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

Vargas, Félix; Rodríguez-Gómez, Isabel; Vargas-Tendero, Pablo; Jiménez, Eugenio; Montiel, Mercedes

doi:10.1530/joe-11-0349

Cited by 62 publications

(58 citation statements)

References 122 publications

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“…31 Thus, it is plausible that low triiodothyronine, as observed in ExFHA women in the current and in previous 10,11 studies, may also contribute to this low renin state. Considering the similarity of body mass index in our 2 groups and the clinical absence of edema, intravascular volume expansion is an unlikely RAAS-suppressive mechanism.…”

Section: Discussionmentioning

confidence: 55%

Discordant Orthostatic Reflex Renin–Angiotensin and Sympathoneural Responses in Premenopausal Exercising-Hypoestrogenic Women

et al. 2015

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Its prevalence is markedly higher in recreationally and competitively exercising women and women with physically demanding jobs (≈1% to 44%) than in sedentary women (≈2% to 5%).2,3 Hypothalamic-pituitary-ovarian suppression in physically active women with FHA (ExFHA) has been related causally to energy deficiency (ie, caloric deficit) in association with high energy expenditure and insufficient energy intake (ie, low caloric intake). 4Circulating estradiol concentrations in women with ExFHA are chronically low and resemble those observed in postmenopausal women and in men. 5,6 In postmenopausal women, estrogen deficiency is associated with increases in blood pressure (BP) and a marked acceleration in the development and progression of atherosclerosis.7 Cardiovascular consequences of premenopausal hypoestrogenemia in ExFHA women are not yet known, but disruption of the menstrual cycle during the reproductive years is also associated with the premature development and progression of coronary artery disease. 8,9 However, in contrast to postmenopausal women, ExFHA women have lower resting systolic blood pressure (SBP) and heart rate (HR) than age-and fitness-matched estrogen-replete physically active women.10,11 The presence of low arterial BP, despite hypoestrogenemia, suggests that estrogen deficiency may have different consequences for BP regulation in premenopausal and postmenopausal women.The sympathetic nervous system and the renin-angiotensinaldosterone system (RAAS) are cornerstones of BP regulation. Estrogen modulates both. In estrogen-deficient Abstract-Our prior observations in normotensive postmenopausal women stimulated the hypotheses that compared with eumenorrheic women, active hypoestrogenic premenopausal women with functional hypothalamic amenorrhea would demonstrate attenuated reflex renin-angiotensin-aldosterone system responses to an orthostatic challenge, whereas to defend blood pressure reflex increases in muscle, sympathetic nerve activity would be augmented. To test these hypotheses, we assessed, in recreationally active women, 12 with amenorrhea (ExFHA; aged 25±1 years; body mass index 20.7±0.7 kg/m 2 ; mean±SEM) and 17 with eumenorrhea (ExOv; 24±1 years; 20.9±0.5 kg/m 2 ), blood pressure, heart rate, plasma renin, angiotensin II, aldosterone, and muscle sympathetic nerve activity at supine rest and during graded lower body negative pressure (−10, −20, and −40 mm Hg). At baseline, heart rate and systolic blood pressure were lower (P<0.05) in ExFHA (47±2 beats/min and 94±2 mm Hg) compared with ExOv (56±2 beats/min and 105±2 mm Hg), but muscle sympathetic nerve activity and renin-angiotensin-aldosterone system constituents were similar (P>0.05). In response to graded lower body negative pressure, heart rate increased (P<0.05) and systolic blood pressure decreased (P<0.05) in both groups, but these remained consistently lower in ExFHA (P<0.05). Lower body negative pressure elicited increases (P<0.05) in renin, angiotensin II, and aldosterone in ExOv, but not in ExFHA (P>0.05). Muscle sympatheti...

