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Ion Channel Group, Department of Cell Physiology and Pharmacology, University of Leicester, Leicester LE1 9HN, United Kingdom
The
vasoconstrictor angiotensin II (ANG II) inhibits several types of
K+ channels. We examined the inhibitory mechanism of ANG II
on voltage-gated K+ (KV) currents
(IKV) recorded from isolated rat
arterial smooth muscle using patch-clamp techniques. Application of 100 nM ANG II accelerated the activation of
IKV but also caused inactivation. These effects were abolished by the AT1 receptor antagonist
losartan. The protein kinase A (PKA) inhibitor Rp-cyclic 3',5'-hydrogen phosphothioate adenosine (100 µM) and an analog of diacylglycerol, 1,2-dioctanyoyl-rac-glycerol (2 µM), caused a significant reduction of IKV. Furthermore, the combination
of 5 µM PKA inhibitor peptide 5-24 (PKA-IP) and 100 µM protein
kinase C (PKC) inhibitor peptide 19-27 (PKC-IP) prevented the
inhibition by ANG II, although neither alone was effective. The ANG II
effect seen in the presence of PKA-IP remained during addition of the
Ca2+-dependent PKC inhibitor Gö6976 (1 µM) but was
abolished in the presence of 40 µM PKC-
translocation inhibitor
peptide. These results demonstrate that ANG II inhibits KV
channels through both activation of PKC- and inhibition of PKA.
potassium channel; activation; inactivation; protein kinase A; protein kinase C
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