title: PTH, chronic renal failure and myocardium.
abstract: The heart is a target organ for parathyroid hormone (PTH), and the action of this hormone on the myocardium may be mediated through the ability of PTH to increase cytosolic calcium ([Ca2+]i) in the myocardial cells. Such a property of PTH may be responsible for rise in [Ca2+]i in chronic renal failure (CRF). Our study examined these issues. The data from this study showed: (1) PTH increases [Ca2+]i of cardiac myocytes, (2) this action is receptor-mediated and is produced by activation of the L-type calcium channels following stimulation of G protein(s), (3) the rise in [Ca2+]i is due to both augmented entry of calcium into the myocytes and mobilization of calcium from sarcoplasmic reticulum by a calcium-induced calcium release mechanism, (4) CRF is associated with a significant rise in basal levels of [Ca2+]i of cardiac myocytes, (5) this effect is mediated by the state of secondary hyperparathyroidism of CRF, and (6) the pathways through which excess PTH in CRF generates this effect include both increased entry of calcium into cardiac myocytes and decreased exit of this ion out of these cells.
authors.affiliation: Department of Medicine, University of Southern California, School of Medicine, Los Angeles 90033, USA.
authors.forename: M
authors.initials: M
authors.lastname: Smogorzewski
mesh_terms: D000818:Animals; D001481:Basal Metabolism; D002118:Calcium / Q000378:metabolism*; D006321:Heart / Q000187:drug effects; D006961:Hyperparathyroidism / Q000150:complications*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000494:pharmacology / Q000502:physiology*; D010446:Peptide Fragments / Q000494:pharmacology; D051381:Rats; D019379:Teriparatide
chemical_list: D010281:Parathyroid Hormone; D010446:Peptide Fragments; D019379:Teriparatide; D002118:Calcium