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Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21224
Although
endothelin (ET)-1 is an important regulator of pulmonary vascular tone,
little is known about the mechanisms by which ET-1 causes contraction
in this tissue. Using the whole cell patch-clamp technique in rat
intrapulmonary arterial smooth muscle cells, we found that ET-1 and the
voltage-dependent K+
(KV)-channel antagonist
4-aminopyridine, but not the
Ca2+-activated
K+-channel antagonist
charybdotoxin (ChTX), caused membrane depolarization. In the presence
of 100 nM ChTX, ET-1 (10
10
to 107 M) caused a
concentration-dependent inhibition of
K+ current (56.2 ± 3.8% at
107 M) and increased the
rate of current inactivation. These effects of ET-1 on
K+ current were markedly reduced
by inhibitors of protein kinase C (staurosporine and GF 109203X) and
phospholipase C (U-73122) or under
Ca2+-free conditions and were
mimicked by activators of protein kinase C (phorbol 12-myristate
13-actetate and
1,2-dioctanoyl-sn-glycerol). These
data suggest that ET-1 modulated pulmonary vascular reactivity by
depolarizing pulmonary arterial smooth muscle, due in part to the
inhibition of KV current that
occurred via activation of the phospholipase C-protein kinase C signal
transduction pathway.
potassium ion; protein kinase C; membrane potential; patch clamp
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