title: Thyroid hormones differentially affect sarcoplasmic reticulum function in rat atria and ventricles.
abstract: The present study was undertaken to compare the effects of hypothyroidism and hyperthyroidism on sarcoplasmic reticulum (SR) Ca(2+)-pump activity, together with assessment of the functional role of SR in providing activator Ca2+ under these altered thyroid states. In response to a shift from hypothyroid to hyperthyroid state, a 10 fold and 2 fold increase in SR Ca(2+)-pump activity in atria and ventricles, respectively, were observed. This was associated with the 8-9 fold increases in atrial contractility (+dT/dt) and relaxation (-dT/dt), but only with a 3-4 fold increase in their ventricular counterparts. Also, the recirculation fraction of activator Ca2+ (RFA) increased to a far greater extent in atria (4 fold) than in papillary muscles, and the relative increment in inhibition of developed tension by ryanodine became 3 times larger in atria than in papillary muscles. A positive force-frequency relationship (FFR) was observed in hypothyroid atria, whereas the hyperthyroid atria, hypothyroid and hyperthyroid papillary muscles showed a negative FFR. These results suggest the greater role of transsarcolemmal (SL) Ca2+ and smaller role of SR Ca2+ in activating contraction in hypothyroid atria compared to other preparations. Thyroid hormones decrease the contribution of SL and increase that of SR in providing activator Ca2+ to the greater extent in atria than in ventricles. This effect of thyroid hormones is based on larger stimulation of SR Ca(2+)-pump in atria compared to ventricles.
authors.affiliation: Department of Pathophysiology, University of Tartu, Estonia.
authors.forename: A
authors.initials: A
authors.lastname: Kaasik
authors.forename: A
authors.initials: A
authors.lastname: Minajeva
authors.forename: K
authors.initials: K
authors.lastname: Paju
authors.forename: M
authors.initials: M
authors.lastname: Eimre
authors.forename: E K
authors.initials: EK
authors.lastname: Seppet
mesh_terms: D008841:Actin Cytoskeleton / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000187:drug effects* / Q000502:physiology; D002316:Cardiotonic Agents; D005260:Female; D006321:Heart / Q000187:drug effects*; D006325:Heart Atria / Q000187:drug effects / Q000378:metabolism; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism; D006980:Hyperthyroidism / Q000139:chemically induced / Q000503:physiopathology*; D007037:Hypothyroidism / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D010210:Papillary Muscles / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012433:Ryanodine / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000187:drug effects* / Q000502:physiology; D013268:Stimulation, Chemical; D013963:Thyroid Hormones / Q000494:pharmacology*
chemical_list: D002316:Cardiotonic Agents; D013963:Thyroid Hormones; D012433:Ryanodine; D000252:Calcium-Transporting ATPases; D002118:Calcium