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

Enalapril maleate is an orally active angiotensin-converting enzyme inhibitor. It lowers peripheral vascular resistance without causing an increase in heart rate. Enalapril 10 to 40 mg/day administered either once or twice daily is effective in lowering blood pressure in all grades of essential and renovascular hypertension, and shows similar efficacy to usual therapeutic dosages of hydrochlorothiazide, beta-blockers (propranolol, atenolol and metoprolol) and captopril. Most patients achieve adequate blood pressure control on enalapril alone or with hydrochlorothiazide. In patients with severe congestive heart failure resistant to conventional therapy, enalapril improves cardiac performance by a reduction in both preload and afterload, and improves clinical status long term. Enalapril appears to be well tolerated, with few serious adverse effects being reported. It does not induce the bradycardia associated with beta-blockers or the adverse effects of diuretics on some laboratory values. In fact, the hypokalaemic effect of hydrochlorothiazide is attenuated by the addition of enalapril. The incidence of the main (but rare) side effects of hypotension in hypovolaemic patients and reduced renal function in certain patients with renovascular hypertension, which are also seen with captopril, might be reduced by careful dosage titration, discontinuation of diuretics, and monitoring of at-risk patients. Thus, enalapril is a particularly worthwhile addition to the antihypertensive armamentarium, as an alternative for treatment of all grades of essential and renovascular hypertension. It also shows promise in the treatment of congestive heart failure.
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PMID:Enalapril. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension and congestive heart failure. 301 86

Enalapril, a potent long-acting angiotensin-converting enzyme inhibitor, was prescribed either alone (n = 9) or in combination (n = 20) with hydrochlorothiazide for 96 weeks in essential hypertensive subjects. Blood pressure was well controlled following both monotherapy or combination therapy. Plasma renin activity was stimulated in all subjects; plasma aldosterone concentration was stimulated only in subjects receiving combination therapy. Glomerular filtration rate (assessed by inulin clearance) was unchanged in subjects with initial clearances greater than 80 ml/min/1.73 m2 but was significantly improved (55%) following either form of therapy in subjects with initial clearances less than or equal to 80 ml/min/1.73 m2. Neither monotherapy nor combination therapy adversely affected 24-hour urinary protein excretion, sodium excretion, or body fluid composition. These results suggest that enalapril, either alone or in combination with hydrochlorothiazide, is effective therapy for mild to moderate hypertension. There are no adverse effect on renal function; indeed, enalapril has the capability of improving renal function in those subjects whose renal function was initially impaired from long-standing hypertension.
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PMID:Long-term effects of enalapril monotherapy and enalapril/hydrochlorothiazide combination therapy on blood pressure, renal function, and body fluid composition. 301 81

Thirty-nine general practice patients with mild to moderate essential hypertension were treated with enalapril 10 to 40 mg once daily alone or in combination with hydrochlorothiazide 12.5 to 25 mg once daily for 20 weeks. Eighty-one percent of patients responded with a satisfactory reduction in supine diastolic blood pressure, and 58% became normotensive. No serious adverse clinical or laboratory effects were noted. Enalapril alone or in combination with low dose diuretic administered once daily was an effective alternative regimen for mild to moderate hypertension.
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PMID:Once daily enalapril in general practice patients with mild to moderate essential hypertension. 301 21

Sixteen patients with an established diagnosis of renovascular hypertension were entered in an open study of enalapril (MK421), an oral angiotensin-converting enzyme (ACE) inhibitor, for treatment of their hypertension. Initial blood pressure was 178.9 +/- 6.3/106.2 +/- 3.1 mm Hg during conventional therapy on a median of 3 different antihypertensive agents. All antihypertensive therapy was ceased and the patients admitted to hospital. Following introduction of enalapril, blood pressure fell to 161.5 +/- 6.9/90.6 +/- 4.1 mm Hg at 24 h (p less than 0.01 systolic and diastolic). Blood pressure control (diastolic blood pressure, phase V, less than 95 mm Hg) was achieved with monotherapy in 7 patients and in a further 5 patients with addition of a diuretic. Renal function was compromised in 4 patients, requiring cessation of enalapril in 2 instances. Enalapril is an oral ACE inhibitor useful in the treatment of renovascular hypertension. Close monitoring of renal function is necessary during the introduction of enalapril therapy in patients with renovascular hypertension.
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PMID:Renovascular hypertension: treatment with the oral angiotensin-converting enzyme inhibitor enalapril. 301 7

This prospective, double-blind, multicenter study compared enalapril plus hydrochlorothiazide with standard triple therapy (STT; hydrochlorothiazide, timolol, and hydralazine) with regard to safety, tolerability, antihypertensive efficacy, and effect on renal function in 75 patients with documented renovascular hypertension. Both groups showed a significant mean decrease in systolic and diastolic blood pressure during the double-blind study, with the enalapril group showing a mean 12 mm greater decrease in systolic blood pressure as compared to STT (less than 0.05). Effective treatment of diastolic hypertension was noted in 96% of the enalapril group as compared to 82% on STT (p less than 0.05). STT failure was seen exclusively in patients with bilateral renal artery stenosis of high grade and frequently in association with impaired renal function. cPAH, a measure of effective renal plasma flow, showed a significant increase in the enalapril group, as compared to the STT (p less than 0.05). In contrast, there was a bimodal response of CIn (GFR): 80% of patients in the enalapril group showed no significant change while 20% (10 patients) showed a mean decrease of 28% along with a 12% increase in CPAH (p less than 0.01). No acute renal failure or toxic side effects were noted in the enalapril group. Enalapril plus hydrochlorothiazide is very effective in treating renovascular hypertension and is without significant toxic side effects. The self-limited increase in serum creatinine seen in 20% of renovascular hypertensive patients receiving enalapril and hydrochlorothiazide may identify a subset of patients with unilateral or bilateral high grade renal artery stenosis who should be treated with angioplasty or operative intervention.
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PMID:A comparison of enalapril plus hydrochlorothiazide with standard triple therapy in renovascular hypertension. 301 2

