In:
American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 280, No. 6 ( 2001-06-01), p. L1138-L1147
Abstract:
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 (K V ) and inward rectifier (K ir ) 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 Ba 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 K V , K ir , and large-conductance Ca 2+ -sensitive K + channels are present in PVs. Immunohistochemistry showed that K ir 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 K ir channels, which may modulate venous return both physiologically and in disease states including pulmonary edema.
Type of Medium:
Online Resource
ISSN:
1040-0605
,
1522-1504
DOI:
10.1152/ajplung.2001.280.6.L1138
Language:
English
Publisher:
American Physiological Society
Publication Date:
2001
detail.hit.zdb_id:
1013184-X
detail.hit.zdb_id:
1477300-4
SSG:
12
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