Drugs online research references
Pflugers Arch. 1995 Feb;429(4):470-6.
Mechanism of the enhancing effect of sorbitol on ileal Ca uptake in rat enterocytes.
Tardivel S, Razanamaniraka L, Drueke T, Lacour B.
Metabolisme Mineral des Mammiferes, EPHE, Faculte de Pharmacie, Chatenay Malabry, France.
The effect of sorbitol on Ca uptake by isolated ileal epithelial cells was investigated. Intestinal cells were isolated from rat ileum by mechanical vibration. 45Ca uptake was approximately 2 times higher in cells exposed to 200 mM sorbitol of D-alanine than in control cells. This enhancing effect of sorbitol on percentage Ca uptake decreased with increasing Ca concentrations in the incubation medium suggesting an effect on Ca entry velocity. The addition of 10 microM nifedipine or 200 microM verapamil to the incubation medium was devoid of any effect on Ca uptake in ileal cells, whereas 100 microM trifluoperazine or chlorpromazine abolished the stimulatory effect of sorbitol. Finally, the effect of sorbitol on isolated cells was independent of a measurable change of cellular ATP content. In conclusion, the stimulatory effect of sorbitol on ileal Ca uptake is probably exerted through mechanisms other than an increase in intracellular ATP concentration. Sorbitol may enhance enterocyte Ca transport via a direct interaction with calmodulin and/or the Ca pump. It may also exert its effect through an inhibition of the basolateral Na Ca exchanger.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7617436&dopt=Abstract
J Electrocardiol. 1996 Apr;29(2):123-30.
Mechanisms of the in vitro effects of amphetamine on rat sinus node automaticity and membrane potentials of atrial fibers.
Aileru AA, Carpentier RG.
Department of Physiology and Biophysics, College of Medicine, Howard University, Washington, DC 20059, USA.
The main objective of this investigation was to clarify the mechanisms of the acute in vitro actions of amphetamine (AMP) on cardiac electrophysiology. Concentrations of AMP ranging from those considered clinically therapeutic to those considered toxic were tested in isolated rat sinoatrial tissues while recording membrane potentials with intracellular microelectrodes. In preparations beating spontaneously, 6.8 nM-2.71 microM AMP exerted a positive chronotropic action that was blocked by propranolol. The positive chronotropic action of 5.43 microM AMP was smaller than that of 2.7 microM AMP and was reversed by propranolol. Neither phentolamine nor atropine blocked this depressant action of AMP. It is concluded that the positive chronotropic action of AMP was beta-adrenergic and that beta-adrenergic block unmasked a negative chronotropic action of a high concentration of AMP, which was neither alpha-adrenergic nor muscarinic. In atrial fibers driven at a constant rate, 54.3 nM AMP prolonged the action potential duration (APD), without affecting the resting membrane potential (RMP), the action potential amplitude (APA), or the maximum velocity of phase 0, while 5.43 microM AMP reduced RMP, APA, and the maximum velocity of phase 0, and increased APD. The prolongation of APD, as well as the decreases of RMP and APA, was not abolished by propranolol, phentolamine, or 4-aminopyridine. Conversely, nifedipine abolished the effects of AMP on all three parameters. In general, AMP produced mainly a prolongation of the action potential. Only a high concentration of AMP decreased RMP and depressed phase 0 of the action potential. The effect of AMP on APD, RMP, and APA essentially involved increasing the influx of calcium through the L-type channels in the sarcolemma.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8728598&dopt=Abstract
irp.nih.nida.gov
This study was designed to investigate the influence of the calcium (Ca2+) channel inhibitors nicardipine, nifedipine, and flunarizine on the protective action of MK-801, LY 235959 [N-methyl-D-aspartate (NMDA) receptor antagonists], and GYKI 52466 (a non-NMDA receptor antagonist) against electroconvulsions in mice. Unlike nicardipine (15 mg/kg) or flunarizine (10 mg/kg) nifedipine (7.5 and 15 mg/kg) potentiated the protective potency of MK-801 (0.05 mg/kg), as reflected by significant elevation of the convulsive threshold (a CS50 value of the current strength in mA producing tonic hind limb extension in 50% of the animals). The protective activity of LY 235959 and GYKI 52466 was reflected by their ED50 values in mg/kg, at which the drugs were expected to protect 50% of mice against maximal electroshock-induced tonic extension of the hind limbs. Nicardipine (3.75 15 mg/kg), nifedipine (0.94-15 mg/kg), and flunarizine (2.5-10 mg/kg) in a dose-dependent manner markedly potentiated the antiseizure efficacy of LY 235959. Flunarizine (5 and 10 mg/kg) was the only Ca2+ channel inhibitor to enhance the protective action of GYKI 52466 against electroconvulsions. Except with MK-801 + flunarizine (motor performance) or GYKI 52466 + flunarizine (long-term memory), combination of NMDA or non-NMDA receptor antagonists with Ca2+ channel inhibitors produced an impairment of motor performance (evaluated in the chimney test) and long-term memory acquisition (measured in the passive avoidance task) as compared with vehicle treatment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9130287&dopt=Abstract
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