Tri-Iodothyronine Increases Intra-Cellular Calcium Levels in Single Rat Myocytes

Lomax, Richard B.; Cobbold, P H; Allshire, Ashley; Cuthbertson, K. S. R.; Robertson, W. R.

doi:10.1677/jme.0.0070077

Cited by 23 publications

(6 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Most known effects involve calcium membrane transport or [Ca 2+ ] i , as shown for effects of triiodothyronine in thymocytes (110), rat liver cells (51), red blood cells lacking a nucleus (30), and rat myocytes (69). The similarity of these effects to rapid effects of steroid hormones is striking, and common distal pathways of intracellular activation may be involved for the two types of hormones.…”

Section: Triiodothyroninementioning

confidence: 99%

Specific, Nongenomic Actions of Steroid Hormones

Wehling

1997

Annu. Rev. Physiol.

622

336

View full text Add to dashboard Cite

Traditionally, steroid hormone action has been described as the modulation of nuclear transcription, thus triggering genomic events that are responsible for physiological effects. Despite early observations of rapid steroid effects that were incompatible with this theory, nongenomic steroid action has been widely recognized only recently. Evidence for these rapid effects is available for steroids of all clones and for a multitude of species and tissues. Examples of nongenomic steroid action include rapid aldosterone effects in lymphocytes and vascular smooth muscle cells, vitamin D3 effects in epithelial cells, progesterone action in human sperm, neurosteroid effects on neuronal function, and vascular effects of estrogens. Mechanisms of action are being studied with regard to signal perception and transduction, and researchers have developed a patchy sketch of a membrane receptor-second messenger cascade similar to those involved in catecholamine and peptide hormone action. Many of these effects appear to involve phospholipase C, phosphoinositide turnover, intracellular pH and calcium, protein kinase C, and tyrosine kinases. The physiological and pathophysiological relevance of these effects is unclear, but rapid steroid effects on cardiovascular, central nervous, and reproductive functions may occur in vivo. The cloning of the cDNA for the first membrane receptor for steroids should be achieved in the near future, and the physiological and clinical relevance of these rapid steroid effects can then be established.

show abstract

Section: Triiodothyroninementioning

confidence: 99%

Specific, Nongenomic Actions of Steroid Hormones

Wehling

1997

Annu. Rev. Physiol.

622

336

View full text Add to dashboard Cite

show abstract

“…There is now increasing evidence that Ca2+ serves as the first messenger for the prompt and plasma membrane-mediated action of T3 in several cell types both in vitro (30,31) and in vivo (32). It has even been demonstrated that T3 increases Ca2+ uptake in rat cardiocytes by phosphorylating Ca2+ channels on the membrane (33).…”

Section: Effects Of Amiodarone (Am)mentioning

confidence: 99%

Dihydropyridine-like effects of amiodarone and desethylamiodarone on thyrotropin secretion and intracellular calcium concentration in rat pituitary

Roussel

Grazzini²,

Guipponi³

et al. 1995

European Journal of Endocrinology

View full text Add to dashboard Cite

Amiodarone (AM) and its major metabolite desethylamiodarone (DEA) are structurally similar to biologically active thyroid hormones. Amiodarone therapy is frequently associated with impairment of thyrotropic function, whose mechanisms are still controversial. Besides its effect on nuclear thyroid hormone binding. AM is able to displace dihydropyridine (DH) binding on membrane preparations from several tissues. By perifusing rat pituitary fragments and measuring thyrotropin (TSH) release we examined: the effect of AM on Ca(2+)-dependent and DHP-sensitive potentiation of the TSH response to thyrotropin-releasing hormone (TRH) induced by either triiodothyronine (T3, perifused for only 30 min before a TRH pulse) or by the prepro-TRH peptide 160-169 (PS4); and the effect of DEA on TRH-induced TSH response in the presence or absence of the DHP nifedipine. We show that AM reverses T3 or PS4 potentiation of the TSH response to TRH; this effect is specific because AM does not modify ionomycin potentiation of that response. In contrast, DEA significantly potentiates the TSH response to TRH and the DHP nifedipine reverses that potentiation. We also tested whether AM would change the acute T3-induced increase in intracellular Ca2+ concentration by measuring intracellular Ca2+ ([Ca2+])i with fura-2 imaging on primary cultures of pituitary cells. We show that AM reverses the effect of T3 on [Ca2+]i as well as the PS4-induced increase in [Ca2+]i. In contrast, DEA increases [Ca2+]i and nifedipine reverses this effect. Our results suggest that AM and DEA display DHP-like effects on TRH-induced TSH release, behaving either as a Ca2+ channel blocker (AM) or as a Ca2+ channel agonist (DEA).

show abstract

“…The results shown here were the means ±sem for four experi¬ ments. This figure shows that neither T2 nor T3 caused a significant increase in PDH activity in heart mitochondria after 30 thymocytes, myocytes and perfused liver, but this effect may be transient (7,9,18,29) T2. The rats used in the experiments reported here had been made hypothyroid by treatment with PTU, which inhibits 5'-iodothyronine deiodinases (21).…”

Section: Effects Of Thyroid Hormones On Pyruvate Dehydrogenase Activitymentioning

confidence: 82%

Studies on the rapid stimulation of mitochondrial respiration by thyroid hormones

O'Reilly

Murphy

1992

Acta Endocrinologica

View full text Add to dashboard Cite

Injection of L-3,5-diiodothyronine (T2) into rats made hypothyroid by 6-n-propyl-2-thiouracil (PTU) increased the respiration rates of subsequently isolated liver mitochondria; this stimulation of respiration by T2 occurred in the presence of cycloheximide and is therefore independent of protein synthesis on cytoplasmic ribosomes. Injection of T3 into PTU-treated rats had a lesser effect than T2 on the respiration rates of subsequently isolated mitochondria; as PTU is an inhibitor of 5\m='\-iodothyronine deiodinases, which convert T3 into T2 in vivo, the rapid stimulation of mitochondrial respiration by T3, which has been shown in a range of systems, may not be due directly to T3 itself, but may be mediated by its deiodination product T2. Injection of T2, or T3, into hypothyroid or euthyroid rats had no effect on the percentage activity of mitochondrial pyruvate hydrogenase assayed 30 min later. The amount of active pyruvate dehydrogenase is regulated by changes in mitochondrial calcium concentration and matrix ATP/ADP ratio; therefore these parameters are not persistently affected by treatment with T3 or T2. In addition, the total amount of pyruvate dehydrogenase present was the same in euthyroid and hypothyroid rats, indicating that the expression of this enzyme is not stringently controlled by thyroid hormone status.

show abstract

Tri-Iodothyronine Increases Intra-Cellular Calcium Levels in Single Rat Myocytes

Cited by 23 publications

References 15 publications

Specific, Nongenomic Actions of Steroid Hormones

Specific, Nongenomic Actions of Steroid Hormones

Dihydropyridine-like effects of amiodarone and desethylamiodarone on thyrotropin secretion and intracellular calcium concentration in rat pituitary

Studies on the rapid stimulation of mitochondrial respiration by thyroid hormones

Contact Info

Product

Resources

About