Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
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PMID:Correlation of left ventricular hypertrophy and its regression by lisinopril with salt-induced hypertension. 284 21

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)
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PMID:Effects of the angiotensin converting enzyme inhibitor, lisinopril, on normal and diabetic rats. 284 85

1. Lisinopril, a new orally active angiotensin converting enzyme inhibitor, was given to eight patients with stable chronic renal failure, in a dose of 5 mg 24 h-1 for 1 week. Creatinine clearance of the subjects ranged from 0.22 to 1.11 ml s-1. Lisinopril pharmacokinetics were studied over 8 days. 2. There was a close correlation between creatinine clearance and total 'area under the curve' over the 8 days of study (r = -0.88, P less than 0.05), and plateau lisinopril concentration and creatinine clearance (r = -0.77, P less than 0.05). 3. Serum angiotensin converting enzyme activity was inhibited in proportion to log serum lisinopril concentration (r = -0.99, P less than 0.001). Calculated IC50 was 47 ng lisinopril ml-1. from pooled data, with individual patients IC50 ranging from 20 to 70 ng lisinopril ml-1. 4. Creatinine clearance was unaltered by treatment. Serum potassium rose to over 5 mmol 1-1 in four patients, without adverse clinical effect.
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PMID:Lisinopril pharmacokinetics in chronic renal failure. 284 71

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.
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PMID:Lisinopril in essential hypertension: a six month comparative study with nifedipine. 285 52

The interactions of blood pressure, salt intake and angiotensin converting enzyme (ACE) inhibition were investigated in the Dahl salt-sensitive (DS) and salt-resistant (DR) strains of rats. Eight-week-old DS and DR (40 of each) were separately randomized to receive a low- (0.4% NaCl) or a high- (8% NaCl) salt diet for 3 weeks. Thereafter the rats were further separated randomly to receive the ACE inhibitor lisinopril (3-8 mg/kg per day) or no drug treatment for 11 weeks. In untreated DS rats blood pressure rose, paralleled by a higher left ventricular mass (ratio left ventricular weight/body weight) irrespective of salt intake. Lisinopril lowered blood pressure to normotensive levels in all groups except DS rats on a high-salt diet, despite doses of up to 100 mg/kg per day, although there was a significant fall in blood pressure. Lisinopril reduced left ventricular mass significantly on the low- but not on the high-salt diet. Plasma renin activity increased on lisinopril treatment in all groups except DS rats on the high-salt diet. Regression of an increased left ventricular mass by ACE inhibition seemed to be impaired by a high salt intake, even when blood pressure was lowered. Therefore, although for regression of left ventricular hypertrophy, reduction of afterload was the leading factor, this might be adversely affected by a high salt intake.
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PMID:Modulation of left ventricular hypertrophy by dietary salt and inhibition of angiotensin converting enzyme. 285 24

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.
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PMID:Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients. 285 65

The effects of orally administered captopril, enalapril and lisinopril on plasma concentrations of angiotensin converting enzyme (ACE), angiotensin II (ANGII) and renin (PRC) were studied over a period of 6 hours in 6 normal subjects. A further 4 subjects received intravenous enalapril and enalaprilic acid (enalaprilat). Captopril (25 mg) by mouth caused a fall in pANGII that reached a nadir 30 to 40 minutes after administration but an effect was hardly apparent after 6 hours. Enalapril (10 mg) by mouth had less marked effects on pACE and pANGII with a decline in levels first apparent 1 hour after administration and the lowest levels reached between 3 and 6 hours. Lisinopril (10 mg) produced a progressive fall in pACE and pANGII from 1 hour to reach the lowest values 6 hours after treatment. Intravenous enalaprilat (5 mg) produced an immediate sustained fall in both pACE and pANGII but intravenous enalapril (7 mg) had a biphasic inhibitory effect.
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PMID:Onset of action of captopril, enalapril, enalaprilic acid and lisinopril in normal man. 285 60

The angiotensin converting enzyme inhibitor, lisinopril, was studied in a cryo-injury model of chronic heart failure. This model is characterized by a progressive decrease in cardiac output starting six weeks after cryo-injury to a 30% decrease in cardiac output 10 weeks after injury. Although histological damage to the myocardial tissue, particularly in the epicardial area, was observed, no significant changes occurred in body weight, mean arterial blood pressure, heart rate or central venous pressure. Daily intraperitoneal injection of 3 mg/kg lisinopril was instituted starting four weeks after injury for a duration of six weeks. Lisinopril completely restored the cardiac output to normal values at the end of this six week period. Thus, converting enzyme inhibition appears to be an effective therapeutic agent in this model of chronic cardiac failure.
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PMID:Effects of lisinopril, a new angiotensin converting enzyme inhibitor in a cryo-injury model of chronic left ventricular failure. 301 31

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.
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PMID:Antihypertensive and hormonal effects of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor in patients with renovascular hypertension. 303 98

The effects of the angiotensin converting enzyme (ACE) inhibitor lisinopril on blood pressure, proteinuria and renal hemodynamics were evaluated in 13 patients with renal disease of different origin. A comparison was made with the effects of conventional antihypertensive therapy. Both drug regimens significantly lowered blood pressure, while only after 12 weeks of treatment with lisinopril, blood pressure was significantly lower than during conventional therapy. Lisinopril reduced proteinuria (by 61 +/- 40%), whereas conventional therapy had no significant effect on protein excretion. During the first eight weeks of treatment with lisinopril, there was a comparable degree of blood pressure reduction with both treatment regimens, whereas urinary protein loss was significantly less during ACE inhibition. There was only a nearly-significant positive correlation between the fall in proteinuria during lisinopril and the concomitant decrease in mean arterial pressure. Glomerular filtration rate decreased from 26.3 +/- 11.6 to 20.6 +/- 9.4 ml/min during treatment with lisinopril. This decrease was not correlated with the fall in proteinuria. A significant positive correlation existed between the fall in urinary protein excretion and both the decrease in overall renal vascular resistance, and the fall in filtration fraction. Although blood pressure lowering by itself could contribute to the antiproteinuric effect of lisinopril, our results suggest that this effect of ACE inhibition is also due to efferent (postglomerular) vasodilation. We conclude that the ACE inhibitor lisinopril effectively reduces blood pressure and proteinuria in renal disease. The latter effect is not only the result of a lower blood pressure, but is probably also due to a fall in intraglomerular capillary pressure.
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PMID:Reduction of proteinuria by angiotensin converting enzyme inhibition. 304 Oct 97


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