Drugs online research references
Biochim Biophys Acta. 1994 Jan 3;1189(1):1-6.
Reversal agent inhibition of the multidrug resistance pump in human leukemic lymphoblasts.
Wigler PW, Patterson FK.
Department of Medical Biology, University of Tennessee Medical Center, Knoxville 37920.
Multidrug resistant cancer cells of the MDR-1 phenotype utilize an ATP-dependent pump to excrete toxic drugs. Rhodamine 123 (R123) is a fluorescent substrate of the MDR pump. An assay for the ATP-dependent initial efflux of R123 from CEM/VLB100 human leukemic lymphoblasts has been developed. The MDR-1 cells were treated with a reversal agent and preloaded with 40.0 nM R123 in buffer at 30 degrees C that contained sodium azide and 2-deoxyglucose. The cells were rinsed with cold buffer and resuspended in L-glutamine/glucose solution at 23 degrees C. The cell suspension was passed through a filter and R123 in the filtrate was detected at 2-s intervals by fluorescence. Efflux of R123 was inhibited by the reversal agents amiodarone, cyclosporin A, Ro11-2933 (DMDP), quinidine, and the optical isomers of propranolol. The MDR pump is stereospecific for the (R)-diastereomer quinidine; however, the (S)-diastereomer quinine is a relatively weak inhibitor of the pump. Cyclosporin A was the most potent inhibitor tested against the efflux of R123 by the MDR pump.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7905747&dopt=Abstract
Pharmacol Biochem Behav. 1993 Dec;46(4):953-8.
Effects of beta-adrenoceptor agonists and antagonists on thermoregulation in the cold in lean and obese Zucker rats.
Carlisle HJ, Dubuc PU, Stock MJ.
Department of Psychology, University of California, Santa Barbara 93106.
This experiment examines whether the thermoregulatory ability of obese Zucker rats is comparable to that of lean rats following treatment with beta-adrenoceptor agonists and antagonists in a cold (-8 degrees C) environment. Half-maximal doses of the nonselective beta-adrenoceptor agonist isoproterenol (ISO) produced net thermolytic (heat loss) effects in both obese and lean rats in an operant lever pressing for radiant heat task. ISO increased the demand for heat, but posttest colonic temperature (Tc) decreased. A low dose of propranolol (100 micrograms/kg) normalized thermoregulatory behavior, Tc, and thermal balance when coadministered with ISO. Activation of thermogenesis with the selective beta 3-agonist BRL 35135 (BRL) reduced heat influx by both obese and lean rats at doses between 2 and 10 micrograms/kg, but no dose-response effects were evident within this range. Posttest Tc and thermal balance indicated no thermolytic effects. No evidence was found for a beta 2-component in the BRL response when a supramaximal dose (40 micrograms/kg) was tested with the selective beta 2-antagonist ICI 118551 (1 mg/kg). These data show that, despite a higher baseline demand for heat, the obese Zucker rat responds to the thermogenic effects of BRL and the thermolytic effects of ISO as does the lean rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7906041&dopt=Abstract
Cardiovasc Res. 1994 Jan;28(1):112-8.
Beta 1 adrenoceptor mediated decrease in pHi in quiescent ventricular myocardium.
Shida S, Nakaya H, Matsumoto S, Kanno M.
Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan.
OBJECTIVE: The aims were to examine the effect of beta adrenergic stimulation on the intracellular pH (pHi) and to compare it with that of alpha adrenergic stimulation in ventricular myocardium. METHODS: Using conventional and ion selective electrodes membrane potential and pHi were measured simultaneously in quiescent papillary muscles of guinea pigs in HEPES or bicarbonate buffered solution. Isoprenaline and propranolol (1 microM) plus phenylephrine (30 microM) were used to stimulate beta and alpha adrenoceptors, respectively. In order to evaluate underlying mechanism(s) of beta adrenoceptor mediated pHi change, effects of Na(+)-H+ exchange, Cl(-)-HCO3- exchange, Na(+)-HCO3- symport, and glycolysis blockers on the pHi change were examined. RESULTS: Isoprenaline (1 microM) produced a decrease in pHi of 0.08(SEM 0.01) pH units and a transient depolarisation of the resting membrane. The isoprenaline induced intracellular acidosis was blocked by the beta 1 blocker atenolol (10 microM) but not by the beta 2 blocker ICI 118,551 (0.1 microM). Forskolin also produced a decrease in pHi of 0.06(0.03) pH units. In contrast, alpha adrenergic stimulation produced an increase in pHi, which was abolished by 1 mM amiloride, an Na(+)-H+ exchange blocker. In the presence of amiloride, the isoprenaline induced decrease in pHi was rather enhanced. 4,4'-Diisothiocyanostilbene-2,2'-disulphonic acid (DIDS, 1 mM), a blocker of Cl(-)-HCO3- exchange and the Na(+)-HCO3- symport system, failed to affect the isoprenaline induced pHi decrease in bicarbonate buffered solution. However, pretreatment with 2-deoxyglucose or iodoacetic acid abolished the isoprenaline induced pHi decrease. CONCLUSIONS: beta 1 Adrenoceptor stimulation causes intracellular acidosis via the enhanced glycolysis, and the Na(+)-H+ exchange system appears to play a compensatory role. The beta 1 adrenoceptor mediated intracellular acidosis may modulate inotropic response to adrenergic stimulation in ventricular myocardium.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7906613&dopt=Abstract
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