Drugs online research references
ukbf.fu-berlin.de
Trabecularmeshwork (TM), a smooth muscle-like tissue with contractile properties, is involved in the regulation of aqueous humor outflow. However, little is known about the regulation of Ca(2+)influx in trabecular meshwork cells. We investigated the influence of acetylcholine and tyrosine kinases on Ca(2+)conductances of bovine TM (BTM) and human TM (HTM) cells using the perforated-patch configuration of the patch-clamp technique and measurements of intracellular free Ca(2+)([Ca(2+)](i)). Depolarization of the cells in the presence of 10 m m Ba(2+)or Ca(2+)led to an activation of inward currents at potentials positive to -30 mV with characteristics typical of L-type Ca(2+)currents: when using 10 m m Ba(2+), maximal inward current and inactivation time constant (tau) increased; the L-type Ca(2+)channel blocker nifedipine (1 microm) reduced and the L-type Ca(2+)channel agonist BayK8644 (5 microm) enhanced maximal inward current.Acetylcholine (100 microm) and carbachol (1 microm) led to an increase in inward Ba(2+)current whereas application of the tyrosine kinase inhibitors genistein (50 microm) and lavendustin A (20 microm) resulted in a decrease in inward current. The application of daidzein (10 microm), an inactive analog of genistein had no effect. Depolarization of the cells with 135 m m K(+)or direct stimulation of L-type channels by application of BayK 8644 led to an increase in [Ca(2+)](i). Carbachol (1 microm) induced an increase in [Ca(2+)](i)which was decreased by application of the tyrosine kinase inhibitor genistein (50 microm). We conclude that HTM and BTM cells express voltage-dependent L-type Ca(2+)channels that influence intracellular Ca(2+)concentration and thus may modulate TM contractility. The activity of L-type Ca(2+)currents is influenced by muscarinic agonists and tyrosine kinases. Copyright 2000 Academic Press.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10712815&dopt=Abstract
salud.unm.edu
Previously, we reported that aortic segments from rats made hypertensive with the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine (L-NNA) exhibit enhanced contractile sensitivity to both alpha2-adrenergic receptor (alpha2-AR) stimulation and to KCl-induced depolarization. We hypothesized that increased contractile responses to these agents was due to a change in the common effector L-type voltage-dependent calcium channel (VDCC). In aortic segments from control and L-NNA-treated rats, contraction to the alpha2-AR agonist UK-14304 stimulated Ca2+ influx but released intracellular Ca2+ only in control arteries. UK-14304-induced contraction was blocked by the VDCC antagonist nifedipine in both control and L-NNA aortas but contraction of aortas from L-NNA-treated rats was blocked by lower concentrations. Calcium imaging studies in fura 2-loaded freshly isolated aortic vascular smooth muscle cells also demonstrated UK-14304-stimulated Ca2+ influx sensitive to nifedipine only in cells from L-NNA-treated rats. We conclude that alpha2-AR contraction in the rat aorta is mediated primarily by Ca2+ influx and that L-NNA-induced hypertension increases the dependence of this contraction on VDCCs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11668088&dopt=Abstract
Acta Physiol Pharmacol Bulg. 1990;16(2):16-20.
Ryodipine-induced enhancement of farmarubicin cytotoxicity against human leukemia cells in vitro.
Mircheva J, Staneva-Stoytcheva D, Ancheva M.
Institute of Pharmacology and Pharmacy, Medical Academy, Sofia.
Ryodipine is a recently developed dihydropyridine calcium channel blocker, chemically similar to nifedipine but with some advantages: light stability, low toxicity, etc. In recent years calcium antagonists have attracted attention not only with their cardiovascular activity but also as drugs increasing the antitumor effect of some cytostatics. In the present work the potentiating effect of ryodipine on the farmarubicin-induced cytotoxicity against K 562 human leukemia cells in vitro was evaluated. The cells were exposed to farmarubicin, ryodipine and combination of both drugs. The results obtained clearly demonstrated that a nontoxic concentration (0.5 microgram/ml) of ryodipine increased (about 5 times) farmarubicin cytotoxicity as the IC50 of the cytostatic was shifted from 1,86 ng/ml on single treatment to 0.37 ng/ml on combined treatment of the cells. The data presented suggest a role for ryodipine in the enhancement of the antitumor activity of some cytostaticts.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2281796&dopt=Abstract
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