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Articles in PresS, published online ahead of print August 22, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00071.2002
Submitted on February 15, 2002
Accepted on August 19, 2002
1 Center for Cardiovascular Diseases, Texas Southern University, College of Pharmacy and Health Sciences, Houston, Texas, USA
2 Physiology, University of Tennessee Health Science Center, Laboratory for Research in Neonatal Physiology, Memphis, Tennessee, USA
* To whom correspondence should be addressed. E-mail: yakubu_ma{at}tsu.edu.
We have investigated the role of [Ca2+]i in endothelin-1 (ET-1) production, effects of potential vasospastic agents on [Ca2+]i, and the presence of L-type voltage-dependent Ca2+-channels in cerebral microvascular endothelial cells. Primary cultures of endothelial cells isolated from piglet cerebral microvessels were established and used in these studies. To investigate the role of extracellular Ca2+ in vasoactive agents induced ET-1 biosynthesis, confluent cells were washed with PBS and exposed to either the thromboxane receptor agonist U-46619 (1 µM), 5-hydroxytryptamine (5-HT; 0.1 mM), or lysophosphatidic acid (LPA; 1 µM) alone or following pretreatment with the Ca2+-chelating agent ethylenediaminetetraacetic acid (EDTA; 100 mM), the L-type Ca2+-channel blocker verapamil (10 µM), or the antagonist of receptor operated Ca2+-channel SKF 96365 HCL (10 µM) for 15 min. ET-1 levels were elevated from 1.2±0.2 (control) to 8.2±2.7 (U-46619), 4.9±1 (5-HT), or 3.9±1.9 (LPA) fmol/µg protein, respectively. Such elevated ET-1 biosynthesis was attenuated following pretreatment of cells with verapamil, EDTA, or SKF 96365 HCL. To investigate the presence of L-type voltage-dependent Ca2+-channels in endothelial cells, the [Ca2+]i signal was determined by fluorimetric measurement using the Ca2+ indicator Fura-2 AM. Superfusion of confluent endothelial cells with U-46619, 5-HT, or LPA significantly increased [Ca2+]i. Pretreatment of endothelial cells with high K+ (60 mM) or the L-type voltage-sensitive Ca2+-channel blocker nifedipine (4 µM) diminished increases in [Ca2+]i induced by the vasoactive agents. The results from these studies indicate that: 1) elevated [Ca2+]i signals are involved in ET-1 biosynthesis induced by specific spasmogenic agents, 2) the increases in [Ca2+]i induced by the vasoactive agents tested involve receptor- as well as L-type voltage-dependent Ca2+-channels, and primary cultures of cerebral microvascular endothelial cells express L-type voltage-dependent Ca2+-channels. Thus, increases in [Ca2+]i occur via activation of potential driven and/ or L-type voltage-dependent Ca2+-channels and may play significant roles in the modification of cerebral microvascular reactivity and modulation of endothelial functions.
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