Drugs online research references
Acta Diabetol. 2000;37(4):185-8.
The influence of the ACE inhibitor lisinopril on the glomerular metabolism of proteolytic enzymes in diabetic rats.
Koenen C, Lang C, Kempe HP, Werle E, Hasslacher C.
Department of Internal Medicine, St. Josef Hospital, Landhausstrasse 25, D-69115 Heidelberg, Germany.
Clinical studies indicate a nephro-protective effect in conjunction with the use of ACE inhibitors. This study's aim was to determine whether ACE inhibitors influence the metabolism of glomerular cells in addition to their known hemodynamic effects. Streptozotocin diabetic rats were treated with lisinopril (DLis 1.5 mg/l water), or hydralazine (Dhyd, 50 mg/l water) over 4 weeks. Untreated diabetic rats (DC) and non-diabetic rats (C) served as controls. After four weeks of treatment, urinary excretion of albumin, blood pressure and metabolic control (Glyc-Hb) were measured. After treatment glomeruli were isolated and homogenized, and beta-NAG and total proteolytic activity against azocasein were measured. Glycated hemoglobin levels were similar in all diabetic groups (DC, 12%, Dhyd, 10%; DLis 11%). Blood pressure of DLis rats (79 +/- 3 mmHg) and DHyd rats (46 +/- 2 mmHg) was lower than that of DC rats (111 +/- 3 mmHg). Urinary albumin excretion of diabetic groups was lowest in DLis. Diabetic rats showed a decrease in glomerular beta-NAG (10 vs. 60.5 U/g protein) and total proteolytic activity against azocasein (148 vs. 170 U/mg protein hour) compared to non-diabetic rats. Lisinopril increased beta-NAG (30 vs. 14 U/g protein) and total proteolytic activity (160.5 vs. 141.5 U/mg protein hour) compared with hydralazine. Our study confirms that the nephro-protective effect of ACE inhibitors is partially due to modulatory effects on the metabolism of basement membrane proteins.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11450501&dopt=Abstract
Jpn J Pharmacol. 2001 Jun;86(2):203-14.
Possible roles of cardiac chymase after myocardial infarction in hamster hearts.
Jin D, Takai S, Yamada M, Sakaguchi M, Yao Y, Miyazaki M.
Department of Pharmacology, Osaka Medical College, Takatsuki City, Japan.
The significance of cardiac chymase after myocardial infarction (MI) was evaluated using a hamster model of MI. At 1, 3, 7, 14, 28 and 56 days after MI, tissues were removed for measurements of angiotensin-converting enzyme (ACE) and chymase activities. The mean infarct size 3 days after left coronary artery ligation was 47.3 +/- 5.9% of the left ventricle circumference. The ratio of left ventricle weight to body weight was significantly increased from 3 days after MI. The level of plasma renin activity in the MI hamsters was significantly increased at the early phase of MI (1-3 days), while no significant changes in plasma ACE activity were observed. The ACE activity in the infarcted left ventricle was significantly increased starting from 3 days after MI and this increase was sustained up to 28 days. The chymase activity in the infarcted left ventricle was significantly increased starting from 1 day after MI and this increase was sustained up to 56 days. The number of chymase-positive mast cells in the infarcted left ventricle was significantly higher than in the sham group 3 and 7 days after operation. Treatment with an angiotensin (Ang) II type 1 receptor antagonist (candesartan cilexetil, 10 mg/kg per day) starting 3 days before the induction of MI significantly reduced the mortality rate during 14 days of observation following MI, whereas treatment with an ACE inhibitor (lisinopril, 20 mg/kg per day) did not. A significant improvement in hemodynamics (maximal negative and positive rates of pressure development, left ventricular systolic pressure and end-diastolic pressure, mean arterial blood pressure) was observed by the treatment with candesartan cilexetil, but not with lisinopril, 3 and 14 days after MI. These results suggested that Ang II produced by chymase may participate in the pathophysiologic state after MI in hamsters.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11459123&dopt=Abstract
Eur Heart J. 1992 Nov;13(11):1540-4.
Effectiveness of the antihypertensive action of lisinopril on left ventricular mass and diastolic filling.
Modena MG, Mattioli AV, Parato VM, Mattioli G.
Department of Cardiovascular Disease, University of Modena, Italy.
The effect of antihypertensive treatment with lisinopril (10 to 20 mg) on left ventricular mass and diastolic function was studied in 35 patients with mild to moderate hypertension. At baseline 6 and 12 months after treatment responders to lisinopril were examined by complete echo Doppler in order to measure left ventricular mass, diastolic and systolic function. Only 30 patients concluded the study follow-up. Lisinopril successfully reduced mean blood pressure (from 122 +/- 10 to 110 +/- 11 mmHg), without modification in heart rate, and left ventricular mass index (from 145 +/- 57 to 116 +/- 42 g.m-2) at month 6, with mild additional reduction at month 12. Isovolumic relaxation time was reduced but still abnormal at months 6 and 12, whereas deceleration time significantly changed only (from 230 +/- 40 to 195 +/- 35 msec) at month 12. Our results indicate that lisinopril is more successful in reducing left ventricular mass than in improving diastolic filling.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1334466&dopt=Abstract
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