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Am J Physiol Regul Integr Comp Physiol 279: R860-R873, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 3, R860-R873, September 2000

Cerebral artery sarcoplasmic reticulum Ca2+ stores and contractility: changes with development

Wen Long, Lubo Zhang, and Lawrence D. Longo

Center for Perinatal Biology, Departments of Physiology/Pharmacology and Obstetrics and Gynecology, School of Medicine, Loma Linda University, Loma Linda, California 92350

To test the hypothesis that sarcoplasmic reticulum (SR) Ca2+ stores play a key role in norepinephrine (NE)-induced contraction of fetal and adult cerebral arteries and that Ca2+ stores change with development, we performed the following study. In main branch middle cerebral arteries (MCA) from near-term fetal (~140 days) and nonpregnant adult sheep, we measured NE-induced contraction and intracellular Ca2+ concentration ([Ca2+]i) in the absence and presence of different blockers. In adult MCA, after thapsigargin (10-6 M), the NE-induced responses of tension and [Ca2+]i were 37 ± 5 and 47 ± 7%, respectively, of control values (P < 0.01 for each). In the fetal artery, in contrast, this treatment resulted in no significant changes from control. When this was repeated in the absence of extracellular Ca2+, adult MCA increases in tension and [Ca2+]i were 32 ± 5 and 13 ± 3%, respectively, of control. Fetal cerebral arteries, however, showed essentially no response. Ryanodine (RYN, 3 × 10-6 to 10-5 M) resulted in increases in tension and [Ca2+]i in both fetal and adult MCA similar to that seen with NE. For both adult and fetal MCA, the increased tension and [Ca2+]i responses to RYN were essentially eliminated in the presence of zero extracellular Ca2+. These findings provide evidence that in fetal MCA, in contrast to those in the adult, SR Ca2+ stores are of less importance in NE-induced contraction, with such contraction being almost wholly dependent on Ca2+ flux via plasma membrane L-type Ca2+ channels. In addition, they suggest that in both adult and fetal MCA, the RYN receptor is coupled to the plasma membrane Ca2+-activated K+ channel and/or L-type Ca2+ channel.

cerebrovascular circulation; vascular smooth muscle; sympathetic nervous system; norepinephrine; intracellular calcium; thapsigargin; cyclopiazonic acid; ryanodine; L-type calcium channel; fetus; adult


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