Drugs online research references
J Appl Physiol. 2000 May;88(5):1690-7.
Effect of captopril on skeletal muscle angiogenic growth factor responses to exercise.
Gavin TP, Spector DA, Wagner H, Breen EC, Wagner PD.
Department of Medicine, University of California San Diego, La Jolla, California 92093-0623, USA. tgavin
ucsd.edu
Acute exercise increases vascular endothelial growth factor (VEGF), transforming growth factor-beta(1) (TGF-beta(1)), and basic fibroblast growth factor (bFGF) mRNA levels in skeletal muscle, with the greatest increase in VEGF mRNA. VEGF functions via binding to the VEGF receptors Flk-1 and Flt-1. Captopril, an angiotensin-converting enzyme inhibitor, has been suggested to reduce the microvasculature in resting and exercising skeletal muscle. However, the molecular mechanisms responsible for this reduction have not been investigated. We hypothesized that this might occur via reduced VEGF, TGF-beta(1), bFGF, Flk-1, and Flt-1 gene expression at rest and after exercise. To investigate this, 10-wk-old female Wistar rats were placed into four groups (n = 6 each): 1) saline + rest; 2) saline + exercise; 3) 100 mg/kg ip captopril + rest; and 4) 100 mg/kg ip captopril + exercise. Exercise consisted of 1 h of running at 20 m/min on a 10 degrees incline. VEGF, TGF-beta(1), bFGF, Flk-1, and Flt-1 mRNA were analyzed from the left gastrocnemius by quantitative Northern blot. Exercise increased VEGF mRNA 4.8-fold, TGF-beta(1) mRNA 1.6-fold, and Flt-1 mRNA 1.7-fold but did not alter bFGF or Flk-1 mRNA measured 1 h after exercise. Captopril did not affect the rest or exercise levels of VEGF, TGF-beta(1), bFGF, and Flt-1 mRNA. Captopril did reduce Flk-1 mRNA 30-40%, independently of exercise. This is partially consistent with the suggestion that captopril may inhibit capillary growth.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10797131&dopt=Abstract
Cardiovasc Surg. 2000 Apr;8(3):192-7.
The effect of captopril on membrane bound enzymes in ischemia-reperfusion injury.
Isbir CS, Dogan R, Farsak B, Ayd1n M.
Department of Cardiovascular Surgery, Marmara University School of Medicine, Istanbul, Turkey.
There is substantial evidence that Na(+)K(+)/Mg(2+) ATPase and Ca(2+)/Mg(2+) ATPase enzymes would effect the membrane integrity. Forty guinea pig (n=10 in each group) hearts were studied in an isolated Krebs-Henseleit solution perfused Langendorff cardiac model. The first group was utilized as the control group. Group 2 hearts were arrested with captopril (200micromol/l) added St Thomas Hospital Cardioplegic Solution (STHCS). Group 3 animals were pretreated with oral captopril (0.3mg/kg/twice a day) for 10days and then arrested with STHCS. Group 4 hearts were again pretreated with oral captopril (0.3mg/kg/twice a day for 10days) arrested with STHCS and reperfused with captopril added Krebs-Henseleit solution (200micromol/l). Hearts were subjected to normothermic global ischemia for 90min and than were reperfused at 37 degrees C. When the treated groups were compared with control, best results were achived by group 4. The Na(+)K(+) and Ca(2+)/Mg(2+) ATPase levels increased from 466.38+/-5.99 to 564.13+/-7.77 and 884.69+/-9.13 to 1254.29+/-5.75 nmol Pi/mg/prot/h respectively (P<0.05). These results suggest that captopril protects the membrane integrity and thus played a role at the recovery of depressed membrane bound Na(+)K(+)/Mg(2+) ATPase and Ca(2+)/Mg(2+) ATPase activity and also in ischemia-reperfusion injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10799827&dopt=Abstract
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