ABSTRACT
In order to explore the mechanism of cardiac damage by PTH, the release of PGI2 from heart cells was measured. The results showed that bPTH ( 1-34) increased the release of 6-keto-PGFla from heart cells in a dose dependent manner. Calcium inophone A23187 also increased the 6-keto-PGF1? release, while EDTA and verapamil reduced it. These suggest that the PGI2 synthesis in heart cells was affected by intra and extracellular calcium. The significance of bPTH( 1-34) induced increase of PGI2 synthesis might be associated with interference of energy metabolism, and then, cell damage.
ABSTRACT
In order to obtain some evidences of the role of parathyroid hormone (PTH) in regulating calcium metabolism, and explore the mechanisms by which PTH regulates calcium in the heart, 45Ca was used to study the influence of bovine PTH1-34 fragment (bPTH1-34) on calcium transsacolemma. The results indicate that bPTH1-34(l?I0-7mol ? L-1) increases beating rate of heart cells under normal state and it markedly increases the rapid (5 min) and the slow (120 min) phases of 45Ca influx in heartcells (under normal, KC1 10-5 mol?L-1 high K+depolarised, NA 10-7mol?L-1receptors activated states), but it could also reduce 45Ca efflux from the cultured heart cells. It suggests that the mechanisms caused by bPTH1-34 which enhances the cytosolic calcium concentration and myocardial beating rate may be related with cAMP level elevated in heart cells.