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Vol. 284, Issue 3, 1122-1131, March 1998
University of Oxford, Department of Pharmacology, Oxford, OX1 3QT,
United Kingdom
The electrophysiological effects of endothelin (ET)-1 were compared in
myocytes isolated from rat small pulmonary artery, basilar artery and
aorta. ET-1 evoked depolarization in all three smooth muscle cell
types. Depolarizing oscillations in membrane current also were observed
in pulmonary and aortic myocytes. In voltage-clamp experiments ET-1
induced a gradual inhibition of the Ca++-independent
outward current (IK) in pulmonary and aortic myocytes, whereas in basilar myocytes ET-1 inhibited the
Ca++-activated K+ current (IK(Ca)).
ET-1 also evoked a transient enhancement of IK(Ca) and
oscillations in inward current in aortic and pulmonary myocytes. The
inward currents were inhibited by caffeine, which suggests
Ca++-dependent activation. Ion-exchange experiments
indicated that in pulmonary myocytes oscillatory currents were caused
solely by the movement of Cl
, whereas in aortic myocytes
they were the consequence of both Ca++-activated
Cl (ICl(Ca)) and nonselective cation currents
(INS). No inward current was evoked in basilar myocytes in
response to ET-1 or photorelease of Ca++, which suggests
that these cells do not possess ICl(Ca). Experiments with
ET receptor ligands indicated that in basilar myocytes ETA receptor stimulation is responsible for IK(Ca) inhibition,
whereas in aortic and pulmonary myocytes ETB and
ETA receptor stimulation mediates inhibition of
IK and activation of ICl(Ca), INS
and IK(Ca), respectively. In the future, it may be possible
to exploit these differential effects of ET-1 pharmacologically to
assist development of tissue-specific modulators for the treatment of
vascular disease.
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