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Laboratoire de Physiologie Cellulaire Respiratoire, Contrat de Recherche Institut National de la Santé et de la Recherche Médicale 9806, Université Bordeaux 2, 33076 Bordeaux, France
The effect of endothelin (ET)-1 on both
cytosolic Ca2+ concentration
([Ca2+]i)
and membrane current in freshly isolated myocytes, as well as on the
contraction of arterial rings, was investigated in rat main pulmonary
artery (RMPA) and intrapulmonary arteries (RIPA). ET-1 (5-100 nM,
30 s) induced a first
[Ca2+]i
peak followed by 3-5 oscillations of decreasing amplitude. In
RMPA, the ET-1-induced
[Ca2+]i
response was fully abolished by BQ-123 (0.1 µM). In RIPA, the response was inhibited by BQ-123 in only 21% of the cells, whereas it
was abolished by BQ-788 (1 µM) in 70% of the cells. In both types of
arteries, the response was not modified in the presence of 100 µM
La3+ or in the absence of external
Ca2+ but disappeared after
pretreatment of the cells with thapsigargin (1 µM) or neomycin (0.1 µM). In RPMA myocytes clamped at 
60 mV, ET-1 induced an
oscillatory inward current, the reversal potential of which was close
to the equilibrium potential for
Cl
. This current was
unaltered by the removal of external
Ca2+ but was abolished by niflumic
acid (50 µM). In arterial rings, the ET-1 (100 nM)-induced
contraction was decreased by 35% in the presence of either niflumic
acid (50 µM) or nifedipine (1 µM). These results demonstrate that
ET-1 via the ETA receptor only in
RMPA and both ETA and
ETB receptors in RIPA induce
[Ca2+]i
oscillations due to iterative Ca2+
release from an inositol trisphosphate-sensitive
Ca2+ store.
Ca2+ release secondarily activates
an oscillatory membrane Cl
current that can depolarize the cell membrane, leading to an influx of
Ca2+, this latter contributing to
the ET-1-induced vasoconstrictor effect.
cytosolic calcium concentration measurement; patch clamp; vascular smooth muscle; niflumic acid; calcium-activated chloride currrent
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