Drugs online research references
Peptides. 1989 Mar-Apr;10(2):431-4.
Angiotensin converting enzyme: substrate inhibition.
Schullek JR, Wilson IB.
Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309-0215.
Phosphate, borate, and Tris inhibit angiotensin converting enzyme (ACE), but HEPES buffer is inert. Measurements of substrate inhibition were made in HEPES buffer at pH 7.0 and 25 degrees C and 37 degrees C. Substrate inhibition was marked and goes to completion. A new equation for substrate inhibitions enables one, under favorable circumstances, to determine whether there is cooperativity in the binding of substrate to the inhibitory and active sites. Cooperativity does occur with ACE using Hipp-His-Leu as substrate. The kinetic parameters were measured (Km = 0.21 mM, K* = 0.65 mM at 37 degrees C). The enzyme concentration (1.94 X 10(-8) M) was determined by titration with lisinopril so that kcat (5 X 10(3) at 37 degrees C) could be determined. Using this value and the molecular weight the specific activity of ACE was calculated for different common buffers. The specific activity in HEPES calculated from Vmax was 33.7 units/mg at 37 degrees C.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2547207&dopt=Abstract
J Hum Hypertens. 1989 Jun;3 Suppl 1:57-62.
Angiotensin-converting enzyme inhibition and compliance of the carotid artery in normotensive and hypertensive rats.
Levy BI, Benessiano J, Poitevin P, Safar ME.
INSERM Unit 141, Hopital Lariboisiere, Paris, France.
To investigate the effects of local application of an angiotensin-converting enzyme inhibitor on the mechanical properties of the arterial wall, the volume/pressure relationship (from 25 to 175 mmHg) in the in vivo isolated carotid artery was measured in normotensive (WKY) and spontaneously hypertensive rats (SHR). The compliance of the carotid artery (CC) was calculated, for each level of pressure, as the slope of the the volume/pressure curve. The carotid artery was less compliant in the SHR strain than in normotensive rats. This rigidity was partly related to an increased tone of the arterial smooth muscle in SHR compared with the WKY. Local incubation with lisinopril (2.3 micrograms/ml) produced a significant increase in the compliance of the carotid artery in both normotensive and hypertensive rats; CC was increased by 23% in WKY rats and by 14% in SHR. Since the goal of antihypertensive treatment may be not only to reduce blood pressure (BP) but also to improve the mechanical properties of the arterial system, the direct effect of lisinopril on the arterial wall may have a major beneficial role.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2550645&dopt=Abstract
Am J Hypertens. 1988 Jul;1(3 Pt 3):214S-216S.
Angiotensin converting enzyme inhibitors. Disparities in the mechanism of their antihypertensive effect.
Garavaglia GE, Messerli FH, Nunez BD, Schmieder RE, Frohlich ED.
Department of Internal Medicine, Ochsner Clinic, New Orleans, LA 70121.
Systemic and renal hemodynamics were studied by invasive and noninvasive techniques in 30 patients with mild to moderate essential hypertension before and after antihypertensive therapy with captopril (12 patients), enalapril (8 patients), and lisinopril (10 patients). All three angiotensin-converting enzyme (ACE) inhibitors reduced arterial pressure to about the same extent: captopril by 14%, enalapril by 18%, and lisinopril by 13%. However, lisinopril produced a significant fall (14%, P less than 0.001) in cardiac output that was not seen with captopril or enalapril therapy. Moreover, lisinopril elicited an increase in renal blood flow (22%, P less than 0.05) that was more marked than that with enalapril (12%) or captopril (4%). Although left ventricular mass was reduced (P less than 0.05) with all three agents, enalapril induced a twofold greater reduction (29%) than captopril (14%) or lisinopril (12%). These findings suggest that systemic and renal hemodynamic effects may be drug specific and not uniform for all ACE inhibitors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2843195&dopt=Abstract
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