| 10926549 |
Sham JS, Crenshaw BR Jr, Deng LH, Shimoda LA, Sylvester JT: Effects of hypoxia in porcine pulmonary arterial myocytes: roles of K (V) channel and endothelin-1. Am J Physiol Lung Cell Mol Physiol. 2000 Aug;279(2):L262-72.
Effects of acute hypoxia on intracellular Ca (2+) concentration ([Ca (2+)](i)) and cell length were recorded simultaneously in proximal and distal pulmonary (PASMCs) and femoral (FASMCs) arterial smooth muscle cells. Reducing PO (2) from normoxia to severe hypoxia (PO (2) < 10 mmHg) caused small but significant decreases in length and a reversible increase in [Ca (2+)](i) in distal PASMCs and a small decrease in length in proximal PASMCs but had no effect in FASMCs, even though all three cell types contracted significantly to vasoactive agonists. Inhibition of voltage-dependent K (+) (K (V)) channel with 4-aminopyridine produced a greater increase in [Ca (2+)](i) in distal than in proximal PASMCs. In distal PASMCs, severe hypoxia caused a slight inhibition of K (V) currents; however, it elicited further contraction in the presence of 4-aminopyridine. Endothelin-1 (10 (-10) M), which itself did not alter cell length or [Ca (2+)](i), significantly potentiated the hypoxic contraction. These results suggest that hypoxia only has small direct effects on porcine PASMCs. These effects cannot be fully explained by inhibition of K (V) channels and were greatly enhanced via synergistic interactions with the endothelium-derived factor endothelin-1. |
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