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

---

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

Lisinopril is a new, long-acting, nonsulfhydryl angiotension-converting enzyme (ACE) inhibitor that is excreted unchanged by the kidney. The antihypertensive efficacy and safety profiles of lisinopril were assessed in 24 patients (15 men, 9 women; mean age 52.3 years; range 21-75 years) with hypertension associated with impaired renal function (glomerular filtration rate GFR 60 ml/min or less), in an open study of 12 weeks' duration. Previous antihypertensive drugs were discontinued at entry into the study. Lisinopril was given orally once daily; the starting dose was 2.5 mg in patients with a GFR of less than 30 ml/min, and 5 mg in all other patients. The dosage of lisinopril was titrated upward to 40 mg daily according to BP response. A diuretic could then be added if hypertension was inadequately controlled. Twenty-three patients completed the study. Mean sitting BP was reduced from 177 +/- 21.2/106 +/- 9.1 mm Hg (mean +/- SD) at entry to the study to 145 +/- 21.4/88 +/- 8.3 mm Hg after 12 weeks of treatment (p less than 0.001). The median dose of lisinopril used was 10 mg (range 2.5-40 mg) and only 4 patients had a diuretic added to the lisinopril. Overall GFR was unchanged during the study: mean baseline value was 37 +/- 16.4 ml/min (range 10-60 ml/min) at the beginning of the study and 40 +/- 21.0 ml/min at the end. As in a previous pharmacokinetic study in similar patients, a tendency toward drug accumulation was noted only in those patients with the most severe renal impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Lisinopril treatment of hypertension in patients with impaired renal function. 283 Nov 15

Lisinopril is a new, nonsulfhydryl angiotensin-converting enzyme inhibitor approved for the treatment of hypertension. After oral administration, 25-29 percent of the dose is absorbed intact; biotransformation is not required for pharmacological activity. Onset of action occurs one to two hours after administration, with effects still present 24 hours later. The major route of elimination is through renal excretion and an elimination half-life of 12.6 hours has been reported in normotensive individuals. In patients with impaired renal function (creatinine clearance less than or equal to 30 ml/min) a longer half-life and accumulation have been observed. Lisinopril 20-80 mg/d has been shown to be as effective as hydrochlorothiazide, nifedipine, and beta-blocking agents in the treatment of essential hypertension. Its efficacy in renovascular hypertension has also been demonstrated. In congestive heart failure (CHF) doses of 2.5-20 mg/d appear to provide hemodynamic effects comparable to those of captopril. Dizziness and cough have been the most frequently reported side effects; rash and proteinuria have also been reported in a small number of patients. Interactions with diuretics, potassium supplements, and possibly with nonsteroidal antiinflammatory agents may occur. Lisinopril appears to be similar in efficacy to other antihypertensive agents in the treatment of essential hypertension and to captopril in the treatment of CHF. Whether lisinopril is safer or more effective than captopril or enalapril in the treatment of hypertension or CHF requires further investigation. Prolonged duration of action of lisinopril allows once daily dosing, unlike captopril for which dosing is required every 8-12 hours or enalapril which may necessitate twice daily dosing.
...
PMID:Lisinopril: a new angiotensin-converting enzyme inhibitor. 283 26

The interaction of salt with hypertension-induced left ventricular hypertrophy and its reversal by inhibition of angiotensin converting enzyme were studied in salt sensitive and salt resistant Dahl rats. Eight-week-old rats were fed either a low or high salt diet for three weeks. The colonies were then further divided and either treated with lisinopril or given no treatment for 11 weeks. Untreated salt sensitive rats had higher blood pressures than salt resistant animals. Left ventricular weight and wall thickness in both untreated salt sensitive groups was higher than in the resistant groups. Therapy lowered blood pressures in all groups but those of the high salt group remained higher than the low salt group. Reduction of left ventricular weight and wall thickness took place in either strain only when salt intake was low. Right ventricular and atrial weights were largely unaffected either by salt intake or drug therapy. Plasma renin activity increased and aldosterone levels decreased with lisinopril therapy in all groups except the salt sensitive, high salt group where both remained unchanged at low levels. Lisinopril was effective in reducing blood pressure and left ventricular hypertrophy, but both effects were severely impaired by high salt intake. The major determinant of left ventricular hypertrophy appeared to be afterload, as shown by a good correlation between left ventricular mass and systolic blood pressure, but there was some indication of a possible independent hypertrophic action of salt.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Correlation of left ventricular hypertrophy and its regression by lisinopril with salt-induced hypertension. 284 21

