Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy and safety of the treatment of arterial hypertension with the ACE-inhibitor quinapril, were evaluated in a multicentre study conducted in Italy. The study, lasting 14 weeks, after a preliminary wash-out period, allowed response-based titration of quinapril dose from 10 mg to 40 mg once a day, with provision to combine additional hydrochlorothiazide (12.5 to 25 mg), in case of persistently high diastolic pressure levels. The efficacy sample included 1267 patients: at therapy week 14, 78.6% of patients were treated with quinapril alone. Global response rate (intent-to-treat) was 83.3%, with a mean reduction of diastolic pressure of 15.8 mmHg (95% confidence interval from 15.5 to 16.2 mmHg). 91 patients reported 126 associated adverse events (7.0%); the most frequently reported event was cough (2.7%). First-dose hypotension was rarely reported (1.3%), even in elderly and diabetic patients.
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PMID:[The Study Group of Quinapril in Arterial Hypertension. The Steering Committee]. 163 Jun 80

The Authors describe a clinical case of a patient affected by arterial hypertension of severe degree (IV grade OMS) that during therapy with ACE inhibitors and diuretics developed acute renal failure that reversed after stopping treatment. The clinical course was quite similar to acute renal failure induced by ACE inhibitors and diuretics in patient with bilateral renal artery stenosis. In interpreting the pathogenesis, the Authors suppose, beside a reductions of effective plasma flow, the coexistence of hyalinosis of renal arterioles. They underline the necessity of monitoring renal function at least in the first weeks of therapy when a treatment with ACE inhibitors and diuretics is started especially in patients with hypertension of high degree and/or reduced renal function.
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PMID:[Acute renal failure caused by treatment with diuretics and ACE inhibitors in the absence of renal artery stenosis]. 163 Jun 98

1. The two isozymes of human angiotensin converting enzyme (ACE; EC 3.4.15.1) have recently been cloned and sequenced. 2. The larger, endothelial isozyme has two highly similar internal domains each bearing a putative catalytic site. In contrast the smaller, testicular isozyme has a single catalytic site corresponding to the C-terminal domain of endothelial ACE and represents the ancestral, non-duplicated form of the gene. 3. Both isozymes are anchored in the plasma membrane by a single hydrophobic transmembrane polypeptide located near the C-terminus, and both are extensively N-glycosylated. 4. The testicular isozyme may also be O-glycosylated. 5. The soluble form of ACE in plasma, seminal fluid and other body fluids appears to be derived from the membrane-bound endothelial isozyme by a post-translational modification. 6. ACE has a complex substrate specificity with peptidyl tripeptidase or endopeptidase action on certain peptides, as well as the classical peptidyl dipeptidase activity. 7. Numerous potent inhibitors of the enzyme have been developed and used successfully in the treatment of hypertension, but some of the observed side effects may be due to inhibition of other zinc metalloenzymes. 8. Both endothelial and testicular ACE are highly conserved between species, indicative of the essential role(s) of the enzyme in blood pressure regulation and other physiological processes.
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PMID:Angiotensin converting enzyme: implications from molecular biology for its physiological functions. 165 Jul 17

With 30 years of experience, it is possible to claim that diuretics are well tolerated antihypertensive drugs producing a significant decrease in systolic and diastolic blood pressure as good as obtained with beta-blockers, converting enzyme inhibitors, calcium antagonists and centrally acting drugs. Recently diuretics have been criticised because of a substantial number of important side-effects, and are disregarded by some authors as first-line agents for the treatment of mild hypertension. Diuretics seem however safe in the majority of hypertensive patients who do not present special problems. Using low doses, which are equally effective, most toxic properties can probably be avoided. Combination therapy, especially with ACE inhibitors, has not only additional effects, but lowers also the potential adverse effects, caused by diuretics. We are convinced that diuretics are still important as first-line agents for the treatment of arterial hypertension in the general population.
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PMID:Diuretics in the treatment of hypertension. 166 46

367 patients with mild-moderate hypertension were included in a multicentre study for the purpose of examining the antihypertensive effect of six weeks of treatment with the ACE-inhibitor lisinopril 10 and 20 mg once daily. Both low-dose and high-dose lisinopril significantly reduced sitting and standing blood pressure values. The fall in blood pressure in the sitting position was slightly but significantly greater among the high-dose group compared with the low-dose group (a 3 mm Hg fall difference in systolic values and a 1 mm Hg fall in diastolic values). No such differences were found in the standing position. Heart rate remained unchanged during lisinopril treatment. Episodes of possible first dose hypotension were reported in six patients. Approximately 90% of the patients in both groups were classified as responders according to defined criteria. The frequency of side-effects was low, and was equal in both treatment groups. An evaluation of reduction in blood pressure, and of response rate and side-effects suggests that an initial dose of 10 mg lisinopril once daily is sufficient, and that this dosage will control blood pressure in the majority of patients.
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PMID:[Treatment of hypertension with the ACE inhibitor lisinopril. A multicenter study of patients with mild to moderate hypertension in general practice]. 165 75

