Myogenic regulation of arterial diameter:: role of potassium channels with a focus on delayed rectifier potassium current

The phenomenon of myogenic constriction of arterial resistance vessels in response to increased intraluminal pressure has been known for over 100 years, yet our understanding of the molecular mechanisms involved remains incomplete. The focus of this paper concerns the potassium (K+) channels that provide a negative feedback control of the myogenic depolarization of vascular smooth muscle cells that is provoked by elevations in intraluminal pressure, and specifically, the contribution of delayed rectifier (K-DR) channels. Our knowledge of the important role played by K-DR channels, as well as their molecular identity and acute modulation via changes in gating, has increased dramatically in recent years. Several lines of evidence point to a crucial contribution by heteromultimeric K(V)1 subunit-containing K-DR channels in the control of arterial diameter and myogenic reactivity, but other members of the K-V superfamily are also expressed by vascular myocytes, and less is known concerning their specific functions. The effect of pharmacological modulation of K-DR channels is discussed, with particular reference to the actions of anorexinogens on K(V)1- and K(V)2-containing K-DR channels. Finally, the need for a greater understanding of the mechanisms that control K-DR channel gene expression is stressed in light of evidence indicating that there is a reduced expression of K-DR channels in diseases associated with abnormal myogenic reactivity and vascular remodelling.