Lisinopril, a long-acting angiotensin-converting enzyme inhibitor, is excreted unchanged by the kidney. To determine how reduced renal function affects the drug's antihypertensive efficacy and safety, we studied 26 patients with hypertension associated with impaired renal function, having glomerular filtration rates (GFRs) of 60 ml/minute or less. These patients were enrolled in an open trial of 12 weeks' duration. They were given single daily doses of lisinopril, starting with 2.5 mg in patients with a GFR of less than 30 ml/minute, and 5 mg in the other patients. The dose was titrated to a maximum of 40 mg daily according to the blood pressure response. A diuretic was then added if required. Mean sitting and standing blood pressures at four, eight, and 12 weeks of treatment were significantly reduced compared with pretreatment values. The median dose of lisinopril was 10 mg daily (range, 2.5 to 40 mg), and only four patients required the addition of a diuretic. The mean GFR was unchanged during the study (36 +/- 16.4 ml/minute at baseline, 39 +/- 20.8 ml/minute after 12 weeks of treatment). Twenty-five patients completed the study. The one patient withdrew because of nausea and vomiting due to reflux esophagitis, which was probably not drug-related. Another patient had transient angioneurotic edema and continued to receive lisinopril. No clinically significant hematologic or biochemical abnormalities were observed. Sixteen patients continued to receive lisinopril for one year. Blood pressure control and GFR were well maintained throughout. Thus, in a group of patients who are often difficult to treat, lisinopril provided highly effective blood pressure control and was generally well tolerated.
...
PMID:Lisinopril in the treatment of hypertensive patients with renal impairment. 284 84

The comparative effects of lisinopril, a third generation angiotensin converting enzyme (ACE) inhibitor, on components of the renin-angiotensin system were assessed in normal and in an animal model of diabetes-related hypertension, the streptozotocin-diabetic rat. Two weeks after injection of streptozotocin the mean systolic blood pressure of diabetic rats was elevated 11% above that of normal rats. This effect was prevented by daily injection of insulin. The mean serum ACE activity was elevated 71% above that of normal rats. Lisinopril reduced systolic blood pressure and inhibited serum ACE activity in both normal and diabetic rats in a dose-response fashion. In normal rats maximum inhibition of blood pressure occurred at a mean dose of 1.0 mg/kg and in the diabetic rat at a mean dose of 5.0 mg/kg. At a mean dose of 5 mg/kg, ACE was inhibited by 100 and 92% in normal and diabetic rats, respectively. Plasma renin activity (PRA) increased sharply in both groups of rats treated with the lower doses of lisinopril, only to decrease at the 5 mg/kg level. At 20 mg/kg, PRA continued to decline in normal animals, but not in diabetic rats. Formation of angiotensin II (Ang II) in both normal and diabetic rats was maximally inhibited at doses of 1.0 and 0.1 mg/kg of lisinopril, respectively without a significantly greater effect at the higher doses of the drug. In separate experiments the effects of chronic treatment with lisinopril at two dosage levels on various physiological parameters of streptozotocin-diabetic rats were compared with the effects of another hypotensive agent, hydralazine, an arteriolar vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effects of the angiotensin converting enzyme inhibitor, lisinopril, on normal and diabetic rats. 284 85

The antihypertensive efficacy and tolerability of lisinopril, a new long acting angiotensin converting enzyme inhibitor, and nifedipine, in a retard formulation, were compared in a randomized six month double-blind study, in 45 patients with essential hypertension. Lisinopril, 20 to 80 mg once daily and nifedipine retard, 20 to 40 mg twice daily, were equally effective in lowering blood pressure and controlling hypertension. There were however significantly more adverse effects (P less than 0.01) reported with nifedipine. No significant differences were observed between groups for laboratory values, although the lisinopril group showed a significant reduction in urinary protein excretion compared to baseline values. Lisinopril and nifedipine have equal efficacy in the treatment of essential hypertension but in this study lisinopril was better tolerated than nifedipine.
...
PMID:Lisinopril in essential hypertension: a six month comparative study with nifedipine. 285 52

The chemistry, pharmacology, pharmacokinetics, clinical use, adverse effects, and dosage of lisinopril are reviewed. Lisinopril, a new nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor, is absorbed in its active form. Like the other ACE inhibitors, it lowers peripheral vascular resistance, with a resultant decrease in blood pressure. Approximately 29% of lisinopril is absorbed after oral administration. No measurable metabolism occurs, and excretion is primarily renal. Accumulation of lisinopril occurs in patients with renal dysfunction; however, dosage adjustment is necessary only when the creatinine clearance is less than 30 mL/min. Lisinopril has been shown to be an effective antihypertensive agent at doses of 10 to 80 mg given once daily in patients with essential and secondary hypertension caused by renal artery stenosis. The effectiveness of lisinopril is comparable to that with diuretics, beta blockers, and calcium-channel antagonists. In patients who are unresponsive to maximal doses of lisinopril alone, addition of another antihypertensive agent may be beneficial. Limited information suggests that lisinopril may be comparable to captopril for the treatment of congestive heart failure. Adverse effects associated with lisinopril are relatively minor and are comparable to those associated with enalapril. Hematological abnormalities have not been reported with lisinopril. Class-related adverse effects include cough, azotemia, angioedema, hypotension, and hyperkalemia. Lisinopril appears to be comparable to other ACE inhibitors for the treatment of hypertension and may be as effective as its predecessors for the treatment of congestive heart failure. Further study is needed to better define a therapeutic niche for lisinopril.
...
PMID:Lisinopril: a nonsulfhydryl angiotensin-converting enzyme inhibitor. 285 60

