Renin-Angiotensin System in Thyroid Dysfunction in Rats

Marchant, Catherine; Brown, Lindsay; Sernia, Conrad

doi:10.1097/00005344-199309000-00016

Cited by 86 publications

(90 citation statements)

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“…Thus, the number of AT1 receptors defines the biological efficacy of angiotensin II. The RAS has also been implicated in cardiovascular pathology, and the upregulation of AT1 receptors in the cardiovascular system has been reported in diseases like thyroid dysfunction, hypertension and myocardial infarction [22][23][24]. Our present findings demonstrate increased densities of the AT1 receptor mRNA and protein in human atrial myocardium of patients suffering from type 2 diabetes.…”

Section: Discussionsupporting

confidence: 71%

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

et al. 2006

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Aims/hypothesis The angiotensin II (type 1) (AT1) receptor mediates many biological effects of the renin-angiotensin system (RAS), leading to remodelling of cardiac tissue. The present study was designed to analyse changes in the function and expression of the AT1 receptor as principal effector of the RAS in myocardium from type 2 diabetic patients compared with non-diabetic myocardium as control. In addition, we determined the effect of treatment with ACE inhibitors or AT1 receptor blockers on expression levels of the receptor in diabetic patients. Methods Gene expression of the AT1 receptor was analysed by quantitative RT-PCR and protein expression was determined by immunoblot analysis in human right atrial myocardium. We investigated functional coupling of the receptors by measuring contractility in isolated trabeculae stimulated with increasing concentrations of angiotensin II. Results Diabetic myocardium showed a significant increase in protein expression (170±16% of control) and median mRNA expression (186% of control) of the AT1 receptor.The additional receptors were functionally coupled, resulting in a stronger inotropic response upon stimulation with angiotensin II (89±5.5% vs 29±1.6% in controls), whereas receptor affinity was similar in both groups. However, myocardium from diabetic patients treated with ACE inhibitors or AT1 receptor blockers showed no increase in AT1 receptor expression. Conclusions/interpretation AT1 receptor expression in myocardium of type 2 diabetic patients is dynamic, depending on the level of glycaemic control and the activity of the RAS. These findings could at least in part explain the strong therapeutic benefit of RAS inhibition in diabetic patients.

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Section: Discussionsupporting

confidence: 71%

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

et al. 2006

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“…The decrease in plasma levels in thyroidectomized rats is partially restored by thyroid hormone treatment (Dzau & Herrmann 1982) and may reflect a reduced synthesis in the liver, given that the liver content and release of angiotensinogen are both lower in thyroidectomized animals (Clauser et al 1983, Jiménez et al 1984. However, contradictory results were reported for plasma angiotensinogen concentrations in adult hyperthyroid rats (Dzau & Herrmann 1982, Jiménez et al 1982, Marchant et al 1993, and no significant changes were observed in hyperthyroid dogs (Sernia et al 1993). Discrepancies among studies may be due to the different durations and dosages of the thyroid hormone treatments used to induce hyperthyroidism.…”

Section: Angiotensinogenmentioning

confidence: 99%

“…These actions of thyroid hormones on renin secretion and renin mRNA are direct and not mediated by changes in sympathetic nervous system activity (Kobori et al 1997a,b). However, the above studies do not rule out the possibility that RAS activity modifications in thyroid Hauger-Klevene & Levin 1976, Jiménez et al 1982, Santos & Ferreira 2007 [ (Jiménez et al 1984);Y (Hauger-Klevene & Levin 1976, Jiménez et al 1982) Angiotensin-converting enzyme [ (Phillips et al 1993) Y , Jiménez et al 1990) Angiotensin II [ (Marchant et al 1993, Garcia del Río et al 1997, Kobori et al 1997a Y (Marchant et al 1993, Kobori et al 1997a New RAS components --Heart Renin Kobori et al 1997a,b, 1999 Marchant et al 1993 [ (Marchant et al 1993) Kidney Renin [ (Bouhnik et al 1981, Kobori et al 1997a,b, Klein & Ojamaa 2001)…”

