Responses of systemic vascular smooth muscle to hypoxia.

The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical activity, which has been shown not to be a simple deprivation of aerobic processes. Strips of rat portal vein (RPV), rabbit ear artery (REA) and rabbit common carotid artery (RCC) were studied under isotonic conditions, contracted by 10(-6) noradrenaline (NA). Reduction of Po2 to less than 3KPa during NA constraction led to relaxation which was rapid and 90% complete in RPV, rapid and 60% in REA: the relaxation began when tissue Po2 was decreasing and was not lower than 5.5 K Pa. RCC responded slowly and only some strips relaxed. The rapidity and magnitude of relaxation for each type of vessel was comparable to that produced by removal of external calcium. Also for any one type of VSM the response to NA was abolished or diminished to a similar extent by preliminary exposure to hypoxia, or by preliminary removal of calcium. Preliminary hypoxia diminished 50 mmol.1(-1) K+ contractions as much as it diminished NA contractions. Preliminary 1-2 hour exposure to hyperoxia diminished the subsequent relaxant effect of hypoxia. Inhibition of glycolysis (iodoacetic acid) had no effect on normoxic NA contraction or on hypoxic relaxation, but prevented or diminished the subsequent recovery on reoxygenation. Low oxygen tension appears to act in VSM as though it interferes with net influx or utilisation of external calcium.