EFFECTS OF HYPOXIA AND OTHER VASOACTIVE AGENTS ON PULMONARY AND CEREBRAL-ARTERY SMOOTH-MUSCLE CELLS

Smooth muscle cells (SMC) were isolated from cat cerebral arteries and three sizes of pulmonary artery (<200-, 200-to 600-, and >800-mum diameter) and used within 72-96 h. Change in cell length in response to hypoxia and other vasoactive agents was measured in a specially constructed cell chamber on an inverted microscope. Pulmonary artery SMC responded to hypoxia differently according to artery size. SMC from <200-and 200- to 600-mum-diameter pulmonary arteries shortened 18.6 +/- 4.85 and 24.2 +/- 2.70%, respectively. However, SMC from >800-mum-diameter pulmonary arteries shortened 0.81 +/- 0.44%. Cerebral artery SMC plated on a flexible polydimethyl siloxane membrane showed loss of tension during exposure to hypoxia. The shortening of SMC from the 200- to 600-mum pulmonary arteries was accompanied by myosin phosphorylation. SMC from >800-mum-diameter pulmonary arteries and cerebral arteries contained myosin that did not phosphorylate during hypoxia. The SMC from both artery types responded to norepinephrine, serotonin, prostaglandin F2alpha, and indomethacin and exhibited alpha-adrenergic receptor population patterns similar to those of intact arteries. The pattern of hypoxic responses exhibited by these nondedifferentiated pulmonary and cerebral artery SMC supports the idea that, at least in the cat, the hypoxic sensor is located within the SMC.