Effect of thyroid hormone on Mg(2+) homeostasis and extrusion in cardiac cells.
The present study investigated the effect of alteration in thyroid hormone level on Mg(2+) homeostasis in cardiac ventricular myocytes. Hyperthyroid conditions increased cardiac myocytes total Mg(2+) content by ~14% as compared to cells from eu-thyroid animals. The excess Mg(2+) was localized predominantly within cytoplasm and mitochondria, and was mobilized into the extracellular compartment by addition of isoproterenol (ISO) or cAMP but not phenylephrine (PHE). Hypothyroid conditions, instead, decreased cardiac myocytes total Mg(2+) content by ~10% as compared to cells from eu-thyroid animals. Also in this case, cytoplasm and mitochondria were the two cellular pools predominantly affected. Under hypothyroid conditions, administration of ISO or cAMP resulted in a decreased Mg(2+) extrusion as compared to that observed in cardiac cells from eu-thyroid animals. Similar changes in cellular Mg(2+) content and transport were observed in cardiac ventricular myocytes isolated from hyper- and hypo-thyroid animals, as well as in cultures of H9C2 cells rendered hyper- or hypo-thyroid under in vitro conditions. Supplementation of thyroid hormone to hypothyroid animals restored Mg(2+) level and transport to levels comparable to those observed in eu-thyroid animals. Taken together, these results indicate that changes in thyroid hormone level have a major effect on Mg(2+) homeostasis and compartmentation in cardiac cells. The enlarged Mg(2+) mobilization via beta- but not alpha(1)-adrenergic receptor stimulation further suggests that beta- and alpha(1)-adrenergic receptors target selectively different Mg(2+) compartments within the cardiac myocyte. These results provide a new rationale to interpret changes in cardiac function under hyper- or hypo-thyroid conditions.
Ballard
Brandon
B
School of Medicine-Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106-4970, USA.
Torres
Lisa M
LM
Romani
Andrea
A
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002451:Cell Compartmentation / Q000187:drug effects; D002469:Cell Separation; D000242:Cyclic AMP / Q000494:pharmacology; D006706:Homeostasis / Q000187:drug effects*; D007037:Hypothyroidism / Q000378:metabolism; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism*; D010477:Perfusion; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013963:Thyroid Hormones / Q000494:pharmacology*; D014284:Triiodothyronine / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D013963:Thyroid Hormones; D014284:Triiodothyronine; D010656:Phenylephrine; D000242:Cyclic AMP; D008274:Magnesium; D007545:Isoproterenol