TY - JOUR
T1 - Potassium channels regulate tone in rat pulmonary veins
AU - Michelakis, Evangelos D.
AU - Weir, E. Kenneth
AU - Wu, Xichen
AU - Nsair, Ali
AU - Waite, Ross
AU - Hashimoto, Kyoko
AU - Puttagunta, Lakshmi
AU - Knaus, Hans Gunther
AU - Archer, Stephen L.
PY - 2001
Y1 - 2001
N2 - 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 role in PV tone is unknown. We show that voltage-gated (Kv) and inward rectifier (Kir) K+ 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 Ba2+, and an outward current, inhibited by 4-aminopyridine. In contrast, PVSMCs lack inward currents, and their outward current is inhibited by tetraethylammonimn (5 mM) and 4-aminopyridine. Several Kv, Kir, and large-conductance Ca2+-sensitive K+ channels are present in PVs. Immunohistochemistry showed that Kir channels are present in PVCMs and PV endothelial cells but not in PVSMCs. We conclude that K+ channels are present and functionally important in rat PVs. PVCMs form sphincters rich in Kir channels, which may modulate venous return both physiologically and in disease states including pulmonary edema.
AB - 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 role in PV tone is unknown. We show that voltage-gated (Kv) and inward rectifier (Kir) K+ 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 Ba2+, and an outward current, inhibited by 4-aminopyridine. In contrast, PVSMCs lack inward currents, and their outward current is inhibited by tetraethylammonimn (5 mM) and 4-aminopyridine. Several Kv, Kir, and large-conductance Ca2+-sensitive K+ channels are present in PVs. Immunohistochemistry showed that Kir channels are present in PVCMs and PV endothelial cells but not in PVSMCs. We conclude that K+ channels are present and functionally important in rat PVs. PVCMs form sphincters rich in Kir channels, which may modulate venous return both physiologically and in disease states including pulmonary edema.
KW - Inward rectifier potassium channels
KW - Pulmonary circulation
KW - Pulmonary edema
KW - Venous tone
KW - Voltage-gated potassium channels
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U2 - 10.1152/ajplung.2001.280.6.l1138
DO - 10.1152/ajplung.2001.280.6.l1138
M3 - Article
C2 - 11350792
AN - SCOPUS:0034983103
SN - 1040-0605
VL - 280
SP - L1138-L1147
JO - American Journal of Physiology - Lung Cellular and Molecular Physiology
JF - American Journal of Physiology - Lung Cellular and Molecular Physiology
IS - 6 24-6
ER -