The purposes of the research were to study the prevalence of C-344T polymorphism and the distribution of aldosterone synthase gene (CYP11B2) genotypes, to analyze the association of aldosterone concentration with aldosterone synthase gene genotypes, to study the features of left ventricular hypertrophy (LVH) by echocardioscopy and identify their association with different genotypes of the aldosterone synthase gene in young patients with arterial hypertension (AH), depending on the presence or absence of concomitant obesity (or overweight). 123 young patients with essential AH (18-44 years old) were examined, the average age was (32,83±0,58) years old, the male/female ratio was 72/51 respectively. All patients were divided into 3 groups: group 1 (n=41) with normal body weight; group 2 (n=40) with overweight; group 3 (n=42) -with obesity. It was revealed that the "pathological" genotypes (CC+CT) of the aldosterone synthase gene C-344T polymorphism were significantly more frequent in patients as with normal body weight and with concomitant obesity or overweight. In concomitant overweight and obesity the average blood aldosterone concentration was significantly higher, that confirms the presence of additional activation of aldosterone synthesis in such comorbid combination and requires further study of the exact mechanism of this type of hyperaldosteronism. Concomitant overweight and obesity significantly influenced on the echocardiographic parameters characterizing LVH processes in young patients with AH with the significant increased proportion of eccentric LVH. "Pathological" genotypes (CT+TT) of the C-344T polymorphism of the aldosterone synthase gene are associated with a higher blood aldosterone concentration and more expressed LVH processes in young patients with AH.
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Endocr Connect
January 2025
P Kamenický, Centre de Référence des Maladies Rares de l'Hypophyse, Le Kremlin-Bicêtre, 94275, France.
Background: Arterial hypertension and left ventricular hypertrophy and remodeling are independent cardiovascular risk factors in patients with Cushing's syndrome. Changes in the renin-angiotensin system and in the mineralocorticoid axis activity could be involved as potential mechanisms in their pathogenesis, in addition to cortisol excess.
Methods: In this ancillary study of our previous study prospectively investigating patients with ACTH-dependent Cushing's syndrome by cardiac magnetic resonance imaging (NCT02202902), 11 patients without any interfering medication were cross-sectionally compared to 20 control subjects matched for age, sex and body mass index.
Int J Mol Sci
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Department of Cardiology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510800, China.
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Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Hypertension remains a global health challenge due to its high prevalence and association with premature morbidity and mortality. Aldosterone, a mineralocorticoid hormone, and its receptor, the mineralocorticoid receptor (MR), are highly implicated in hypertension pathogenesis. Aldosterone synthase is the sole enzyme responsible for producing aldosterone in humans.
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East Coast Institute for Research, 3550 University Blvd S #101, Jacksonville, FL, USA.
Patients with hypertension are at an increased risk of cardiovascular disease and death. Resistant hypertension, or hypertension that is unsuccessfully treated with multiple antihypertensive medications, further exacerbates the complications and negative outcomes for patients. A new pathway, via aldosterone synthesis inhibition, is currently being studied as a method to reduce blood pressure values in patients who are currently taking other antihypertensive medications.
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Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Aldosterone-producing adenoma (APA) is a leading cause of primary aldosteronism (PA), a condition marked by excessive aldosterone secretion. CYP11B2, the aldosterone synthase, plays a critical role in aldosterone biosynthesis and the development of APA. Despite its significance, encoding regulatory mechanisms governing CYP11B2, particularly its degradation, remain poorly understood.
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