We investigated the linkage between high blood pressure and the ACE gene in the F2 generation between SHRSP/Izm and WKY/Izm. The male F2 rats were categorized into 3 genotypes according to a microsatellite polymorphism in the ACE gene. Significantly high blood pressure was observed in the SHRSP homozygotes when it was compared to the blood pressure of the heterozygotes. Further, after 2 or 3 months salt-loading, the blood pressure was significantly higher in the SHRSP homozygotes than in the heterozygotes and the WKY homozygotes. The heterozygotes had a blood pressure similar to that in the WKY homozygotes, indicating that the effect of the ACE gene genotype was recessive. Salt appetite was neither correlated with the salt-sensitivity nor cosegregated with the ACE genotype. The results indicate that the locus of ACE gene associates with the development of hypertension, especially salt-sensitive hypertension.
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PMID:Blood pressure cosegregates with a microsatellite of angiotensin I converting enzyme (ACE) in F2 generation from a cross between original normotensive Wistar-Kyoto rat (WKY) and stroke-prone spontaneously hypertensive rat (SHRSP). 166 4

Ambulatory blood pressure and heart rate monitoring were used for comparing the antihypertensive effect of a 1-week treatment with enalapril and lisinopril 10 mg once daily (double-blind crossover placebo-controlled study). Twelve outpatients with mild to moderate hypertension were treated. Both drugs had a significant and identical hypotensive effect. Neither drug affected the diurnal rhythm of blood pressure or heart rate. Therefore the two drugs are equipotent antihypertensive agents. Both drugs inhibited ACE activity to a highly significant extent, but in this regard lisinopril was more effective than enalapril. However, lisinopril's greater ACE inhibition was not accompanied by a greater hypotensive effect. The clinical value of this difference is not yet established.
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PMID:Different hemodynamic (24-h ambulatory blood pressure monitoring) and renin-inhibiting effect of a 1-week treatment with enalapril and lisinopril. 166 62

The long-term oral administration of TA-6366 (5 mg/kg/day) from 4-weeks old impeded the genetic hypertension development with only a slight decrease in heart rate in spontaneously hypertensive rats (SHRs). However, the lower dose (1 mg/kg/day) of TA-6366 did not affect the development, but it lowered blood pressure after the development was almost accomplished. Concomitantly, relative heart weights in both the groups were markedly decreased to almost the same degree. The reduction of ACE activity in the aorta, brain and lung of both groups was found at 24 hr after the final administration, particularly at the 5 mg/kg/day dose; and that of the aorta was kept at almost the same low level even on the 9th day after withdrawal. After withdrawal of TA-6366 (5 mg/kg/day), the significant decrease in blood pressure was sustained at least for 10 weeks. The beneficial effect of TA-6366 on the hypertension development in SHRs seems to be related to its strong and long-lasting ACE inhibition, especially in the vasculature.
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PMID:Pharmacological studies on TA-6366, a new ACE inhibitor: II. Effect of long-term administration from the pre-hypertensive stage on blood pressure, relative heart weight and ACE activity of various tissues in spontaneously hypertensive rats (SHRs). 166 18

Therapeutic agents for the treatment of hypertension in the elderly are the well known basic antihypertensive drugs (Diuretics, beta-blocking agents, calcium antagonists and ACE-inhibitors). Choice is determined by concomittant diseases increasing with age. In the elderly patient the assessment of benefit and risk is particularly essential. Drugs should therefore not be installed without exact information of the patient and be started at the smallest possible dose. If tolerance is good the dose may be raised of prescription of an additional drug be evaluated cautiously.
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PMID:[Hypertension in the old age: how to treat it?]. 167 86

The three approaches (physiopathological, epidemiological and pharmacological) to the management of hypertension should converge to provide a personalized prescription of the most appropriate treatment to prevent and/or cure the cardiovascular complications of hypertension: hypertensive left ventricular hypertrophy and the risks directly related to it (haemodynamic, arrhythmic, ischaemic) may be corrected by certain antihypertensive agents (methyldopa, ACE inhibitors, some calcium antagonists) although there is no proof as yet of the benefits of this intervention (which could suppress the adaptation to the increased wall stress of the left ventricle); malignant hypertension and its cardiovascular complications have almost disappeared with modern antihypertensive therapy. Cardiac failure can be effectively prevented and cured when exclusively related to hypertension. When diastolic pressures are lowered by 8-10 mmHg cerebrovascular risk is reduced by a half and coronary risk by a quarter. Cardiovascular mortality related to hypertension is thus reduced by 20% and total mortality is thereby significantly decreased; the large scale clinical trials which provided these data were performed in the years 1965-1985 with diuretic therapy relayed by (or compared with) betablockers from 1980 onwards. These two families remain the drugs of reference in the prevention and treatment of the cardiovascular complications of hypertension. Personalized description of antihypertensive therapy should take into account the degree of risk and previous cardiovascular complications of the hypertensive patient: betablockers eventually associated with calcium antagonists are to be preferred in cases of hypertension with coronary artery disease and/or arrhythmias, severe hypertension and hypertension complicated by cardiac failure are good indications for ACE inhibitors without prejudicing other therapeutic options necessary in certain contexts, in particular aspirin therapy in patients with previous transient ischemic cerebral attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of hypertension and cardiovascular complications]. 168 21


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