Drugs online research references
Insect Biochem Mol Biol. 2001 Jan;31(1):87-95.
In vitro degradation of the Neb-Trypsin modulating oostatic factor (Neb-TMOF) in gut luminal content and hemolymph of the grey fleshfly, Neobellieria bullata.
Zhu W, Vandingenen A, Huybrechts R, Baggerman G, De Loof A, P Poulos C, Velentza A, Breuer M.
Zoological Institute, Katholieke Universiteit Leuven, B-3000, Leuven, Belgium.
The unblocked hexapeptidic Trypsin Modulating Oostatic Factor of the fleshfly, an inhibitor of both trypsin and ecdysone biosynthesis, resists very well proteolytic breakdown by enzymes present in the lumen of the gut of previtellogenic fleshflies. However, when incubated in hemolymph of adult flies, females and males, its half-life time is a mere 0.5 min. In hemolymph of last instar larvae, this value increases to about 1.5 min. Whereas PMSF, a potent inhibitor of serine proteases has no effect, captopril and lisinopril, both known to be specific inhibitors of mammalian angiotensin I converting enzyme (ACE), effectively inhibit TMOF breakdown in fly hemolymph. Digestion of Neb-TMOF by recombinant Drosophila AnCE on itself results in identical degradation products as with total hemolymph. In both cases ESI-Qq-oa-Tof mass spectrometry demonstrated the appearance of peptide fragments with the sequences NPTN, LH and NP. These observations not only confirm the reported presence of circulating ACE-like activity in flies but also strongly suggest that in flies this hemolymph ACE-like activity might be involved in the regulation of the oostatic activity as exerted by Neb-TMOF.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11102838&dopt=Abstract
rug.ac.be
Capillary electrophoretic separation of eight inhibitors of the angiotensin-converting enzyme, viz., enalapril, lisinopril, quinapril, fosinopril, perindopril, ramipril, benazepril and cilazapril, was investigated with respect to the following parameters: pH of the running buffer, organic modifiers and surfactants. The most critical parameter is the pH of the running buffer. The addition of sodium dodecyl sulfate had a negative influence on the peak symmetry, and selectivity was not improved. The separation of the eight compounds can be performed by means of two phosphate buffers (each 100 mM) at pH 7.0 and pH 6.25, respectively. This combination is necessary for the selective identification of structurally related substances because of their similar pKa values.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11105846&dopt=Abstract
J Mol Cell Cardiol. 2000 Dec;32(12):2239-47.
Angiotensin II type 1 receptor blockade abolishes specific K(ATP)channel gene expression in rats with myocardial ischemia.
Akao M, Sakurai T, Horie M, Otani H, Takano M, Kouchi I, Murakami T, Sasayama S.
Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan.
The cardiac ATP-sensitive potassium (K(ATP)) channel is potentially composed of an inward rectifier potassium channel (Kir6.1 and/or Kir6.2) subunit and the cardiac type of sulfonylurea receptor (SUR2A). We reported that cardiac Kir6.1 mRNA and protein are specifically upregulated in the non-ischemic as well as the ischemic regions in rats with myocardial ischemia, suggesting that humoral and/or hemodynamic factors are responsible for this regulation. In the present study, pretreatment with TCV-116, an angiotensin (Ang) II type 1 receptor antagonist, completely inhibited the upregulation of Kir6.1 mRNA and protein expression in both regions of rat hearts subjected to 60 min of coronary artery occlusion followed by 24 h of reperfusion; whereas pretreatment with lisinopril, an Ang converting enzyme (ACE) inhibitor, partly inhibited this upregulation. Except for rats pretreated with TCV-116, Kir6.1 mRNA levels were positively correlated with those for brain natriuretic peptide (BNP), a molecular indicator of regional wall stress, in both the non-ischemic and the ischemic regions. Plasma Ang II levels were not elevated in rats with control myocardial ischemia compared with sham rats. Thus, the stress-related induction of cardiac Kir6.1 mRNA and protein expression under myocardial ischemia is inhibited by pretreatment with an AT1 antagonist, but also in part by an ACE inhibitor, suggesting that activation of local renin-angiotensin system may play a role. Copyright 2000 Academic Press.
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