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Articles in PresS, published online ahead of print May 30, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00925.2001
Submitted on October 24, 2001
Accepted on May 24, 2002
1 Physiology, Justus-Liebig-Universitat Giessen, Giessen, Germany
2 Pathophysiology, Universitatsklinikum Essen, Essen, Germany
3 Innere Medizin, Universitatsklinikum Giessen, Giessen, Germany
* To whom correspondence should be addressed. E-mail: klaus-dieter.schlueter{at}physiologie.med.uni-giessen.de.
Parathyroid hormone-related peptide (PTHrP) is expressed throughout the cardiovascular system and able to dilate vessels. This study investigates whether mechanical forces generated by changes in regional perfusion influence PTHrP release from the coronary vascular bed. Experiments were performed in vitro on saline perfused rat hearts or isolated coronary endothelial cells exposed to cyclic strain and in vivo in anaesthesized pigs. In vitro, PTHrP release from saline perfused rat hearts strongly correlated to coronary flow (r=0.84). Increasing coronary flow from 5 to 10 ml/min increased PTHrP release from 442±42 to 1563±167 pg/min. Increasing viscosity of the perfusate did not change basal PTHrP release. Increasing flow without a concomitant increase in pressure did not led to an increase in release rate, but reduction in pressure under flow-constant conditions reduced PTHrP release rate. Cyclic strain induced a strain-dependent release of PTHrP from endothelial cells which was inhibited by the addition of a calcium chelating agent. In vivo, there was a net release of PTHrP in the coronary circulation and decreases in coronary flow and pressure decreased PTHrP release rate. Bradykinin in the presence of constant pressure increased PTHrP release, probably via increasing intracellular calcium concentration in coronary endothelial cells. In summary, mechanical forces evoked by blood flow can trigger a constant PTHrP release.
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