This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Choi, J. Articles by Hester, R. L. Search for Related Content PubMed PubMed Citation Articles by Choi, J. Articles by Hester, R. L. Related Collections Endothelium/vascular type/nitric oxide Cell signalling/signal transduction

(Hypertension. 2002;39:581.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Calcium-Dependent Synthesis of Prostacyclin in ATP-Stimulated Venous Endothelial Cells

Jaehwa Choi; Leah W. Hammer; Robert L. Hester

From the Department of Physiology and Biophysics, University of Mississippi Medical Center (J.C., L.W.H., R.L.H.), Jackson, Miss.

Correspondence to Dr Robert L. Hester, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216-4505. E-mail rhester{at}physiology.umsmed.edu

Prostacyclin is a powerful vasodilator that is released from vascular endothelial cells. Previous studies in our laboratory have indicated that arachidonic acid metabolites from venous endothelium play an important role in the dilation of adjacent arterioles during muscle stimulation. Furthermore, recent studies have suggested that ATP released from red blood cells during hypoxia stimulates dilation of arterioles. We tested the hypothesis that an ATP-induced increase in intracellular Ca²⁺ in venous endothelium promotes prostacyclin synthesis. Small branches of femoral veins were isolated from male golden hamsters, placed in a 1 mL bath, and cannulated for perfusion with 3-(N-morpholino) propanesulfonic acid (MOPS)-buffered physiological salt solution at 37°C. Prostacyclin synthesis was determined by enzyme immunoassay of bath solution. Perfusion of veins with ATP increased prostacyclin synthesis from 50±5 to 627±46 pg/mL (n=49). ATP-induced prostacyclin synthesis was inhibited by removal of extracellular Ca²⁺, chelation of intracellular Ca²⁺ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) (10 µmol/L for 10 minutes), and preincubation with cytosolic phospholipase A₂ (PLA₂) inhibitors, AACOCF₃, and bromoenol lactone. Changes in intracellular Ca²⁺ in cultured human venous endothelial cells were assessed by fura-2 spectrofluorometry. ATP induced a transient Ca²⁺ peak within seconds, and the subsequent Ca²⁺ plateau was abolished by removal of extracellular Ca²⁺. An increase in prostacyclin synthesis was detected in these cells 2 minutes after application of ATP. These findings suggest that the ATP-induced increase in intracellular Ca²⁺ stimulates prostacyclin synthesis in venous endothelial cells.

Key Words: microcirculation • prostacyclin • veins • endothelium

This article has been cited by other articles:

				L. W. Hammer, C. R. Overstreet, J. Choi, and R. L. Hester ATP stimulates the release of prostacyclin from perfused veins isolated from the hamster hindlimb Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2003; 285(1): R193 - R199. [Abstract] [Full Text] [PDF]