Drugs online research references
J Pharm Sci. 1989 Dec;78(12):995-8.
Intestinal absorption mechanism of dipeptide angiotensin converting enzyme inhibitors of the lysyl-proline type: lisinopril and SQ 29,852.
Friedman DI, Amidon GL.
College of Pharmacy, University of Michigan, Ann Arbor 48109-1065.
The intestinal absorption mechanism of two nonsulfhydril lysyl-proline angiotensin converting enzyme (ACE) inhibitors, lisinopril (1) and SQ 29,852 (2; [(S)-1-[6-amino-2-[[hydroxy (4-phenylbutyl)-phosphinyl]oxy[-1-oxohexyl]-L-proline) were investigated in rats using a single-pass perfusion method. Compound 2 is well absorbed from rat jejunum, whereas lisinopril absorption is relatively low. The permeability of both ACE inhibitors is concentration dependent and is decreased by the dipeptide Tyr-Gly and by cephradine, indicating a nonpassive absorption mechanism via the peptide carrier-mediated transport system. Compound 2 is well absorbed by a nonpassive mechanism, in parallel with a small passive component. The estimated dimensionless carrier parameters for 2 are J*max = 0.16, Km = 0.08 mM, P*c = 2.0, and P*m = 0.25; for lisinopril, passive absorption is not significant and its absorption is nonpassive: J*max = 0.032, Km = 0.082 mM, and P*c = 0.39 (where J*max is the maximal flux, Km is the Michaelis constant, P*c is the carrier permeability, and P*m is the passive permeability). These results offer a mechanistic explanation for the prolonged ACE inhibition and the low oral bioavailability of lisinopril, and for the nonlinear pharmacokinetics of 2.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2559191&dopt=Abstract
Cas Lek Cesk. 1993 Dec 6;132(23):709-14.
[Lisinopril in the monotherapy of patients with essential hypertension: the effect of therapy on glucose and lipid metabolism]
[Article in Slovak]
Gajdos M, Spustova V, Dzurik R.
Oddelenie Klinickej Farmakologie Ustavu Preventivnej a Klinickej Mediciny, Bratislava.
Twenty patients with mild or medium severe essential hypertension were treated with lisinopril (Prinivil), 20 or 40 mg resp. by the oral route per day. After six weeks of treatment the mean values of systolic pressure declined from 169 +/- 4.38 mm Hg to 149 +/- 3.96 mm Hg and the diastolic pressure from 108 +/- 0.99 mm Hg to 91 +/- 1.77 mm Hg. The differences were statistically significant. In 40% of the patients it was necessary to increase the daily dose of lisinopril to 40 mg. When this was used, the mean values of systolic pressure declined to 140 +/- 3.18 mm Hg and those of diastolic pressure declined to 85 +/- 1.43 mm Hg during the subsequent six weeks. The blood pressure of all investigated patients was within the range of reference values. The authors recorded a positive effect on the glucose metabolism in particular in patients with impaired glucose tolerance. The mean blood sugar levels during the second hour following glucose administration during the oGTT declined from 9.81 +/- 0.54 mmol/l before treatment to 7.28 +/- 0.79 mmol/l after 12 weeks of lisinopril treatment. The values of immunoreactive insulin after the mentioned intervals declined from 82.49 +/- 5.6 to 34.94 +/- 8.37 microM/ml. The investigated parameters of the lipid spectrum did not change after 12 weeks of treatment. The authors did not observe any marked side-effects of treatment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8293440&dopt=Abstract
Am J Kidney Dis. 1988 Jun;11(6):499-507.
Effect of lisinopril monotherapy on renal hemodynamics.
Reams GP, Bauer JH.
Department of Medicine, University of Missouri School of Medicine, Columbia.
Nineteen essential hypertensive patients were entered into a protocol to assess the BP, humoral and renal effects of the angiotensin converting enzyme inhibitor, lisinopril (MK 521, 20 to 80 mg once daily), administered for 52 weeks. Specifically monitored prior to, and following 12 and 52 weeks of lisinopril monotherapy were plasma renin activity and plasma aldosterone, the clearances of creatinine, inulin and para-aminohippurate, and the 24-hour urinary excretion of protein. BP was well controlled. Plasma renin activity was stimulated, and plasma aldosterone was suppressed throughout the entire protocol. In contrast to the reported short-term and long-term renal effects of enalapril, lisinopril (a lysine analog of enalapril) had no short-term effect on renal function: glomerular filtration rate, effective renal plasma flow, filtration fraction (FF), renal vascular resistance (RVR), and protein excretion were all unchanged. However, following long-term therapy, both FF and RVR were decreased. Lisinopril appears to convey no specific renal pharmacological benefit.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2837083&dopt=Abstract
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