Drugs online research references
Dev Pharmacol Ther. 1993;20(1-2):72-85.
Developmental differences in the electrophysiological response of isolated canine Purkinje fibers to adrenergic stimulation during simulated ischemia.
Fenrich A, Hamra M.
Department of Pediatrics, Baylor College of Medicine, Houston, Tex.
Developmental differences in adrenergic responsiveness may cause age-related changes in the cellular response to ischemia. Standard microelectrode techniques were used in isolated young and adult canine Purkinje fibers to determine the effect of simulated ischemia ([K+]o = 10 mM, pH 6.7, pO2 < 25 mm Hg) alone or with adrenergic stimulation on the rhythmic activity in spontaneously beating Purkinje fibers and on transmembrane potentials and delayed afterdepolarizations in paced Purkinje fibers (basic cycle length = 800-300 ms). The adrenergic agonists used were phenylephrine (5 x 10(-8) M) and isoproterenol (1 x 10(-6) M). For all automatic fibers studied, the control maximum diastolic potential in adults (-96 +/- 1 mV, n = 37) and in the young (-98 +/- 1 mV, n = 36) went to -62 +/- 1 mV during ischemia in both groups and returned to -96 +/- 2 mV with reperfusion. The incidence of rhythmic activity (expressed as percent) during ischemia alone was similar at both ages: adults, 22%; young, 25%. The incidence of ectopic activity with phenylephrine superfusion during ischemia for adults was 63%, an effect blocked by prazosin (1 x 10(-6) M) but not by propranolol (2 x 10(-7) M); the incidence for the young was 25%. Isoproterenol caused ectopic rhythms in 86% of young fibers and 17% of adult fibers (p < 0.05 young vs. adult). During reperfusion the return to control rhythm was slower in adults after ischemia alone or ischemia + alpha-adrenergic stimulation with phenylephrine. There were no age-related differences in the transmembrane potential response of paced fibers to ischemia or reperfusion, and there were no delayed afterdepolarizations with interruption of pacing at 800, 500, or 300 ms in either group. These data suggest that age-related differences in adrenergic responses alter the cellular response to an ischemic insult. To the extent that an ectopic beat may initiate an abnormal rhythm, these differences in sensitivity to adrenergic agonists may lead to developmental differences in arrhythmogenic potential during ischemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7924767&dopt=Abstract
Hepatology. 1994 Oct;20(4 Pt 1):1002-8.
Calmodulin expression during rat liver regeneration.
Agell N, Pujol MJ, Lopez-Girona A, Bosch M, Rosa JL, Bachs O.
Departament de Biologia Cel.lular, Facultat de Medicina, Universitat de Barcelona, Spain.
We have investigated the messenger RNAs expressed from the three calmodulin genes during rat liver regeneration. The results revealed that all the calmodulin transcripts increased from 8 hr after a partial hepatectomy, although differences in the timing and the level of expression from the three genes were observed. Calmodulin I transcripts peaked at 16 hr, whereas calmodulin II and calmodulin III progressively increased from 8 to 24 hr. At 24 hr after surgery, calmodulin I, calmodulin II and the 2.3 kb calmodulin III transcripts reached values of a 6-fold increase, whereas the 0.8 kb product of calmodulin III increased 25-fold. At 30 hr the levels of all the calmodulin transcripts were similar to those observed at 24 hr. The transcription rates of the three calmodulin genes augmented after hepatectomy (calmodulin I and calmodulin II twofold and calmodulin III fourfold), indicating that the elevation of the calmodulin transcripts could be, at least partially, the result of this increase in the transcription rates. The total calmodulin concentration also increased twofold at 24 hr after hepatectomy. We also report that the administration of the beta-adrenergic blocker, D,L-propranolol inhibited the accumulation of calmodulin protein without significantly affecting the increase of the messenger RNAs. These results indicate that the expression of calmodulin observed during liver regeneration could be regulated by cyclic AMP at the translational or posttranslational level.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7927201&dopt=Abstract
Am J Physiol. 1994 Oct;267(4 Pt 1):C969-79.
Coexisting beta-adrenoceptor subtypes: significance for thermogenic process in brown fat cells.
Zhao J, Unelius L, Bengtsson T, Cannon B, Nedergaard J.
Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, Sweden.
The possible significance of the coexisting beta 1-, beta 2-, and beta 3-adrenoceptors in brown adipose tissue for the thermogenic response was investigated. Oxygen consumption of isolated hamster brown fat cells was analyzed as a measure of thermogenesis. Thermogenesis could be evoked not only by the physiological agent norepinephrine but also by BRL-37344 and CGP-12177. No evidence for biphasic inhibition curves was found with either the selective beta 1-antagonist ICI-89406, the beta 2-antagonist ICI-118551, or the beta 1/beta 2-nonselective beta-antagonist propranolol against 1 microM norepinephrine; pI50 (the negative logarithm of the inhibitory constant for an antagonist, as estimated from the dose-response curve for an antagonist vs. a constant agonist concentration) values for ICI-89406 and ICI-118551 were very low (4-5), implying nonselective inhibition; the pI50 for propranolol was approximately 6 (as expected for the beta 3-receptor). Even with suboptimal norepinephrine, no biphasic inhibition was found. CGP-12177 at concentrations where it is primarily an antagonist to the beta 1-receptor did not influence the dose-response curve for either norepinephrine or BRL-37344. BRL-37344- or CGP-12177-induced thermogenesis was inhibited by the beta-antagonists in a manner similar to norepinephrine-induced thermogenesis. Schild plots for propranolol inhibition of norepinephrine-, isoprenaline-, BRL-37344- and CGP-12177-induced thermogenesis yielded similar pA2 (the negative logarithm of the inhibitory constant for an antagonist, as calculated from a series of agonist dose-response curves at different antagonist concentrations) (approximately 5.5), for interaction with either agonist, implying that the same receptor was stimulated by all agonists. Thus, despite the fact that different beta-receptor subtypes coexist in the tissue, we find no evidence for the participation of beta 1- or beta 2-receptors in the thermogenic response. Within the resolution of the experiments, the results therefore imply that it is predominantly or solely the beta 3-receptor that is coupled to thermogenesis, and it is via this beta-adrenergic receptor that not only norepinephrine but also CGP-12177 and BRL-37344 induce thermogenesis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7943293&dopt=Abstract
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