Thyroid disorders and nitric oxide in cardiovascular adaptation to hypovolemia

Ogonowski, Natalia; Piro, Giselle; Pessah, Déborah; Arreche, Noelia; Puchulu, Bernardita; Balaszczuk, Ana M.; Fellet, Andrea L.

doi:10.1530/joe-16-0203

Cited by 5 publications

(6 citation statements)

References 27 publications

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“…These findings were like those obtained by us previously and were discussed previously. 21 The hemodynamics changes let us to evaluate the mitochondrial function in the experimental groups. The determination of this function was achieved by measuring O 2 consumption in presence of saturating concentrations of the respective substrates.…”

Section: Discussionmentioning

confidence: 99%

“…This finding agreed with those found by several authors. [16][17][18][19][20][21][22][23] This effect could be probably controlled by a variety of mechanisms such as reduced content and activity of some components of the electron transport chain, alterations of mitochondrial membranes permeability as well as changes in lipid composition. 23,24 Additionally, Mukherjee et al, 25 showed that complex I activity was inhibited in hypothyroid submitochondrial particles, whereas T 3 supplementation upregulated electron transport chain complexes.…”

Section: Discussionmentioning

confidence: 99%

“…This result would be disagreed with several authors who showed in other tissues like liver and skeletal muscle, an increased mtNOS expression in hypothyroidism. [16][17][18][19][20][21][22][23][24][25][26] That is, hypothyroidism is associated with a lower activity of complex I and lower mtNOS protein level in mitochondrial heart compared with Eut animals. Parihar et al showed a similar result suggesting that rat liver and brain mtNOS are functionally associated with mitochondrial respiration chain complex I.…”

Section: Discussionmentioning

confidence: 99%

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Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia

Ogonowski¹,

Valdez²,

Zaobornyj³

et al. 2018

EMIJ

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After 28 days of treatment, the animals were anesthetized with urethane (1 g/kg ip). A tracheotomy was performed using polyethylene AbstractThe aim of the present work was to examine the effect of thyroid state on rat heart mitochondria function during hypovolemia. Sprague-Dawley rats treated with T 3 (hyper, 20 μg/100 g body weight) or 0.02% methimazole (hypo, w/v) for 28 days. Hypovolemia was induced by acute hemorrhage. O2 uptake, complex I activity and mitochondrial nitric oxide synthase (mtNOS) protein levels were determined in heart mitochondria. The malate-glutamate-supported state 3 respiration decreased and increased in hypo and hyperthyroid rats, while state 4 respirations did not change. Complex I activity and mtNOS protein levels were decreased in hypothyroid rats even in acute hypovolemia. Hyperthyroidism did not change these parameters. In summary, this study showed, for the first time, interesting findings that heart mitochondrial function is altered during thyroid disorder and acute hypovolemia. Heart mitochondrial nitric oxide, modulating oxygen uptake, may be involved in the adaptative response to assure the cardiomyocytes survives in this experimental condition. Citation: Ogonowski N, Valdez LB, Zaobornyj T, et al. Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia

Ogonowski¹,

Valdez²,

Zaobornyj³

et al. 2018

EMIJ

Self Cite

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“…Measurements were taken in the right parasternal short axis plane at the level of the mitral valve leaflets. All determinations were made according to the guidelines of the American Society of Echocardiography (Ogonowski et al., 2016 ).…”

Section: Methodsmentioning

confidence: 99%

Thyroid hormone disorder and the heart: The role of cardiolipin in calcium handling

