Intracellular and extracellular calcium utilization during hypoxic vasoconstriction of cyclostome aortas

Abstract

Hypoxic vasoconstriction (HV) is an intrinsic response of mammalian pulmonary and cyclostome aortic vascular smooth muscle. The present study examined the utilization of calcium during HV in dorsal aortas (DA) from sea lamprey and New Zealand hagfish. HV was temporally correlated with increased free cytosolic calcium (Ca[Formula: see text]) in lamprey DA. Extracellular calcium (Ca[Formula: see text]) did not contribute significantly to HV in lamprey DA, but it accounted for 38.1 ± 5.3% of HV in hagfish DA. Treatment of lamprey DA with ionomycin, ryanodine, or caffeine added to thapsigargin-reduced HV, whereas HV was augmented by BAY K 8644. Methoxyverapamil (D600) in zero Ca[Formula: see text] did not affect HV in lamprey DA, nor did it prevent further constriction when Ca[Formula: see text] was restored during hypoxia in hagfish DA. Removal of extracellular sodium (Na[Formula: see text]) caused a constriction in both species. Lamprey DA relaxed to prehypoxic tension following return to normoxia in zero Na[Formula: see text], whereas relaxation was inhibited in hagfish DA. Relaxation following HV was inhibited in lamprey DA when Na[Formula: see text] and Ca[Formula: see text] were removed. These results show that HV is correlated with [Ca2+]c in lamprey DA and that Na+/Ca2+ exchange is used during HV in hagfish but not lamprey DA. Multiple receptor types appear to mediate stored intracellular calcium release in lamprey DA, and L-type calcium channels do not contribute significantly to constriction in either cyclostome.