We compared exercise responses in two groups of hypertensive patients treated with an angiotensin converting enzyme (ACE) inhibitor (lisinopril, 20-80 mg/day, n = 17) or a cardioselective beta-blocker (atenolol, 50-200 mg/day, n = 9). Measurements were made at rest and during exercise at 25 W (2.7 mets) and at 50 W (3.8 mets) on a bicycle ergometer (where mets is exercising oxygen consumption/resting oxygen consumption) after 4 weeks of placebo, and again after 12 weeks of drug administration. Both drugs reduced (P less than 0.05) mean arterial pressure. Atenolol caused significant decreases in the heart rate (approximately 25%) and cardiac output (approximately 26%; Defares CO2 rebreathing), and significant increases in total peripheral resistance (approximately 30%) and arteriovenous O2 content (approximately 20%). Lisinopril decreased (P less than 0.05) stroke volume. At the same exercise intensity systolic blood pressure, arteriovenous O2 and total peripheral resistance were lower (P less than 0.05) and the heart rate was higher (P less than 0.05) after lisinopril than after atenolol. After the treatment of hypertension with the ACE inhibitor the responses to exercise were less restrictive than those after treatment with the cardioselective beta-blocker.
...
PMID:Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients. 285 65

The antihypertensive and hormonal effects of a new ACE-inhibitor, lisinopril (MK-521), was studied in 11 patients with renal arterial stenosis (bilateral in 1). Oral doses exceeding 5 mg a day significantly reduced blood pressure (BP), the maximum fall occurring 6 h after taking the drug. At higher doses (20-80 mg/day) sustained antihypertensive effects persisted for 24 h. Lisinopril was equally effective in lowering supine and standing BP. When the drug was given stepwise in increasing doses, (5, 10, 20, 40, and in 5 cases 80 mg/day) the BP was successively normalized in 10 of 11 patients (supine BP less than 90 mmHg). 3 patients with low renin hypertension (LRH) responded less well to monotherapy on long-term treatment with lisinopril than the others. A significant increase in heart rate was observed, initially and after 1 month of treatment. After 5 days treatment with increasing doses the plasma concentrations of angiotensin II (AII) and aldosterone (Aldo) fell significantly to very low concentrations. However, on long term treatment (3 months) suppression of AII and Aldo did not always take place. A concomitant decrease in 24 h urinary aldosterone excretion occurred. No changes in renal function or other biochemical tests except for a slight increase in S-K were observed. There were no adverse side-effects. We conclude that lisinopril is an effective and safe medication for renovascular hypertension.
...
PMID:Antihypertensive and hormonal effects of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor in patients with renovascular hypertension. 303 98

The U.S. Food and Drug Administration designed the trough-to-peak ratio as an instrument for the evaluation of long-acting antihypertensive drugs, but the ratios are usually reported without accounting for interindividual variability. This study investigated how the trough-to-peak ratio would be affected by interindividual and intraindividual variability and by smoothing of the diurnal blood pressure profiles. The ambulatory blood pressure was recorded on placebo in 143 hypertensive patients (diastolic pressure on conventional measurement > 95 mm Hg). After 2 months, the recordings were repeated on 10 mg (n = 66) or 20 mg (n = 77) lisinopril given once daily between 7 and 11 PM. The baseline-adjusted trough-to-peak ratios were determined from diurnal blood pressure profiles with 1-hour precision. Lisinopril reduced (+/- SD) the 24-hour pressure by 16 +/- 17 mm Hg for systolic and 10 +/- 10 mm Hg for diastolic (P < .001). According to the usual approach, disregarding interindividual variability, the trough-to-peak ratio was 0.72 for systolic pressure and 0.67 for diastolic pressure. In the 143 patients the ratios were not normally distributed. They were the same on both lisinopril doses. When interindividual variability was accounted for, the median trough-to-peak ratio was 0.34 (P5 to P95 interval, -0.46 to 0.87) for systolic pressure and 0.26 (-0.44 to 0.84) for diastolic pressure. In 66 patients examined twice on 10 mg lisinopril at a median interval of 32 days, the trough-to-peak ratios were characterized by large intraindividual variability.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Dec
PMID:The trough-to-peak ratio as an instrument to evaluate antihypertensive drugs. The APTH Investigators. Ambulatory Blood Pressure and Treatment of Hypertension Trial. 749 Jan 53


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---