Intrapulmonary veins (PVs) contribute to pulmonary vascular resistance, but
the mechanisms controlling PV tone are poorly understood. Although smooth
muscle cell (SMC) K+ channels regulate tone in most vascular beds, their ro
le in PV tone is unknown. We show that voltage-gated (K-V) and inward recti
fier (K-ir) K+ channels control resting PV tone in the rat. PVs have a coax
ial structure, with layers of cardiomyocytes (CMs) arrayed externally aroun
d a subendothelial layer of typical SMCs, thus forming spinchterlike struct
ures. PVCMs have both an inward current, inhibited by low-dose Ba2+, and an
outward current, inhibited by 4-aminopyridine. In contrast, PVSMCs lack in
ward currents, and their outward current is inhibited by tetraethylammonium
(5 mM) and 4-aminopyridine. Several K-V, K-ir, and large-conductance Ca2+-
sensitive K+ channels are present in PVs. Immunohistochemistry showed that
K-ir channels are present in PVCMs and PV endothelial cells but not in PVSM
Cs. We conclude that K+ channels are present and functionally important in
rat PVs. PVCMs form sphincters rich in K-ir channels, which may modulate ve
nous return both physiologically and in disease states including pulmonary
edema.