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Section: Discussionmentioning

confidence: 55%

Discordant Orthostatic Reflex Renin–Angiotensin and Sympathoneural Responses in Premenopausal Exercising-Hypoestrogenic Women

et al. 2015

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“…Notably, findings from animal studies treated with thyroid hormones suggest that the regulation of ACE transcription and activity are tissue-dependent. An increase in ACE expression and activity were observed in the kidney of these animals (80). Fluctuations of renin and angiotensinogen levels by the presence or absence of thyroid hormones may consequently affect AT II levels.…”

Section: Thyroid the Kidney And The Renin-angiotensin Systemmentioning

confidence: 82%

“…In addition, thyroid hormones induce ACE synthesis in endothelial cells (79). Decreased ACE concentrations were found in neonatal and adult rats with hypothyroidism, whereas elevated serum ACE levels were reported in human and animals with hyperthyroidism (80). Moreover, the correlation between serum ACE levels and thyroid hormones levels is positive (80).…”

Section: Thyroid the Kidney And The Renin-angiotensin Systemmentioning

confidence: 99%

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

et al. 2014

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Thyroid hormones may directly affect the kidney and altered kidney function may also contribute to thyroid disorders. The renal manifestations of thyroid disorders are based on hemodynamic alterations or/and to direct effects of thyroid hormones. The renin-angiotensin system plays a crucial role in the cross-talk between the thyroid and the kidney. Hypothyroidism may be accompanied by an increase of serum creatinine and reduction of glomerular filtration rate (GFR), whereas hyperthyroidism may increase GFR. Treatment of thyroid disorders may lead to normalization of GFR. Primary and subclinical hypothyroidism and low triiodothyronine (T3) syndrome are common features in patients with chronic kidney disease (CKD). In addition low levels of thyroid hormones may predict a higher risk of cardiovascular and overall mortality in patients with end-stage renal disease. The causal nature of this correlation remains uncertain. In this review, special emphasis is given to the thyroid pathophysiology, its impact on kidney function and CKD and the interpretation of laboratorial findings of thyroid dysfunction in CKD.

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“…The presence of ACE, Ang II type 1 (AT1R) and type 2 (AT2R) receptors and Ang II in different cells supports the concept of local RAS [23]. The local RAS seems to be regulated independently from the circulating system in a specific manner depending on the cell type and extracellular stimulus [24]. Despite that it can interact with the circulating system and complement it.…”

Section: Tissue and Intracellular Rasmentioning

confidence: 66%

Involvement of the Renin‐Angiotensin System in Atherosclerosis

Kolaković¹,

Živković²,

Stanković³

2017

Renin-Angiotensin System - Past, Present and Future

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The renin-angiotensin system (RAS) is a well known for its role in the regulation of the blood pressure (BP). Angiotensin II (Ang II), the main mediator of the RAS, may act either, as a systemic molecule or a locally produced factor. Within the vessel wall it has significant proinflammatory role by inducing the oxidative stress, secretion of inflammatory cytokines and adhesion molecules. Ang II could trigger proliferation of vascular smooth muscle cells (VSMC) and its migration to the outer layer of the vessel wall. It could induce the release of matrix metalloproteinase (MMPs), from human VSMC and thus increase susceptibility to rupture of atherosclerotic lesions. Binding of Ang II to AT1R/AT2R could have opposing actions in vascular injury. The ACE2/Ang (1-7)/Mas axis of the RAS also opposes the unfavourable actions of ACE/Ang II/ATR1 axis. Inhibition of RAS could reduce inflammation-associated processes in vasculature, independently of lowering BP. RAS is significantly modulated by the genes coding for this system. Certain genetic variants (SNPs) in the RAS genes have been denoted as the functional ones and have been associated with hypertension, cardiovascular phenotypes and atherosclerosis. Also, the genetic components of the RAS interfere with the regulators of gene expression by microRNAs (miRs).

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

Cited by 62 publications

References 122 publications

Discordant Orthostatic Reflex Renin–Angiotensin and Sympathoneural Responses in Premenopausal Exercising-Hypoestrogenic Women

Discordant Orthostatic Reflex Renin–Angiotensin and Sympathoneural Responses in Premenopausal Exercising-Hypoestrogenic Women

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

Involvement of the Renin‐Angiotensin System in Atherosclerosis

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