Intracellular calcium in the control of osteoclast function. I. Voltage-insensitivity and lack of effects of nifedipine, BAYK8644 and diltiazem.
We have recently demonstrated that in the rat osteoclast, a rise in the ambient calcium concentration induces a rapid elevation of cytosolic calcium, and that this phenomenon is accompanied by a complete inhibition of osteoclastic bone resorption. Here, we have attempted to characterise the electrophysiological nature of the putative 'calcium-activated' calcium channel. We have established that calcium influx into the osteoclast that occurs on exposure to elevated extracellular calcium is independent of membrane voltage and is insensitive to modulation by organic calcium channel modulators, namely nifedipine, BAYK8644 and diltiazem. The latter compounds were also unable to block the reduction of cell spread area and the inhibition of bone resorption produced in response to elevated extracellular calcium levels.
Datta
H K
HK
Cell Biology Unit, Royal Postgraduate Medical School, London, UK.
MacIntyre
I
I
Zaidi
M
M
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology*; D000818:Animals; D001862:Bone Resorption / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D004110:Diltiazem / Q000494:pharmacology*; D008564:Membrane Potentials; D009543:Nifedipine / Q000494:pharmacology*; D010010:Osteoclasts / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D004110:Diltiazem; D009543:Nifedipine; D002118:Calcium