Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Freshly dispersed interstitial cells from the rabbit urethra were studied by using the perforated-patch technique. When cells were voltage clamped at -60 mV and exposed to 10 microM norepinephrine (NE) at 80-s intervals, either large single inward currents or a series of oscillatory inward currents of diminishing amplitude were evoked. These currents were blocked by either phentolamine (1 microM) or prazosin (1 microM), suggesting that the effects of NE were mediated via alpha(1)-adrenoceptors. NE-evoked currents were depressed by the blockers of Ca(2+)-activated Cl(-) currents, niflumic acid (10 microM), and 9-anthracenecarboxylic acid (9-AC, 1 mM). The reversal potential of the above currents changed in a predictable manner when the Cl(-) equilibrium potential was altered, again suggesting that they were due to activation of a Cl(-) conductance. NE-evoked currents were decreased by 10 microM cyclopiazonic acid, suggesting that they were dependent on store-released Ca(2+). Inhibition of NE-evoked currents by the phospholipase C inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (100 microM) suggested that NE releases Ca(2+) via an inositol 1,4,5-trisphosphate (IP(3))-dependent mechanism. These results support the idea that stimulation of alpha(1)-adrenoceptors releases Ca(2+) from an IP(3)-sensitive store, which in turn activates Ca(2+)-activated Cl(-) current in freshly dispersed interstitial cells of the rabbit urethra. This elevates slow wave frequency in these cells and may underlie the mechanism responsible for increased urethral tone during nerve stimulation.
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PMID:Characterization of norepinephrine-evoked inward currents in interstitial cells isolated from the rabbit urethra. 1217 45

Measurements were made (using fast confocal microscopy) of intracellular Ca2+ levels in fluo-4 loaded interstitial cells isolated from the rabbit urethra. These cells exhibited regular Ca2+ oscillations which were associated with spontaneous transient inward currents recorded under voltage clamp. Interference with D-myo-inositol 1,4,5-trisphosphate (IP3) induced Ca2+ release using 100 microm 2-aminoethoxydiphenyl borate, and the phospholipase C (PLC) inhibitors 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate and U73122 decreased the amplitude of spontaneous oscillations but did not abolish them. However, oscillations were abolished when ryanodine receptors were blocked with tetracaine or ryanodine. Oscillations ceased in the absence of external Ca2+, and frequency was directly proportional to the external Ca2+ concentration. Frequency of Ca2+ oscillation was reduced by SKF-96365, but not by nifedipine. Lanthanum and cadmium completely blocked oscillations. These results suggest that Ca2+ oscillations in isolated rabbit urethral interstitial cells are initiated by Ca2+ release from ryanodine-sensitive intracellular stores, that oscillation frequency is very sensitive to the external Ca2+ concentration and that conversion of the primary oscillation to a propagated Ca2+ wave depends upon IP3-induced Ca2+ release.
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PMID:Calcium oscillations in interstitial cells of the rabbit urethra. 1576 Sep 47