Abstract

Exposure to hypoxia caused an increase in the hematocrit and right heart weight of experimental rats, but did not affect calcium-45 uptake by pulmonary arterial smooth muscle cells. However, autoradiographic studies showed that hypoxia apparently caused a shift of 45-Ca from primarily extracellular sites in arteries of control rats to intracellular sites in tissues of hypertensive rats. Cytochemical studies of calcium distributions in pulmonary arterial smooth muscle cells support the autoradiographic data and show that in both rats and swine the majority of pyroantimonate granules occur extracellularly in control tissues. In contrast, hypoxic tissues displayed a greatly reduced number of granules in extracellular sites and an increase in the amount of precipitate in intracellular sites. In pulmonary arterial smooth muscle cells from hypoxic rats most of the precipitate was associated with the caveolae intracellulares, while in corresponding cells from hypoxic swine the majority of the pyroantimonate granules were localized to the sarcoplasmic reticulum. Hypoxia may produce pulmonary hypertension by interfering with the ability of the arterial smooth muscle cells to maintain transmembrane ionic gradients, thus producing an effective increase in cytoplasmic calcium levels. The increased calcium may then activate the contractile apparatus to produce a sustained vasoconstriction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47664/1/441_2004_Article_BF00223235.pd

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