TY - JOUR
T1 - Evidence for a dihydropyridine-sensitive and conotoxin-insensitive release of noradrenaline and uptake of calcium in adrenal chromaffin cells
AU - Owen, P. J.
AU - Marriott, D. B.
AU - Boarder, M. R.
PY - 1989/5/1
Y1 - 1989/5/1
N2 - It has been suggested that neuronal voltage-sensitive calcium channels (VSCC) may be divided into dihydropyridine (DHP)-sensitive (L) and DHP-insensitive (N and T), and that both the L and the N type channels are attenuated by the peptide blocker ω-conotoxin. Here the effects of ω-conotoxin on release of noradrenaline and uptake of calcium in bovine adrenal chromaffin cells were investigated. Release of noradrenaline in response to 25 mM K+, 65 mM K+, 10 nM bradykinin or 10 μM prostaglandin E1 was not affected by ω-conotoxin in the range 10 nM-1 μM. 45Ca2+ uptake stimulated by high K+ and prostaglandin was attenuated by 1 μM nitrendipine and enhanced by 1 μM Bay K 8644; these calcium fluxes were not modified by 20 nM ω-conotoxin. With superfused rat brain striatal slices in the same medium as the above cell studies, release of dopamine in response to 25 mM K+ was attenuated by 20 nM ω-conotoxin. These results show that in these neurone-like cells, release may be effected by calcium influx through DHP-sensitive but ω-conotoxin-insensitive VSCC, a result inconsistent with the suggestion the ω-conotoxin blocks both L-type and N-type neuronal calcium channels.
AB - It has been suggested that neuronal voltage-sensitive calcium channels (VSCC) may be divided into dihydropyridine (DHP)-sensitive (L) and DHP-insensitive (N and T), and that both the L and the N type channels are attenuated by the peptide blocker ω-conotoxin. Here the effects of ω-conotoxin on release of noradrenaline and uptake of calcium in bovine adrenal chromaffin cells were investigated. Release of noradrenaline in response to 25 mM K+, 65 mM K+, 10 nM bradykinin or 10 μM prostaglandin E1 was not affected by ω-conotoxin in the range 10 nM-1 μM. 45Ca2+ uptake stimulated by high K+ and prostaglandin was attenuated by 1 μM nitrendipine and enhanced by 1 μM Bay K 8644; these calcium fluxes were not modified by 20 nM ω-conotoxin. With superfused rat brain striatal slices in the same medium as the above cell studies, release of dopamine in response to 25 mM K+ was attenuated by 20 nM ω-conotoxin. These results show that in these neurone-like cells, release may be effected by calcium influx through DHP-sensitive but ω-conotoxin-insensitive VSCC, a result inconsistent with the suggestion the ω-conotoxin blocks both L-type and N-type neuronal calcium channels.
UR - http://www.scopus.com/inward/record.url?scp=0024604756&partnerID=8YFLogxK
U2 - 10.1111/j.1476-5381.1989.tb11933.x
DO - 10.1111/j.1476-5381.1989.tb11933.x
M3 - Article
C2 - 2470457
AN - SCOPUS:0024604756
VL - 97
SP - 133
EP - 138
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 1
ER -