Drugs online research references
Biochem Pharmacol. 1994 Mar 29;47(7):1121-6.
Stability and in vitro absorption of captopril, enalapril and lisinopril across the rat intestine.
Zhou XH, Li Wan Po A.
Drug Delivery Research Group, School of Pharmacy, Queen's University of Belfast, U.K.
In vitro absorption of three angiotensin converting enzyme (ACE) inhibitors, captopril, enalapril and lisinopril, and their stabilities in aqueous buffer as well as their resistance to intestinal and dermal tissue homogenates were investigated. The results demonstrate that the spontaneous oxidation of captopril, enalapril and lisinopril followed first-order degradation kinetics in McIlvaine's citrate-phosphate buffer. The degradation rates for enalapril and lisinopril were much slower than that for captopril. With the former two ACE inhibitors, the first-order rate constants of breakdown in the presence of dermal homogenate were not significantly different from the control values. Intestinal homogenate increased the decomposition of both of these inhibitors when compared to the enzyme-free control systems. On the other hand, the first-order rates of disappearance of captopril in the presence of both dermal and intestinal homogenates were lower than in the enzyme-free system. The extent of reduction was proportional to the amount of homogenate added. This suggests that tissue homogenates prevent the oxidation of captopril to its disulphide dimer. Transport experiments show that the amounts of ACE inhibitors transferred from solution on the mucosal side increased linearly with incubation time over the 2 hr of study. The rates of transfer from the mucosal side to the serosal side had the following rank order: captopril > enalapril > lisinopril roughly in the ratio 1:1.13:1.27. Addition of harmaline caused a significant reduction in the transfer rate of captopril compared to the control system, which strongly suggests that captopril is transported by a sodium-dependent carrier-mediated process across intestinal tissue.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8161340&dopt=Abstract
Kidney Int. 1992 Jul;42(1):46-55.
Blood pressure-independent effect of angiotensin inhibition on vascular lesions of chronic renal failure.
Kakinuma Y, Kawamura T, Bills T, Yoshioka T, Ichikawa I, Fogo A.
Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee.
Previous studies in experimental models of progressive renal failure have shown that the capacity of antihypertensive drugs to protect glomeruli from sclerosis is often unpredictable from their effect on systemic blood pressure. The present study was undertaken to ascertain whether this systemic blood pressure-independent structure-preserving effect of antihypertensives, particularly angiotensin II converting enzyme inhibitors (ACEI), is confined to the glomerulus or not, as well as whether this effect is mediated via angiotensin II (Ang II). The following experimental drug regimens were used in the rat model of subtotal nephrectomy (sNPX): so-called triple therapy [TRX; a combination of reserpine 5 mg/liter drinking water (DW), hydralazine 80 mg/liter DW and hydrochlorothiazide 25 mg/liter DW], or ACEI (either captopril, CPL, 600 mg/liter DW, enalapril, ENL, 400 mg/liter DW or lisinopril, LSL, 200 mg/liter DW), or a novel Ang II receptor antagonist (Ang IIR, L-158,809, 20 mg/liter DW). These dosages were identified in pilot studies to be the minimum required to control systemic blood pressure in the early phase up to 12 weeks. In addition, a separate group was treated with a higher dose of L-158,809 (80 mg/liter DW) with equipotent systemic pressor effect. Treatment was initiated eight weeks after subtotal nephrectomy following renal biopsy, and animals were sacrificed at 16 weeks. In ACEI treated rats, carotid arterial wall thickening (WT), defined as ratio of media thickening to radius of outer vessel wall, was similar to normal age-matched control (0.073 in all ACEI treated rats, vs. 0.074 in normal control) and significantly less than with TRX (ratio 0.118) or untreated sNPX (0.130). Even more remarkably, coronary arteriole WT in ACEI-treated rats averaged 0.139, a value less than one half and one third of TRX (0.298) and untreated sNPX control (0.388), respectively. Similar results were obtained for mesenteric artery WT. These findings were closely paralleled by changes of glomerular sclerosis. In untreated sNPX control rats, glomerular sclerosis increased from biopsy to autopsy specimens by an average of 458%. Although TRX dampened the degree of increase in sclerosis to on average 212%, this protective effect was far less than that achieved by ACEI. In the latter, sclerosis increased on average only 65% from biopsy to autopsy. Although all ACEIs were more effective than TRX, captopril and lisinopril groups showed greatest benefit at these doses. Ang IIR also protected renal and extrarenal structures with 34% increase of sclerosis index in low dose and WT 0.088, 0.117 and 0.112, respectively in carotid, mesenteric and coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1635354&dopt=Abstract
Am J Med. 1988 Sep 23;85(3B):38-43.
Antihypertensive and renal effects of lisinopril in older patients with hypertension.
Laher MS, Donohoe JF, Kelly JG, Doyle GD.
Department of Medicine and Pathology, James Connolly Hospital, Dublin, Ireland.
The antihypertensive efficacy and safety of lisinopril were assessed in 60 older patients with a mean age of 75 years (range, 65 to 85 years) in a 12-week open study. Mean ( +/- SEM) blood pressure while sitting was reduced from 190/106 +/- 3.3/1.8 mm Hg at entry to 162/89 +/- 3.2/1.6 mm Hg after 12 weeks of treatment (p less than 0.001). There was no significant alteration in heart rate, and postural hypotension did not occur. Mean glomerular filtration rate at entry was 61.6 +/- 3.4 ml/minute and was unchanged after 12 weeks of therapy at 62.2 +/- 3.0 ml/minute. Fourteen patients continued to receive lisinopril for a period of one year. Blood pressure remained controlled throughout and heart rate remained unchanged. There was a significant reduction in mean arterial pressure from 128.8 +/- 1.9 mm Hg to 105.1 +/- 1.5 mm Hg (p less than 0.001). Biochemical parameters remained unaltered. There was a significant increase in renal blood flow (p less than 0.025) and a corresponding reduction in renovascular resistance (p less than 0.001) following long-term therapy with lisinopril. Thus, lisinopril was generally well-tolerated and highly effective in lowering blood pressure in older hypertensive patients, whereas at the same time renal function was not adversely changed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2844086&dopt=Abstract
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