Section: Reninmentioning

confidence: 99%

“…The stage of life at which there is a deficit in thyroid hormone influences the synthesis and release of angiotensinogen in this situation, as is the case for other RAS components. Plasma angiotensinogen levels in adult rats were not altered by propylthiouracil-induced hypothyroidism (Jiménez et al 1982), but reduced levels were observed in thyroidectomized animals during early stages of development (Bouhnik et al 1981, Jiménez et al 1982, Marchant et al 1993. The decrease in plasma levels in thyroidectomized rats is partially restored by thyroid hormone treatment (Dzau & Herrmann 1982) and may reflect a reduced synthesis in the liver, given that the liver content and release of angiotensinogen are both lower in thyroidectomized animals (Clauser et al 1983, Jiménez et al 1984.…”

Section: Angiotensinogenmentioning

confidence: 99%

“…An increase or deficit in thyroid hormone changes renin and angiotensinogen levels and consequently affects AII levels. The rise in PRA and plasma angiotensinogen observed in hyperthyroidism is associated with increased plasma AII levels, which are reduced in hypothyroidism (Marchant et al 1993, Kobori et al 1997a. However, the action of thyroid hormones on angiotensin receptors is tissue-dependent.…”

Section: Aii and Aii Receptorsmentioning

confidence: 99%

See 2 more Smart Citations

The renin–angiotensin system in thyroid disorders and its role in cardiovascular and renal manifestations

Vargas¹,

Rodríguez-Gómez²,

Vargas-Tendero³

et al. 2011

Journal of Endocrinology

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Thyroid disorders are among the most common endocrine diseases and affect virtually all physiological systems, with an especially marked impact on cardiovascular and renal systems. This review summarizes the effects of thyroid hormones on the renin-angiotensin system (RAS) and the participation of the RAS in the cardiovascular and renal manifestations of thyroid disorders. Thyroid hormones are important regulators of cardiac and renal mass, vascular function, renal sodium handling, and consequently blood pressure (BP). The RAS acts globally to control cardiovascular and renal functions, while RAS components act systemically and locally in individual organs. Various authors have implicated the systemic and local RAS in the mediation of functional and structural changes in cardiovascular and renal tissues due to abnormal thyroid hormone levels. This review analyzes the influence of thyroid hormones on RAS components and discusses the role of the RAS in BP, cardiac mass, vascular function, and renal abnormalities in thyroid disorders.

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Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

Axelband

Dias

Ferrão

et al. 2010

Journal Cellular Physiology

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Thyroid hormones play a wide range of important physiological activities in almost all organism. As changes in these hormones levels-observed in hypothyroidism and hyperthyroidism-promote serious derangements of the cardiovascular system, it is important to know their mechanisms of action. Although the classic genomic actions which are dependent on interaction with nuclear receptors to modulate cardiac myocytes genes expression, there is growing evidence about T(3) and T(4)-triggered nongenomic pathways, resulted from their binding to plasma membrane, cytoplasm, or mitocondrial receptors that leads to a rapidly regulation of cardiac functions. Interestingly both actions converge to amplify thyroid hormone effects on cardiovascular system. T(3) and T(4) nongenomic actions modify inotropic and chronotropic effects, cardiac action potential duration, cardiac growth, and myocyte shape by protein translation through protein kinases-dependent signaling cascades, which include PKA, PKC, PI3K, and MAPK, and changes on ion channels and pumps activity. In respect to the decreased systemic vascular resistance seen in hyperthyroidism, T(3) appears to activate NOS or ATP-sensitive K(+) channels. In addition, a novel biologically active T(4)-derived metabolite has been described, 3-iodothyronamine, T(1)AM, which also acts through membrane receptors to mediate nongenomic cardiac effects. This metabolite influences the physiological manifestations of thyroid hormone actions by inducing opposite effects from those stimulated by T(3) and T(4), such as negative inotropic and chronotropic effects. Therefore, beyond genomic and nongenomic effects of thyroid hormones, it is crucial for there to be an equilibrium between T(3) or T(4) and T(1)AM levels for maintaining cardiac homeostasis.

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Renin-Angiotensin System in Thyroid Dysfunction in Rats

Cited by 86 publications

References 0 publications

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

The renin–angiotensin system in thyroid disorders and its role in cardiovascular and renal manifestations

Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

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