A microlarval development assay for the detection of anthelmintic resistance in sheep nematodes.
The inhibitory effects of calcium channel blockers; nifedipine and two new compounds, mebudipine and dibudipine, on contractions of isolated guinea-pig common bile duct were investigated. All the compounds tested induced a concentration-dependent reduction of the amplitude of contractile response to electrical stimulation and all the compounds displaced concentration-response curve of calcium chloride to the right in a concentration-dependent manner. The pIC50 values for these compounds acting on electrically stimulated common bile duct were calculated as: dibudipine: 8.50 +/- 0.17; mebudipine: 8.27 +/- 0.20; nifedipine: 7.96 +/- 0.07. The compounds also antagonized the contractile response of K+-depolarized guinea-pig common bile duct to cumulative concentration of calcium. However the inhibitory effect of these compounds were not significantly different.
In the case control studies a group given diuretics +/- other treatments (but not including one of the index drugs) provided a reference group with a relative risk (RR) of 1.0. In the matched case control study the adjusted RR for a CCB without a diuretic was 1.32 (95% CI 0.64-2.70) for IHD mortality and 1.05 (95% CI 0.60-1.84) for cardiovascular mortality. Similar results were observed for methyldopa, BBs and ACE inhibitors. The results in the unmatched case control analysis were also similar. The longitudinal study comparing all those treated for over 1 year with a CCB with all other treatments showed a RR for total mortality of 1.03 (95% CI 0.85-1.25). The longitudinal study of total mortality according to treatment initiated at 3-12 months found results of a similar magnitude for CCBs, methyldopa and BBs.
Despite affecting ocular and systemic perfusion parameters, exercise and smoking did not alter OPA, suggesting functional isolation, i.e. autoregulation of the choroidal and/or ophthalmic artery circulation in healthy volunteers. Low OPA in LTG was increased by nifedipine only in vasospastic LTG patients, suggesting different, vasotonus-related pathologies. Calcium channel blockers and other vasodilators may be useful in vasoreactive LTG patients with reduced OPA.
TXYF formula inhibits colon contraction in rats. This may be related to activation of specific potassium channels and inhibition of extracellular calcium internal flow.
A 1-year, prospective, open-label pilot study.
Adalat experimentally showed a pronounced dose-dependence of vasodilation and long-term aftereffects, which allows the CA to be regarded as the most attractive agent for the intraoperative preparation of an autoarterial shunt.
In our study, approximately every 5th older patient was prescribed at least one PIM. For the future an ongoing update of the Beers criteria to further include newer agents and an adaptation to the different situation in European countries is desirable.
A search of the literature was performed using MEDLINE (1966-September 2006), EMBASE Drugs and Pharmacology (1980-September 2006), and Current Contents/Clinical Medicine (week 24, 2005-week 30, 2006). Package inserts from lercanidipine, nifedipine, felodipine, and amlodipine were also reviewed for comparison of adverse effects.
Postovulatory aging induced morphological features characteristics of abortive SEA in a time-dependent manner in vivo as well as in vitro. The extracellular Ca(2+) increased rate of abortive SEA during initial period of culture, while co-addition of a nifedipine (L-type Ca(2+) channel blocker) protected against postovulatory aging-induced abortive SEA. However, CI induced morphological features characteristics of egg activation (EA) in a dose-dependent manner. As compare to control, an increase of cytosolic free Ca(2+) level (1.42 times) induced abortive SEA, while further increase of cytosolic free Ca(2+) level (2.55 times) induced EA.
Oligopeptides originating from ingested meal stimulate the secretion of various gastrointestinal hormones, but the mechanism is unknown. In this study, we show that transfection of oligopeptide transporter 1 (PEPT1) in STC-1 cells, a murine enteroendocrine cell line, evokes di-peptide-stimulated hormone secretion in a pH-dependent manner. Measurement of membrane potentials shows that PEPT1- transfected STC-1 cells are depolarized by di-peptide glycyl-glycine but not by glycine monomer. Glycyl-glycine stimulation induces a rise in the intracellular calcium concentration in PEPT1-transfected STC-1 cells. The secretion induced by glycyl-glycine in PEPT1-transfected STC-1 cells was blocked by nifedipine, a Ca(2+) channel blocker, suggesting that the secretion is triggered by Ca(2+) influx through L-type voltage-dependent Ca(2+) channels. These data suggest that PEPT1 mediates oligopeptide-induced hormone secretion in enteroendocrine cells.
Four impurities in the bulk drug of nifedipine were detected by means of high performance liquid chromatography coupled with quadrupole time of fight mass spectrometry (HPLC-QTOF MS). A Kromasil C18 HPLC column (250 mm x 4.6 mm, 5 microm) was used with methanol-water (60:40, v/v) as mobile phase. The column temperature was maintained at 35 degrees C with an ultraviolet (UV) detection wavelength of 235 nm for analysis. The eluates were detected with a UV detector and a quadrupole time of fight mass spectrometer in positive mode. The sample was infused into the mass spectrometer from the HPLC system through a T-junction with a splitting ratio of 3:1. The ion source temperature was set at 320 degrees C and the electrospray ionization (ESI) needle voltage was always set at 4 000 V. Nitrogen was used as the drying gas and nebulizer gas. The protonated molecular ions were selected for determining the structures, and their fragmentation pathways were deduced. Based on the fragmentation behavior of nifedipine, the structures of 3 impurities were identified and one of them was identified as 3-ethyl-5-methyl-2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, which was an unknown impurity to the best of our knowledge. An other impurity was identified by the comparison of the retention time and tandem mass spectra with the standard substance. The four proposed structures were all confirmed by exact mass evidence. The results indicated that the described method can be effectively applied to perform the identifications in nifedipine and its impurities.