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1 Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen; 2 Abteilung für Pathophysiologie, Universitätsklinikum Essen, D-45122 Essen; and 3 Abteilung für Innere Medizin, Universitätsklinikum Giessen, D-35392 Giessen, Germany
10.1152/ajpheart.00925. 2001.
Parathyroid hormone-related peptide (PTHrP) is expressed
throughout the cardiovascular system and is able to dilate vessels.
This study investigated 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 anesthetized pigs. In vitro, PTHrP release from
saline-perfused rat hearts was strongly correlated with coronary flow
(r = 0.84). Increasing coronary flow from 5 to 10 ml/min increased PTHrP release from 442 ± 42 to 1,563 ± 167 pg/min. Increasing the viscosity of the perfusate did not change basal
PTHrP release. Increasing flow without a concomitant increase in
pressure did not lead 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 that 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 the PTHrP release rate. Bradykinin in the presence of
constant pressure increased PTHrP release, probably by increasing the
intracellular calcium concentration in coronary endothelial cells. In
summary, mechanical forces evoked by blood flow can trigger a constant PTHrP release.
shear stress; endothelium; nitric oxide
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