Enalapril is a new angiotensin converting enzyme inhibitor which, when absorbed by the digestive tract, is converted to enalaprilat. This metabolite is, in fact, the active form of enalapril. Its duration of action is sufficiently long so that enalapril can be administered in a single daily dose. Enalapril has been proved to be a highly effective therapeutic agent which is well tolerated by patients with arterial hypertension or severe congestive heart failure.
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PMID:Clinical pharmacology of the angiotensin converting enzyme inhibitor, enalapril. 302 10

Although it has been recognized that enalapril lowers blood pressure by reducing the total peripheral vascular resistance, its direct effect on blood vessels is largely unknown. Little information is available about the influence of enalapril on the different vascular regions. Ten patients with moderate essential hypertension were treated with enalapril 20 mg daily in a double-blind, placebo controlled cross-over study for six weeks during each period. Blood pressure and heart rate were measured in supine, sitting and standing position. Venous capacity was derived from pressure volume curves plotted simultaneously at forearm and calf. Arterial blood flow at rest and during reactive hyperemia was measured at calf and finger by plethysmography. Enalapril increases venous capacity in upper and lower limbs in patients with moderate essential hypertension. Also, there is vasodilation of calf and finger arteries both at rest and during reactive hyperemia. Finger and calf arteries contribute to the decrease of the total peripheral vascular resistance during treatment with enalapril; thus, ACE inhibition is capable of correcting the increased peripheral resistance which often is the main cause of arterial hypertension.
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PMID:Vasodilator effects of enalapril in patients with arterial hypertension. 302 12

The purpose of this study was to define the effect of the angiotensin-converting enzyme inhibitor, enalapril maleate, on blood pressure, renal function, protein excretion, and potassium homeostasis in patients with hypertension associated with moderate to severe renal dysfunction. Nine patients, having an initial inulin clearance between 9 and 48 mL/min/1.73 m2, were treated with enalapril monotherapy (n = 6) or enalapril/furosemide (n = 3) combination therapy. Systolic and diastolic blood pressures were well controlled. Supine plasma renin activity was stimulated; the supine plasma aldosterone level was suppressed, with a resultant increase in the serum potassium level. Clinical hyperkalemia was not observed. Glomerular filtration rate, assessed by inulin and creatinine clearances, was not significantly changed. Effective renal plasma flow, assessed by paraaminohippurate clearance was significantly increased, with a resultant decrease in filtration fraction. Importantly, urinary protein excretion was markedly reduced. These results suggest that enalapril therapy produces efferent arteriolar dilitation with preservation of the glomerular filtration rate. Enalapril therapy may also blunt the effects of angiotensin II on transglomerular passage of protein, as demonstrated by reduced proteinuria. These findings suggest that interruption of the renin-angiotensin system in patients with preexisting renal disease may have renal protective effects.
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PMID:Effect of enalapril in subjects with hypertension associated with moderate to severe renal dysfunction. 302 60

Teprotide, a nonapeptide isolated from the venom of a Brazilian pit viper, Bothrops jararaca, was the first angiotensin converting enzyme (ACE) inhibitor to be discovered and tested. It was found to be an effective, non-toxic antihypertensive agent as well as an afterload-reducing agent for patients with congestive heart failure (CHF). The primary activity of teprotide resulted from blockade of the angiotensin I converting enzyme--the pivotal step in the renin-angiotensin-aldosterone system (RAAS), and consequent reductions in angiotensin II levels. There was limited clinical testing for teprotide because of: its scarcity; the need for parenteral administration; and the subsequent discovery and synthesis of captopril, the first orally active angiotensin converting enzyme inhibitor. Captopril is the prototype oral angiotensin converting enzyme inhibitor and has been extensively studied since the initiation of formal studies in 1976. Perhaps one of the most closely researched drugs in modern times, the experience with captopril now includes more than 12,000 patients studied in formalized trials and over 4,000,000 patients treated world-wide by physicians for hypertension and congestive heart failure. Enalapril (MK421) is the first of what appears to be a growing number of analogues which are structurally and pharmacodynamically different from captopril; yet, they possess the same capacity for inhibiting the activity of angiotensin converting enzyme. The side effect profile of enalapril (and presumably future) angiotensin converting enzyme inhibitors appears to be similar to captopril, though clearly more experience is needed with newer agents. The initial use of captopril was troubled by a relatively high incidence of side effects which will form the focus of this discussion. Partially the result of incomplete pharmacokinetic information, captopril was administered in early studies at dosages now recognised to be far in excess of those necessary for drug action. In addition, dosages were given without regard for deficiencies of renal function, now known to be the main excretory route of captopril. The population of those patients studied frequently had chronic, treatment-resistant hypertension, often associated with concomitant end-organ disease (especially renal disease); and many additional factors further complicating the clinical setting, e.g. a relatively high incidence of collagen vascular disease and immunosuppressive treatments.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse reactions with angiotensin converting enzyme (ACE) inhibitors. 302 83

Enalapril was used to treat five patients with pulmonary arterial hypertension secondary to congenital cardiopathy, three with ventricular septal defect, one with arterial septal defect, and one with patent ductus arteriosus. The dose of enalapril was 20 mg/day. All patients underwent pretreatment and posttreatment cardiac catheterization. It was concluded that enalapril may be a useful drug in the treatment of pulmonary arterial hypertension secondary to congenital cardiopathy.
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PMID:Hemodynamic changes with enalapril in pulmonary arterial hypertension secondary to congenital heart disease. 302 17


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