Acute hypoxia increases cytosolic calcium in fetal pulmonary artery smooth muscle cells
Cornfield, D.N.; Stevens, T.; McMurtry, I.F.; Abman, S.H.; Rodman, D.M.
American Journal of Physiology 265(1 Pt 1): L53-L56
1993
ISSN/ISBN: 0002-9513 PMID: 8338182 Document Number: 416272
We studied the effect of acute hypoxia on the cytosolic calcium concentration ((Ca-2+)-i) of fetal vascular smooth muscle cells (SMC) from late gestation fetal lambs. We tested the following hypotheses: 1) fetal pulmonary artery (PA) SMC sense hypoxia; 2) hypoxia stimulates transmembrane Ca-2+ influx causing increased basal (Ca-2+)-i and Ca-2+ responses to pharmacological vasoconstrictors; and 3) the response is unique to SMC from small (near resistance) PA. Fetal SMC were isolated from the proximal and distal pulmonary (DPA) and carotid arteries of late-gestation ovine fetuses, maintained in culture for 5-14 days prior to study, and studied with dual-excitation microfluorimetry using fura 2. Acute hypoxia caused a 233% increase in (Ca-2+)-i in distal PA SMC (P lt 0.01), which was absent in low extracellular calcium bath. (Ca-2+)-i increased transiently in normoxic DPA SMC treated with angiotensin II, and oscillations in (Ca-2+)-i occurred (amplitude gtoreq 30 nM). In hypoxic DPA SMC the increase in (Ca-2+)-i was sustained and oscillations were attenuated or absent. (Ca-2+)-i in proximal PA SMC did not change with exposure to acute hypoxia and carotid artery SMC (Ca-2+)-i decreased by 13% (P lt 0.05). We conclude that fetal SMC isolated from the DPA of late-gestation ovine fetuses directly sense decreased oxygen tension with an increase in (Ca-2+)-i that is dependent on the entry of extracellular Ca-2+.