Abstract:Background: Sodium homeostasis is disrupted in many cardiovascular diseases, which makes non-invasive sodium storage assessment desirable. In this regard, sodium MRI has shown its potential to reveal differences in sodium content between healthy and diseased tissues as well as treatment-related changes of sodium content. When different tissues are affected disparately, simultaneous assessment of these compartments is expected to provide better information about sodium distribution, reduce examination time, and… Show more
“…These results consolidate the notion that cardiac function deterioration induced by excessive aldosterone is largely dependent on salt status. Recently, Christa et al found that PA patients showed treatment-reversible significantly higher tissue sodium signals in the myocardium, calf muscle, and skin compared to healthy controls ( Christa et al, 2019 ; Christa et al, 2022 ). This is a novel explanation for the relationship between sodium and LV hypertrophy in PA. BNP is a neurohormone that is activated by volume expansion and pressure overload of cardiac ventricles ( Epshteyn et al, 2003 ), In the present study, our results show that TASK −/− mice exhibit obvious sodium retention and a rise in BNP and β-MHC mRNA levels in LV tissue.…”
The goal of this paper is to elucidate the effects of sodium restriction on hypertension and left ventricular (LV) hypertrophy in a mouse model with primary aldosteronism (PA). Mice with genetic deletion of TWIK-related acid-sensitive K (TASK)-1 and TASK-3 channels (TASK−/−) were used as the animal model of PA. Parameters of the LV were assessed using echocardiography and histomorphology analysis. Untargeted metabolomics analysis was conducted to reveal the mechanisms underlying the hypertrophic changes in the TASK−/− mice. The TASK−/− adult male mice exhibited the hallmarks of PA, including hypertension, hyperaldosteronism, hypernatremia, hypokalemia, and mild acid-base balance disorders. Two weeks of low sodium intake significantly reduced the 24-h average systolic and diastolic BP in TASK−/− but not TASK+/+ mice. In addition, TASK−/− mice showed increasing LV hypertrophy with age, and 2 weeks of the low-sodium diet significantly reversed the increased BP and LV wall thickness in adult TASK−/− mice. Furthermore, a low-sodium diet beginning at 4 weeks of age protected TASK−/− mice from LV hypertrophy at 8–12 weeks of age. Untargeted metabolomics demonstrated that the disturbances in heart metabolism in the TASK−/− mice (e.g., Glutathione metabolism; biosynthesis of unsaturated fatty acids; amino sugar and nucleotide sugar metabolism; pantothenate and CoA biosynthesis; D-glutamine and D-glutamate metabolism), some of which were reversed after sodium restriction, might be involved in the development of LV hypertrophy. In conclusion, adult male TASK−/− mice exhibit spontaneous hypertension and LV hypertrophy, which are ameliorated by a low-sodium intake.
“…These results consolidate the notion that cardiac function deterioration induced by excessive aldosterone is largely dependent on salt status. Recently, Christa et al found that PA patients showed treatment-reversible significantly higher tissue sodium signals in the myocardium, calf muscle, and skin compared to healthy controls ( Christa et al, 2019 ; Christa et al, 2022 ). This is a novel explanation for the relationship between sodium and LV hypertrophy in PA. BNP is a neurohormone that is activated by volume expansion and pressure overload of cardiac ventricles ( Epshteyn et al, 2003 ), In the present study, our results show that TASK −/− mice exhibit obvious sodium retention and a rise in BNP and β-MHC mRNA levels in LV tissue.…”
The goal of this paper is to elucidate the effects of sodium restriction on hypertension and left ventricular (LV) hypertrophy in a mouse model with primary aldosteronism (PA). Mice with genetic deletion of TWIK-related acid-sensitive K (TASK)-1 and TASK-3 channels (TASK−/−) were used as the animal model of PA. Parameters of the LV were assessed using echocardiography and histomorphology analysis. Untargeted metabolomics analysis was conducted to reveal the mechanisms underlying the hypertrophic changes in the TASK−/− mice. The TASK−/− adult male mice exhibited the hallmarks of PA, including hypertension, hyperaldosteronism, hypernatremia, hypokalemia, and mild acid-base balance disorders. Two weeks of low sodium intake significantly reduced the 24-h average systolic and diastolic BP in TASK−/− but not TASK+/+ mice. In addition, TASK−/− mice showed increasing LV hypertrophy with age, and 2 weeks of the low-sodium diet significantly reversed the increased BP and LV wall thickness in adult TASK−/− mice. Furthermore, a low-sodium diet beginning at 4 weeks of age protected TASK−/− mice from LV hypertrophy at 8–12 weeks of age. Untargeted metabolomics demonstrated that the disturbances in heart metabolism in the TASK−/− mice (e.g., Glutathione metabolism; biosynthesis of unsaturated fatty acids; amino sugar and nucleotide sugar metabolism; pantothenate and CoA biosynthesis; D-glutamine and D-glutamate metabolism), some of which were reversed after sodium restriction, might be involved in the development of LV hypertrophy. In conclusion, adult male TASK−/− mice exhibit spontaneous hypertension and LV hypertrophy, which are ameliorated by a low-sodium intake.
