Drugs online research references
Am J Physiol. 1989 Jun;256(6 Pt 1):C1267-72.
Neuraminidase selectively enhances transient Ca2+ current in cardiac myocytes.
Yee HF Jr, Weiss JN, Langer GA.
Department of Medicine, University of California Los Angeles School of Medicine 90024-1760.
Sialic acid, an anionic sugar moiety found peripherally on membrane glycoconjugates, is specifically hydrolyzed from the cell surface by neuraminidase. Because neuraminidase has previously been demonstrated to augment myocardial cell calcium content, the effects of neuraminidase on Ca channel function were studied on voltage-clamped guinea pig ventricular myocytes. In 25-50% of cells, neuraminidase treatment (0.12 U/ml for 20 min) enhanced current through the transient (T) Ca channel by 304 +/- 35% without significantly altering the magnitude of the long-lasting (L) Ca channel current. Exposure to neuraminidase did not affect the voltage dependence of activation or inactivation, nor did it affect the selective inhibition of the T-channel current by amiloride or the L-channel current by nifedipine. After neuraminidase treatment, the T-channel current inactivated more rapidly (time constant decreasing from 8.9 +/- 0.9 to 7.7 +/- 0.6 ms), whereas there was no change in the rate of inactivation of the L-channel current. Neuraminidase treatment removed approximately 20% of the total cellular sialic acid. These results indicate that neuraminidase treatment selectively modulates the function of the T Ca channel in ventricular myocytes, possibly through removal of sarcolemmal sialic acid, suggesting that glycosylation of membrane macromolecules may influence membrane function.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2544097&dopt=Abstract
Res Commun Mol Pathol Pharmacol. 1999;106(1-2):87-96.
In vivo effects of calcium entry blockers on human parathyroid adenoma cells with special reference to calcium sensing ability and the hormone secretion.
Horikawa Y, Nakajima H, Iizuka K, Imagawa A, Tomita K, Shiba E, Takai S, Miyagawa J, Kuwajima M, Namba M, Hanafusa T, Matsuzawa Y.
Second Department of Internal Medicine, Osaka University Medical School, Suita, Japan.
We evaluated the effects of calcium-entry blockers on parathyroid hormone (PTH) secretion by human parathyroid adenoma cells in vitro. Nifedipine and bamidipine inhibited PTH secretion, while diltiazem had no significant effect. Cytosolic calcium concentrations were measured by use of the calcium-sensitive fluorescent dye fluo-3 with confocal laser scanning microscopy. Nifedipine increased the cytosolic concentration of calcium, whereas diltiazem decreased it. Results suggest that, in parathyroid adenoma cells, regulation of PTH secretion with respect to intracellular calcium concentration would be maintained despite differing response of intracellular calcium concentration following exposure to calcium-entry blockers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11127811&dopt=Abstract
Cell Signal. 2001 Oct;13(10):711-6.
Maitotoxin-induced calcium entry in human lymphocytes: modulation by yessotoxin, Ca(2+) channel blockers and kinases.
de la Rosa LA, Alfonso A, Vilarino N, Vieytes MR, Yasumoto T, Botana LM.
Department of Pharmacology, Faculty of Veterinary, University of Santiago de Compostela, Lugo 27002, Spain.
We have studied the effect of the ciguatera-related toxin maitotoxin (MTX) on the cytosolic free calcium concentration ([Ca(2+)]i) of human peripheral blood lymphocytes loaded with the fluorescent probe Fura2 and the regulation of MTX action by different drugs known to interfere in cellular Ca(2+) signalling mechanisms and by the marine phycotoxin yessotoxin (YTX). MTX produced a concentration-dependent elevation of [Ca(2+)]i in a Ca(2+)-containing medium. This effect was stimulated by pretreatment with YTX 1 microM and NiCl(2) 15 microM. The voltage-independent Ca(2+) channel antagonist 1-[beta-[3-(4-methoxyphenyl)propoxyl]-4-methoxyphenyl]-1H-imidazole hydrochloride (SKF96365) blocked the MTX-induced [Ca(2+)]i elevation, while the L-type channel blocker nifedipine had no effect. Pretreatment with NiCl(2) or nifedipine did not modify YTX-induced potentiation of MTX effect, and SKF96365-induced inhibition was reduced in the presence of YTX, which suggest different pathways to act on [Ca(2+)]i. Preincubation with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide.2HCl (H-89) or genistein (10 microM) also had no effect on the MTX-induced [Ca(2+)]i increment. In contrast, the PKC inhibitor bisindolilmaleimide I (GF109203X 1 microM) potentiated the MTX effect, whereas phosphatidylinositol (PI) 3-kinase inhibition with wortmannin (10 nM) reduced the MTX-elicited Ca(2+) entry. In summary, MTX produced Ca(2+) influx into human lymphocytes through a SKF96365-sensitive, nifedipine-insensitive pathway. The MTX-induced [Ca(2+)]i elevation was stimulated by the marine toxin YTX through a mechanism insensitive to SKF96365, nifedipine or NiCl(2). It was also stimulated by the divalent cation Ni(2+) and PKC inhibition and was partially inhibited by PI 3-kinase inhibition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11602181&dopt=Abstract
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