HUMAN PARATHYROID-HORMONE DILATES BOTH PIG CORONARY AND HUMAN INFERIOR EPIGASTRIC ARTERIES BY A CYCLIC-AMP-DEPENDENT PATHWAY

Human parathyroid hormone (hPTH (1-38)) induced concentration-dependen t relaxations in Prostaglandin F2alpha-preconstricted pig coronary art eries in vitro. Removal of endothelial cells or pretreatment with nitr o-L-arginine, a specific inhibitor of the endothelium-derived relaxing factor (EDRF) synthesis, impaired, although to a small extent. hPTH-i nduced relaxations. Human PTH-, but not bradykinin- or nitroglycerin-i nduced relaxations were potentiated in the presence of the cyclic AMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Human PTH also relaxed preconstricted human inferior epigastric arteries in vitro. In accordance to pig coronary arteries, this relaxation was pot entiated in the presence of IBMX. However, the human internal thoracic (mammary) artery did not respond to hPTH (1 - 100 nM). Thus, acute va sodilatory effects of hPTH may not be present in all human arteries. T he physiological signficance of this phenomenon is not known. This rel axation, at least in pig arteries, is mediated to a small extent by th e release of EDRF. In addition, this relaxation appears to be mainly m ediated in both pig and human arteries by a smooth muscle cyclic AMP p athway.