“…Previous studies mainly led by Titze’s group have shown that tissue sodium reservoir expands and contracts depending on the salt intake ( 9 ). Increased muscle and skin sodium concentrations have furthermore been observed in patients with refractory hypertension, primary aldosteronism, heart failure and insulin resistance ( 11 , 12 , 14 , 15 , 17 ), most of which are associated with increased activity of GC and MC ( 18 , 19 , 20 ).…”
Section: Discussionmentioning
confidence: 99%
“…Since 23 Na is a nucleus with a fast multi-exponential signal decay a relevant part of the signal could not be detected with the sequence used due to the echo time of 2.01 ms. Consequently, we do not report absolute values of tissue sodium but the relative sodium signal intensity (rSSI) which is the 23 Na signal intensity of the calf muscle relative to a reference vial containing an aqueous solution with a concentration of 100 mmol/L that was scanned with every participant. This concentration was chosen to avoid bias during calibration, as it provided a signal-to-noise ratio high enough for calibration (11,15) while even higher concentrations might have induced image artifacts outside the vial.…”
Section: Methodsmentioning
confidence: 99%
“…Non-invasive assessment of tissue sodium has been made possible by sodium MRI ( 23 Na-MRI). Increased muscle and skin sodium concentrations have been associated with refractory hypertension, primary aldosteronism, heart failure and even insulin resistance, suggesting that tissue sodium overload might be an independent cardiovascular risk factor ( 11 , 12 , 13 , 14 , 15 ).…”
Objective
Replacement therapy in primary adrenal insufficiency (PAI) with corticosteroids modulates sodium homeostasis. Serum sodium is, however, prone to osmotic shifts induced by several additional factors besides corticosteroids and does not always reliably reflect treatment quality. Non-osmotic tissue storage can be visualized by sodium MRI (23Na-MRI) and might better reflect corticosteroid activity.
Design
Longitudinal study of 8 patients with newly diagnosed PAI and cross-sectional study in 22 patients with chronic PAI is reported here. Comparison was made with matched healthy controls.
Methods
Using a 23Na-MRI protocol on a 3T scanner, relative sodium signal intensities (rSSI) to signal intensities of the reference vial with 100 mmol/L of sodium were determined in the muscle and skin of the lower calf.
Results
In newly diagnosed patients, tissue rSSI (median, range) were reduced and significantly increased after treatment initiation reaching levels similar to healthy controls (muscle: from 0.15 (0.08, 0.18) to 0.18 (0.14, 0.27), P = 0.02; skin: from 0.12 (0.09, 0.18) to 0.18 (0.14, 0.28), P < 0.01). Muscle rSSI was significantly higher in patients with chronic PAI compared to controls (0.19 (0.14, 0.27) vs 0.16 (0.12, 0.20), P < 0.01). In chronic PAI, skin rSSI significantly correlated with plasma renin concentration.
Conclusion
23Na-MRI provides an additional insight into sodium homeostasis, and thus the quality of replacement therapy in PAI, as tissue sodium significantly changes once therapy is initiated. The increased tissue sodium in patients with chronic PAI might be an indication of over-replacement.
“…The hormones secreted by adrenal gland play an important role in the metabolism ( Sevilla et al, 2013 ), regulation of blood pressure ( Reincke et al, 2021 ), and homeostasis of sodium or glucose ( Kuo et al, 2015 ; Christa et al, 2022 ). Natural products may influence secretion of hormones from adrenal gland.…”
Section: Effect Of Natural Products On Hormones Secreted By the Adren...mentioning
The cortex of adrenal gland produces glucocorticoid, mineralocorticoid, and androgen. The medulla of adrenal gland secrets catecholamines. These hormones play an important role in regulating blood pressure, metabolism, and homeostasis of glucose or electrolytes. Hypersecretion or hyposecretion by the adrenal gland will cause a complex cascade of hormone effects and lead to diseases, including Addison’s disease, Cushing’s syndrome, and congenital adrenal cortical hyperplasia. Skin is the largest organ of body. It provides protection and acts as a barrier against external damage factors like infectious organisms, chemicals, and allergens. Endocrinologic disorders often induce cutaneous abnormalities. According to the previous evidences, natural products have the potential properties for attenuating skin disorders and improving dermatologic symptoms by inhibiting inflammation through MAPK or PI3K/AKT-dependent NF-κB pathways. The natural products may also promote skin wound healing by inhibiting the production of matrix metalloproteinase-9. We systematically searched the relevant articles from databases, including PubMed, Embase, and Cochrane library databases, to review the effects of natural products on skin disorders. This article summarized the effects of natural products on skin inflammation caused by abnormal hormone secreted by adrenal gland. And the published papers indicated that natural products might be a potential source for treating skin diseases.
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