Abstract:
:Endothelin (200 nM) evoked a rapid rise in [Ca2+]i which was then followed by a maintained elevation of [Ca2+]i. The initial transient can be explained by the release of stored Ca2+ whilst the maintained plateau is likely to be an influx of Ca2+ as it was partially inhibited by nifedipine (5 microM) and the remaining component abolished by the removal of extracellular Ca2+. Vasopressin (1 nM) evoked a similar response which also showed a nifedipine insensitive component to it's plateau phase. Endothelin also evoked oscillations in [Ca2+]i; these where characterised by a rapid rising phase followed by a slower decline, with no 'pacemaker' rise in [Ca2+]i preceding the rising phase. The oscillations were inhibited by the addition of 5 microM nifedipine or the removal of extracellular Ca2+ suggesting they are at least in part dependent on voltage gated Ca2+ entry.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Simpson AW,Ashley CCdoi
10.1016/0006-291x(89)91108-xsubject
Has Abstractpub_date
1989-09-29 00:00:00pages
1223-9issue
3eissn
0006-291Xissn
1090-2104pii
0006-291X(89)91108-Xjournal_volume
163pub_type
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