Drugs online research references
Kidney Int Suppl. 1989 Nov;27:S154-62.
Effect of dietary protein intake and angiotensin converting enzyme inhibition in Heymann nephritis.
Kaysen GA, Davies RW, Hutchison FN.
Department of Medicine, Veteran's Administration Medical Center, Martinez, California.
The effect of diets containing 8.5%, 21% or 40% protein on growth, urinary albumin excretion and serum albumin concentration was determined in rats with Heymann nephritis and in non-nephrotic control animals. Urinary albumin excretion was greater in nephrotic rats with each increment in dietary protein intake, and serum albumin concentration tended to be least in nephrotic rats fed 40% protein. Albuminuria decreased spontaneously and serum albumin concentration increased in nephrotic rats fed 8.5% protein for 25 days. Enalapril treatment caused a further reduction in urinary albumin excretion and an increase in serum albumin concentration in nephrotic rats fed 8.5% protein. Albuminuria did not decrease nor did serum albumin concentration increase in nephrotic rats fed 40% protein without enalapril treatment, but enalapril caused a significant reduction in urinary albumin excretion and an increase in serum albumin concentration in nephrotic rats fed either 8.5% or 40% protein. The rate of growth in normal rats was greatest when they were fed 21% protein, compared to either 8.5% or 40% protein. Growth rate was significantly reduced in nephrotic rats, regardless of dietary protein intake and regardless of treatment with enalapril, but the 21% protein diet still induced the most rapid rate of growth. Growth rate was not significantly different in nephrotic rats fed either 40% or 8.5% protein. The difference in weight between pair fed nephrotic and control animals fed 21% protein was due to a decrease in carcass and skin weight in nephrotic animals. Carcass protein was significantly reduced in the nephrotic animals, and carcass saponafiable fat tended to be reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2561514&dopt=Abstract
J Cardiovasc Pharmacol. 1993 Aug;22(2):259-63.
Effect of enalapril on intracellular resistance and conduction velocity in rat ventricular muscle.
De Mello WC, Crespo MJ, Altieri P.
Department of Pharmacology, School of Medicine Medical Sciences Campus, San Juan, Puerto Rico 00936-5067.
The effect of enalapril on the intracellular resistance (ri) and conduction velocity was investigated in isolated rat trabeculae. The results indicated a decline in the internal resistance of 35.5% (SE +/- 3.3) and an increase in conduction velocity of 58.7% (SE +/- 6.6). The action potential duration was not altered, but the resting potential was increased by 10.5 mV (SE +/- 4.4). Enalaprilat had no effect on ri probably because the molecule is a diacid and does not cross the cell membrane. These findings indicate that the renin-angiotensin system is involved in the modulation of cell communication in cardiac muscle and that the beneficial effect of the drug in patients with congestive heart failure is, in part, related to an improvement of electrical synchronization of heart cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7692167&dopt=Abstract
Drug Metab Dispos. 1998 Apr;26(4):324-31.
Intracellular and not intraluminal esterolysis of enalapril in kidney. Studies with the single pass perfused nonfiltering rat kidney.
Sirianni GL, Pang KS.
Department of Pharmacology, University of Toronto, Ontario, Canada.
Two possible sites of renal metabolism exist: intracellular, by enzymes within the peritubular cells, and intraluminal, by ecto-enzymes embedded on the brush border membrane. The esterolysis of enalapril to its dicarboxylate metabolite, enalaprilat, was studied in the isolated perfused, nonfiltering rat kidney preparation (NFK) and compared with that observed for the isolated perfused rat kidney (IPK) to ascertain the site of metabolic conversion. For the NFK, filtration was obliterated with the high oncotic pressure (8% bovine serum albumin in plasma) and ligation of the ureter, thus preventing enalapril from reaching intraluminal sites by filtration. The steady-state renal plasma clearance of enalapril in the NFK was 2.0 ml/min/g, a value similar to that (2.1 ml/min/g) observed previously for the IPK. The rate of appearance of enalaprilat, the metabolite, in venous plasma for the NFK (30 +/- 3% of the input rate of enalapril) was also comparable with that for the IPK (27 +/- 4%). Further, identification of the site of enalapril metabolism (cellular or luminal) was aided by simulations based on physiological models and parameters obtained previously on the renal handling of enalapril and enalaprilat. These parameters were optimized to match closely the experimental observations. The predicted total and metabolic renal clearances for the IPK or for the NFK were similar for both the "cellular model" and "luminal model": in both instances, values for the NFK were 59-65% of those for the IPK. By contrast, predictions for the venous output rate of enalaprilat (as a percent of the input rate of enalapril) were different: the "cellular model" predicted no change in value between the NFK and the IPK, whereas metabolite appearance was greatly magnified for the NFK (289% that of the IPK) with luminal metabolism. The lack of difference in venous outflow of enalaprilat for the NFK and IPK was more congruent with the notion of intracellular and not intraluminal esterolysis of enalapril.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9531519&dopt=Abstract
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