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1 Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, and 2 Augusta Veterans Affairs Medical Center, Augusta, Georgia 30912; 3 Yale University School of Medicine, New Haven, Connecticut 06520; and the 4 University of Virginia, Charlottesville, Virginia 22908
Acute parathyroid hormone exposure induces vascular smooth muscle relaxation. In contrast, continuous infusion of parathyroid hormone leads to vasoconstriction and an elevation of blood pressure. Despite the known effects of parathyroid hormone on vascular smooth muscle, possible direct effects on the vascular endothelium have not previously been investigated. Using a human umbilical vein endothelial cell line, we found that parathyroid hormone increased both intracellular calcium and cellular cAMP content in these endothelial cells. Furthermore, exposure of these cells to increasing concentrations of parathyroid hormone stimulated both [3H]thymidine incorporation and endothelin-1 secretion. Parathyroid hormone/parathyroid hormone-related peptide receptor mRNA could be detected at low levels in these cells. In summary, these data demonstrate that endothelium-derived cells contain functional parathyroid hormone receptors. The potential physiological role of these receptors remains to be determined.
endothelial cells; intracellular calcium; adenosine 3',5'-cyclic monophosphate; parathyroid hormone
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