Potassium channels regulate tone in rat pulmonary veins

Intrapulmonary veins (PVs) contribute to pulmonary vascular resistance, but the mechanisms controlling PV tone are poorly understood. Although smooth muscle cell (SMC) [K.sup.+] channels regulate tone in most vascular beds, their role in PV tone is unknown. We show that voltage-gated (Kv) and inward rectifier ([K.sub.ir]) [K.sup.+] channels control resting PV tone in the rat. PVs have a coaxial structure, with layers of cardiomyocytes (CMs) arrayed externally around a subendothelial layer of typical SMCs, thus forming spinchterlike structures. PVCMs have both an inward current, inhibited by low-dose [Ba.sup.2+], and an outward current, inhibited by 4-aminopyridine. In contrast, PVSMCs lack inward currents, and their outward current is inhibited by tetraethylammonium (5 mM) and 4-aminopyridine. Several Kv, [K.sub.ir], and large-conductance [Ca.sup.2+]-sensitive [K.sup.+] channels are present in PVs. Immunohistochemistry showed that [K.sub.ir] channels are present in PVCMs and PV endothelial cells but not in PVSMCs. We conclude that [K.sup.+] channels are present and functionally important in rat PVs. PVCMs form sphincters rich in [K.sub.ir] channels, which may modulate venous return both physiologically and in disease states including pulmonary edema. inward rectifier potassium channels; voltage-gated potassium channels; venous tone; pulmonary circulation; pulmonary edema