Drugs online research references
Agric Biol Chem. 1991 Jul;55(7):1695-9.
Enzymatic properties of dipeptidyl carboxypeptidase from Bacillus pumilus.
Nagamori Y, Kusaka K, Fujishima N, Okada S.
Ezaki Glico Biochemical Research Laboratories, Osaka, Japan.
Enzymatic properties of dipeptidyl carboxypeptidase (DCP) from Bacillus pumilus were investigated. The enzyme was more active on tri- and tetrapeptides than angiotensin-converting enzyme (ACE) from rabbit lung. The presence of chloride ion is essential for the hydrolysis. The Km value of angiotensin I for the enzyme was 0.119 x 10(-3) M. The enzyme was not inhibited by the mammalian ACE inhibitors lisinopril and enalaprilat. The enzyme is readily inhibited by EDTA but restored by Co2+, Mn2+, and Zn2+. Therefore, it seems to be a zinc-metallo protease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1368711&dopt=Abstract
Can J Microbiol. 1990 Jan;36(1):56-9.
Determination of peptidyl dipeptidase activity in 24 bacterial species.
Stevens J, Fanburg BL, Lanzillo JJ.
Department of Medicine, New England Medical Center Hospital, Boston, MA 02111.
Of 24 bacterial species examined for lisinopril refractive peptidyl dipeptidase activity, only 8 contained activity. Activity in Pseudomonas maltophilia was more than fourfold higher than that of any other species. Pseudomonas maltophilia may be unique among bacteria in possessing high peptidyl dipeptidase activity that is both EDTA inhibitable and lisinopril resistant.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2185870&dopt=Abstract
Br J Pharmacol. 1994 Feb;111(2):555-60.
Increased arterial distensibility induced by the angiotensin-converting enzyme inhibitor, lisinopril, in normotensive rats.
Makki T, Talom RT, Niederhoffer N, Amin F, Tankosic P, Mertes PM, Atkinson J.
Laboratoire de Pharmacologie Cardio-vasculaire, Faculte de Pharmacie, Nancy, France.
1. We investigated possible structural correlates of the beneficial effect of chronic angiotensin-converting enzyme inhibition (ACEI) with lisinopril on the aortic distensibility of normotensive rats. 2. Experiments were performed in young (4-month old), normotensive, Wistar rats which received lisinopril in their drinking water (0.9 or 9 mg kg-1 day-1) for 9 months. 3. Following ACEI treatment, rats were pithed and aortic pulse wave velocity was measured during the progressive rise in mean arterial blood pressure produced by i.v. infusion of the alpha 1-adrenoceptor agonist, phenylephrine. The slope of the regression line relating aortic pulse wave velocity to mean arterial blood pressure was taken as an index of aortic distensibility. Following this, the aorta was fixed in situ at a normotensive pressure level and histomorphometry was performed. We also measured the calcium content of the aortic wall by atomic absorption. 4. The lower dose of lisinopril failed to lower systolic arterial blood pressure (unanaesthetized rat) or mean arterial blood pressure (pithed rat). Chronic ACEI with the higher dose of lisinopril lowered both systolic arterial blood pressure (104 +/- 6 mmHg, controls 133 +/- 4 mmHg, unanaesthetized), and mean arterial blood pressure (27 +/- 1 mmHg, controls 34 +/- 2 mmHg, pithed). 5. Although the lower dose of lisinopril did not lower blood pressure, it did improve aortic distensibility as revealed by a fall in the slope relating aortic pulse wave velocity (Y) to mean arterial blood pressure (X). Values were 5.7 +/- 0.7, 3.8 +/- 0.6 and 2.7 +/- 0.3 in controls, and in low and high ACEI groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8004398&dopt=Abstract
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