Parathyroid hormone causes a transient rise in intracellular ionized calcium in vascular smooth muscle cells.
The effect of parathyroid hormone on intracellular calcium concentration in vascular smooth muscle cells in culture was studied. Human PTH 1-34 (hPTH (1-34)) caused a transient rise in intracellular calcium in a dose-dependent manner at physiological concentrations. The effect of PTH was mimicked by dibutyryl cyclic AMP and inhibited by a PTH receptor antagonist. The effect of PTH was increased in parallel with extracellular calcium concentration and a sustained response was observed when extracellular calcium was 2 mM or higher. The PTH action was blocked by nisoldipin, a calcium antagonist, but not by ouabain, a Na, K-ATPase inhibitor. These data indicate that PTH increases intracellular calcium through its receptor via opening calcium channels. A possible role of this effect in the regulation of vascular tone is also discussed.
Kawashima
H
H
Department of Cell Biology, Tsukuba Research Laboratories, Yamanouchi Pharmaceutical Co., Ltd., Ibaraki, Japan.
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002460:Cell Line; D003593:Cytoplasm / Q000378:metabolism; D004533:Egtazic Acid / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D015737:Nisoldipine / Q000494:pharmacology; D010281:Parathyroid Hormone / Q000494:pharmacology*; D051381:Rats
D002121:Calcium Channel Blockers; D010281:Parathyroid Hormone; D015737:Nisoldipine; D004533:Egtazic Acid; D003994:Bucladesine; D002118:Calcium