AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 281: H2480-H2489, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 6, H2480-H2489, December 2001

Angiotensin II inhibits and alters kinetics of voltage-gated K+ channels of rat arterial smooth muscle

Y. Hayabuchi, N. B. Standen, and N. W. Davies

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-epsilon translocation inhibitor peptide. These results demonstrate that ANG II inhibits KV channels through both activation of PKC-epsilon and inhibition of PKA.

potassium channel; activation; inactivation; protein kinase A; protein kinase C


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