Potassium channels in vascular smooth muscle: a pathophysiological and pharmacological perspective

Abstract Potassium (K + ) ion channel activity is an important determinant of vascular tone by regulating cell membrane potential ( MP ). Activation of K + channels leads to membrane hyperpolarization and subsequently vasodilatation, while inhibition of the channels causes membrane depolarization and then vasoconstriction. So far five distinct types of K + channels have been identified in vascular smooth muscle cells ( VSMC s): Ca +2 ‐activated K + channels ( BK C a ), voltage‐dependent K + channels ( K V ), ATP ‐sensitive K + channels ( K ATP ), inward rectifier K + channels (K ir ), and tandem two‐pore K + channels (K 2 P). The activity and expression of vascular K + channels are changed during major vascular diseases such as hypertension, pulmonary hypertension, hypercholesterolemia, atherosclerosis, and diabetes mellitus. The defective function of K + channels is commonly associated with impaired vascular responses and is likely to become as a result of changes in K + channels during vascular diseases. Increased K + channel function and expression may also help to compensate for increased abnormal vascular tone. There are many pharmacological and genotypic studies which were carried out on the subtypes of K + channels expressed in variable amounts in different vascular beds. Modulation of K + channel activity by molecular approaches and selective drug development may be a novel treatment modality for vascular dysfunction in the future. This review presents the basic properties, physiological functions, pathophysiological, and pharmacological roles of the five major classes of K + channels that have been determined in VSMC s.