the clinical response to ACE inhibitors in African patients.
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PMID:Angiotensin converting enzyme inhibitors in cardiovascular and renal disease in Africans: a review. 190 20

Physical exercise can increase urinary albumin excretion rate (UAER) in diabetic patients without microalbuminuria at rest (stage II diabetic nephropathy) or with baseline microalbuminuria (stage III diabetic nephropathy). The aim of this study was to compare the acute effects of captopril, an ACE inhibitor, and nifedipine, a calcium channel blocker, on exercise-induced microalbuminuria in hypertensive insulin-dependent (Type I) and non-insulin-dependent (Type II) diabetic patients with early stage nephropathy. Non-obese diabetic patients, 13 Type I (7 with stage II and 6 with stage III nephropathy) and 14 Type II (6 with stage II and 8 with stage III nephropathy), with hypertension, WHO stages I-II, underwent five submaximal cycloergometric tests: the first two in basal conditions, the other three after 24 hour administration of captopril (25 mg twice daily), placebo (1 tab twice daily) or nifedipine AR (20 mg twice daily) according to a randomised, double-blind design. Acute administration of both captopril and nifedipine was able to reduce exercise-induced microalbuminuria in hypertensive Type I and Type II diabetic patients regardless of the stage of their nephropathy. Captopril reduced systolic blood pressure less than nifedipine, in both Type I and Type II diabetics, but was more effective than nifedipine in blunting exercise-induced microalbuminuria, especially in Type I diabetics.
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PMID:Albuminuria induced by exercise in hypertensive type I and type II diabetic patients: a randomised, double-blind study on the effects of acute administration of captopril and nifedipine. 192 Mar 40

Latent diabetic nephropathy with no complication such as retinopaty and hypertension was treated with Alacepril, an ACE inhibitor. This study enrolled 10 patients with microalbuminuria ranging from 5 mg/day (5 mg/gCr) to 50 mg/day (30 mg/gCr). Histological changes due to diabetic nephropathy were confirmed by renal biopsy performed in 4 of 10 patients. All the patients were divided into 2 groups; 5 patients were given 25 mg of Alacepril for 6 months and the remaining 5 patients were employed as the control. As the results, the mean blood pressure was decreased from 92.7 +/- 9.0 mmHg to 87.3 +/- 11.3 mmHg in Alacepril group but these changes were not statistically significant. Microalbuminuria were significantly decreased from 17.33 +/- 7.82 mg/gCr to 10.43 +/- 4.14 mg/gCr during 6 months in the Alacepril group while in the control group, no significant changes were observed in blood pressure and microalbuminuria. Creatinine clearances were not significantly changed in both groups. These findings suggest that Alacepril is useful in improving microalbuminuria of latent diabetic nephropathy.
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PMID:[Treatment of latent diabetic nephropathy with ACE inhibitor alacepril]. 192 Sep 34


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