Drugs online research references
Eur J Pharmacol. 1996 Oct 24;314(1-2):91-8.
Pulmonary versus systemic effects of vasodilator drugs: an in vitro study in isolated intrapulmonary and mesenteric arteries of neonatal piglets.
Perez-Vizcaino F, Villamor E, Moro M, Tamargo J.
Department of Pharmacology, School of Medicine, Universidad Complutense, Madrid, Spain.
The ability of several vasodilators to inhibit the responses to noradrenaline and U46619 (a thromboxane A2 analog) in isolated pulmonary and mesenteric arteries of neonatal piglets was compared. In pulmonary arteries, acetylcholine produced endothelium-dependent relaxations (pIC50 = about 6.8) while, in mesenteric arteries, a relaxant (< or = 10(-7) M) or a contractile response (> or = 10(-6) M) was observed. Sodium nitroprusside produced relaxant effects in pulmonary and mesenteric arteries contracted by noradrenaline (pIC50 = 6.6 and 6.0, respectively) and U46619 (pIC50 = 5.4 and 6.7, respectively). ATP induced an endothelium-independent relaxation in pulmonary arteries (pIC50 = about 4) but in mesenteric arteries it produced weak relaxant effects. In resting mesenteric arteries, ATP induced a concentration-dependent contraction which was not observed in pulmonary arteries. Prostaglandin E1 induced a contractile effect whereas, at higher concentrations, a relaxant response was observed. The alpha-adrenoceptor antagonist tolazoline had no effect on arteries contracted by U46619 but relaxed arteries contracted by noradrenaline being slightly more potent in mesenteric than in pulmonary arteries (pIC50 = 5.1 and 4.8, respectively). Nifedipine (> 10(-7) M) relaxed both arteries, mesenteric being more sensitive than pulmonary arteries and noradrenaline more sensitive than U46619-induced contractions. In conclusion, differences in the relaxant effects for all vasodilators were found depending on the artery, the vasoconstrictor used or both. However, ATP was the only drug which, regardless of the concentration or vasoconstrictor used, produced greater relaxant effects in pulmonary than in mesenteric arteries.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8957223&dopt=Abstract
Biochim Biophys Acta. 1996 Nov 8;1314(1-2):43-8.
Volume regulation and the efflux of amino acids from cells in incubated slices of rat cerebral cortex. II. Dependence on Ca2+ ions.
Law RO.
Department of Cell Physiology and Pharmacology, University of Leicester, UK.
The efflux of gamma-aminoisobutyric acid (GABA) and L-glutamate from pre-loaded cells in rat cerebral cortical slices has been studied during interventions designed to affect the availability of intracellular Ca2+ during hyposmotic swelling and membrane depolarization due to raised extracellular K+. Calmodulin-dependent acceleration of amino acid efflux in hyposmotic media, with cell swelling less than would be predicted on the basis of perfect osmometric behaviour (see Ref. [1]), was unaffected by Ca-ionophore in the presence of external Ca2+ or by the omission of external Ca2+, but was suppressed by pre-exposure of slices to thapsigargin (2 microM), which is reported to deplete cytosolic Ca2+, and by TMB-8 (0.5 mM), which blocks release of Ca2+ from internal stores. TMB-8 also led to significant cell swelling. The effects of TMB-8 were reversed by Ca-ionophore. Raised external K+ (54 mM) led to accelerated amino acid efflux which required calmodulin activation and was blocked by (i) omission of external Ca2+, (ii) the voltage-sensitive Ca2+ channel blocker nifedipine (1 microM), (iii) the anion transport inhibitor DIDS (25 microM for GABA, 100 microM for L-glutamate, see Ref. [1]), and (iv) the -SH group acetylator N-ethylmaleimide. TMB-8 was without effect in high K+ media. These results suggest that while enhanced amino acids efflux probably occurs through the same population of Ca/calmodulin-dependent, DIDS-sensitive pathways following hyposmotic shock or membrane depolarization, the source of Ca2+ ions required for the activation of these pathways may depend upon which of these acceleratory stimuli is applied.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8972716&dopt=Abstract
Zhonghua Yi Xue Za Zhi (Taipei). 1996 Nov;58(5):341-7.
A model for investigating effect of shock waves on intracellular calcium mobilization.
Chen WC, Jan CR, Lee YH, Ou HC, Huang JK, Tseng CJ.
Division of Surgery, Veterans General Hospital-Kaohsiung, Taipei, Taiwan, R.O.C.
BACKGROUND: Shock wave lithotripsy (SWL) has become a non-invasive standard treatment for urolithiasis; however, it has some unwanted bioeffects. A cell model using calcium (Ca) imaging of cultured Madin-Darby canine kidney (MDCK) cells has been established in this laboratory to study the effects of shock waves on intracellular free Ca mobilization of renal tubular cells. METHODS: Digital video imaging of fura-2 fluorescence was used to measure both resting and stimulated intracellular free Ca concentrations in single cultured MDCK cells. Pharmacological agents including adenosine-5'-trisphosphate (ATP), bradykinin and thapsigargin, were used as Ca mobilizing agents. RESULTS: ATP, bradykinin and thapsigargin all elicited a robust transient increase in intracellular Ca concentration. CONCLUSIONS: A cell model was established to investigate the effect of shock waves on single kidney cells. This provided an opportunity to determine how shock waves affect the regulation of intracellular Ca concentrations in kidney cells; in addition, it allows investigation, for the first time at the single cell level, of whether blocking Ca entry in kidney cells plays any role in the mechanism by which some Ca channel blockers, e.g. nifedipine and verapamil, protect patients of urolithiasis from shock wave-induced renal damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9037850&dopt=Abstract
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