D’Angelo

Martinez

Arreche

et al. 2023

Experimental Physiology

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New Findings What is the central question of this study?Do alterations in thyroid status affect haemodynamic parameters and echocardiographic measurements in the rat postnatal heart, and calcium handling, contractility, relaxation and cardiolipin content in isolated rat cardiomyocytes? What is the main finding and its importance?An imbalance in phospholipids of the mitochondrial membrane such as cardiolipin is related to defects in mitochondrial function. T3‐dependent cardiolipin signals contribute to the maintenance of mitochondrial homeostasis and involve Ca2+ handling, this pathway being more important in hypothyroidism. Abstract The objective of this study was to evaluate whether alterations in thyroid status affect (1) haemodynamic parameters and echocardiographic measurements in the rat postnatal heart, and (2) calcium handling, contractility, relaxation and cardiolipin content in isolated rat cardiomyocytes. Sprague–Dawley rats aged 2 months treated with T3 (hyperthyroid, 20 μg/100 g body weight) or 0.02% methimazole (hypothyroid, w/v) for 28 days. Heart function was evaluated by echocardiography. Measurements of mean arterial pressure (MAP), heart rate, Ca2+ transients, cardiomyocyte shortening, number of spontaneous contractions per minute and cardiolipin (CL) content were performed. Thyroid disorders were associated with changes in pacemaker activity without modifications of MAP. Thyroid disorder induced changes in left ventricular diameter which were correlated with modifications of cardiac contractility (altered cell shortening and sarcoplasmic reticulum Ca2+ content). Endocrine disorders altered cardiomyocyte relaxation (reduction in the time to 50% re‐lengthening and the time to 50% Ca2+ decay). Thyroid disorder increased the number of spontaneous contractions per minute (an index of pro‐arrhythmogenic behaviour). CL content was increased only in hypothyroid rats. Changes in CL content, CL composition and CL–protein interaction in mitochondria from hypothyroid animals are responsible for alterations of contractile and relaxation cardiac function. This mechanism may be not be involved in T3‐treated rats. Maintenance of euthyroidism is of crucial importance to preserve cardiac performance. An imbalance in relation to phospholipids of the mitochondrial membrane such as CL is related to defects in mitochondrial function. T3‐dependent CL signals contribute to the maintenance of mitochondrial homeostasis and involve Ca2+ handling, this pathway being more important in hypothyroidism.

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“…The production of nitric oxide (NO) is regulated by APOE polymorphism [48]. Altered NO levels have been associated with migraine/TTH and thyroid dysfunction [49][50][51][52]. There is increased production of NO in APOE E4 carriers because of increased oxidative stress, suggesting a higher relative risk of E4 towards headache [53,54].…”

Section: Apoementioning

confidence: 99%

Migraine and thyroid dysfunction: Co‐occurrence, shared genes and biological mechanisms

Tasnim

Nyholt

2023

Euro J of Neurology

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Background and purpose: Migraine and thyroid dysfunction, particularly hypothyroidism, are common medical conditions and are known to have high heritability. Thyroid function measures, thyroid stimulating hormone (TSH) and free thyroxine (fT4), are also known to be genetically influenced. Although observational epidemiological studies report an increased co-occurrence of migraine and thyroid dysfunction, a clear and combined interpretation of the findings is currently lacking. A narrative review is provided of the epidemiological and genetic association evidence linking migraine, hypothyroidism, hyperthyroidism and thyroid hormones TSH and fT4.Methods: An extensive literature search was conducted in the PubMed database for epidemiological, candidate gene and genome-wide association studies using the terms migraine, headache, thyroid hormones, TSH, fT4, thyroid function, hypothyroidism and hyperthyroidism.Results: Epidemiological studies suggest a bidirectional relationship between migraine and thyroid dysfunction. However, the nature of the relationship remains unclear, with some studies suggesting migraine increases the risk for thyroid dysfunction whilst other studies suggest the reverse. Early candidate gene studies have provided nominal evidence for MTHFR and APOE, whilst more recently genome-wide association studies have provided robust evidence for THADA and ITPK1 being associated with both migraine and thyroid dysfunction.Conclusions: These genetic associations improve our understanding of the genetic relationship between migraine and thyroid dysfunction, provide an opportunity to develop biomarkers to identify migraine patients most likely to benefit from thyroid hormone therapy, and indicate that further cross-trait genetic studies have excellent potential to provide biological insight into their relationship and inform clinical interventions.

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Thyroid disorders and nitric oxide in cardiovascular adaptation to hypovolemia

Cited by 5 publications

References 27 publications

Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia

Thyroid hormones and heart mitochondrial nitric oxide under hypovolemia

Thyroid hormone disorder and the heart: The role of cardiolipin in calcium handling

Migraine and thyroid dysfunction: Co‐occurrence, shared genes and biological mechanisms

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