Thyroid status and postnatal changes in subsarcolemmal distribution and isoform expression of rat cardiac dihydropyridine receptors

Wibo, Maurice; Féron, Olivier; Zheng, Lei; Maleki, M; Kolář, František; Godfraind, Théophile

doi:10.1016/s0008-6363(97)00228-9

Cited by 13 publications

(3 citation statements)

References 36 publications

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“…Wibo et al. 22 also reported that the maturation of dihydropyridine receptor (a voltage L type calcium channel) was postponed after the induction of hypothyroidism in fetal and neonate rats and induced ionic imbalance in the heart tissue. In addition, Meehan et al 23 reported that thyroid hormone deficiency in fetal life decreased the level of energy in cardiac cells due to the reduction in the expression of cytochrome c oxidase isoforms and vital enzyme for the production of energy in the electron transport chain in the heart tissue during development period.…”

Section: Discussionmentioning

confidence: 99%

Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

Yousefzadeh¹,

Jeddi²,

Alipour³

2016

Arquivos Brasileiros De Cardiologia

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Background:Thyroid hormone deficiency during fetal life could affect the cardiac function in later life. The mechanism underlying this action in fetal hypothyroidism (FH) in rats has not been elucidated thus far.Objective:The aim of this study is to evaluation the effect of FH on cardiac function in male rats and to determine the contribution of α-myosin heavy chain (MHC) and β-MHC isoforms.Methods:Six pregnant female rats were randomly divided into two groups: The hypothyroid group received water containing 6-propyl-2-thiouracil during gestation and the controls consumed tap water. The offspring of the rats were tested in adulthood. Hearts from the FH and control rats were isolated and perfused with langendroff setup for measuring hemodynamic parameters; also, the heart mRNA expressions of α- MHC and β-MHC were measured by qPCR.Results:Baseline LVDP (74.0 ± 3.1 vs. 92.5 ± 3.2 mmHg, p < 0.05) and heart rate (217 ± 11 vs. 273 ± 6 beat/min, p < 0.05) were lower in the FH rats than controls. Also, these results showed the same significance in ±dp/dt. In the FH rats, β-MHC expression was higher (201%) and α- MHC expression was lower (47%) than control.Conclusion:Thyroid hormone deficiency during fetal life could attenuate normal cardiac functions in adult rats, an effect at least in part due to the increased expression of β-MHC to α- MHC ratio in the heart.

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Section: Discussionmentioning

confidence: 99%

Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

Yousefzadeh¹,

Jeddi²,

Alipour³

2016

Arquivos Brasileiros De Cardiologia

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“…During cardiac E-C coupling, brief openings of L-type Ca 2ϩ channels activate RyRs by the mechanism of Ca 2ϩ -induced Ca 2ϩ release (3,11) to generate Ca 2ϩ T that activate contraction. In turn, L-type Ca 2ϩ channels are inactivated (5,37) and terminate SR Ca 2ϩ release, thus allowing the SERCA2 and the sarcolemmal Na ϩ /Ca 2ϩ exchanger (NCX) to resequester or extrude Ca 2ϩ from the cytosol to cause relaxation. Within this frame, the results obtained here, together with our previous data on SR calcium regulatory proteins, provide the rationale to theorize about the mechanism underlying the variations in E-C coupling between acclimated and nonacclimated hearts.…”

Section: Contractile Force and Ca 2ϩ Handling By Acclimated Myocytesmentioning

confidence: 99%

“…Several models of E-C coupling (5,37) suggest that a RyRs/DHPR ratio of 6 -7/1 is required for RyRs activation in the rat heart. Altered cross-talk between these two components in several pathological conditions is responsible for changes in myocyte contractility.…”

Section: Contractile Force and Ca 2ϩ Handling By Acclimated Myocytesmentioning

confidence: 99%

Altered Ca²⁺handling and myofilament desensitization underlie cardiomyocyte performance in normothermic and hyperthermic heat-acclimated rat hearts

Cohen

Kanana

Zoizner

et al. 2007

Journal of Applied Physiology

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Heat acclimation (AC) improves cardiac mechanical and metabolic performance. Using cardiomyocytes and isolated hearts from 30-day and 2-day acclimated rats (AC and AC-2d, 34 degrees C), we characterized cellular contractile mechanisms under normothermic (37 degrees C) and hyperthermic (39-42 degrees C) conditions. To determine contractile responses, Ca2+ transients (Ca2+ T), sarcoplasmic reticulum (SR) Ca2+ pool size (fura-2/indo-1 fluorescence), force generation [amplitude systolic motion (ASM)], L-type Ca2+ channels [dihydropyridine receptor (DHPR)], ryanodine receptors (RyRs), and total (PLBt) and phosphorylated phospholamban [serine phosphorylated (PLBs) and theonine phosphorylated (PLBtr)] proteins and transcripts were measured (Western blot, RT-PCR). Cardiac mechanical performance was measured using a Langendorff system. We demonstrated that AC and AC-2d increased Ca2+ T amplitude (148% and 147%, respectively) and twitch force (180% and 130%, respectively) and desensitized myofilaments, as indicated by a rightward shift in the ASM-Ca2+ relationships, despite no change in SR Ca2+ pool size. Hence, generation of higher Ca2+ T underlies greater force development in AC and AC-2d myocytes. In isolated hearts, ryanodine administration eliminated differences between AC and control (C) hearts, implying an important role for RyRs in that acclimation phase. Increased expression of DHPR and RyRs, and decreased PLBs/PLBt in AC hearts only, suggest that different pathways increase force generation in the AC-2d vs. AC myocytes. At basal beating rates, hyperthermia (39-41 degrees C) enhanced pressure generation in AC hearts. C hearts failed to restitute pressure beyond 39 degrees C. Increased beating frequency produced negative inotropic response. In C cardiomyocytes, hyperthermia elevated basal cytosolic Ca2+ and tension, Ca2+ T, and ASM. AC myocytes enhanced Ca2+ T but showed myofilament desensitization, suggesting its involvement in cardiac protection against hyperthermia. Collectively, both Ca2+ turnover and myofilament responsiveness are important adaptive acclimatory targets during normothermic and hyperthermic conditions.

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Modulation of Electrical Properties by Ions, Hormones, and Drugs

Hiraoka

2002

Comprehensive Physiology

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Thyroid status and postnatal changes in subsarcolemmal distribution and isoform expression of rat cardiac dihydropyridine receptors

Abstract: Hypothyroidism impaired the early postnatal maturation of dihydropyridine receptors as regards both their concentration into junctional structures and the decrease in the relative expression of alpha 1-subunit mRNA variants typical of foetal heart.

Cited by 13 publications

References 36 publications

Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

Altered Ca²⁺handling and myofilament desensitization underlie cardiomyocyte performance in normothermic and hyperthermic heat-acclimated rat hearts

Modulation of Electrical Properties by Ions, Hormones, and Drugs

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Thyroid status and postnatal changes in subsarcolemmal distribution and isoform expression of rat cardiac dihydropyridine receptors

Abstract: Hypothyroidism impaired the early postnatal maturation of dihydropyridine receptors as regards both their concentration into junctional structures and the decrease in the relative expression of alpha 1-subunit mRNA variants typical of foetal heart.

Cited by 13 publications

References 36 publications

Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

Altered Ca2+handling and myofilament desensitization underlie cardiomyocyte performance in normothermic and hyperthermic heat-acclimated rat hearts

Modulation of Electrical Properties by Ions, Hormones, and Drugs

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Altered Ca²⁺handling and myofilament desensitization underlie cardiomyocyte performance in normothermic and hyperthermic heat-acclimated rat hearts