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Department of Physiology, University of Virginia, Charlottesville, Virginia 22903; Department of Physiology, University Autonoma de San Luis Potosi, 78210 San Luis Potosi; and the Instituto Politecnico Nacional de Mexico, Mexico City, DF 11340 Mexico
Coronary flow regulates cardiac
functions, and it has been suggested that endothelial membrane
glycosylated proteins are the primary shear stress mechanosensors. Our
hypothesis was that if these proteins are the sensors for flow, then
intracoronary perfusion of lectins or specific antibodies should
differentially depress coronary flow-enhanced responses of different
parenchymal cell types such as auricular-ventricular (A-V) nodal cells
(dromotropic effect), contractile myocytes (inotropic effect), and
junctional Purkinje-muscle cells (spontaneous ventricular rhythm). The
coronary flow stimulatory effects on A-V delay and spontaneous
ventricular rhythm were selectively depressed by six of eight lectins.
None of the lectins depressed the coronary flow inotropic effect.
Antibodies against endothelial surface proteins,
v
5-integrin
and sialyl-Lewisb glycan,
depressed the dromotropic but not the inotropic effects of coronary
flow, whereas the vascular cell adhesion molecule 1 antibody had no
effect on the dromotropic, but enhanced the inotropic, effect. The fact
that lectins and antibodies differentially depressed regional coronary
flow effects suggests that there is a chemical distinctiveness in their
intravascular endothelial cell surfaces. However, nonselective
cross-linking of endothelial glycocalyx proteins with 2,000-kDa
dextran-aldehyde or vitronectin indistinctively depressed the
dromotropic and inotropic effects of coronary flow. These results
indicate that coronary flow-induced stress acts on specific structures
located in the capillary intravascular membrane glycocalyx.
mechanical transmission-transduction; shearing forces; extracellular matrix molecules; mechanosensors; endothelial extracellular mediators; glycoproteins; capillary perfusion; intravascular endothelial glycoproteins
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