Components of the adrenocortical system (adrenal and blood corticosteroid hormones and hepatic and renal 11beta-hydroxysteroid dehydrogenase activity) and also activity of the most important enzyme of the renin-angiotensin system, tissue and blood angiotensin converting enzyme (ACE) have been investigated in dynamics of alloxan diabetes. The study has shown that the initial period of diabetes is characterized by activation of synthesis and secretion of adrenocortical hormones into blood. High blood glucose and glucocorticoid honnones increase activity of the renin-angiotensin system in lungs and decrease ACE secretion into blood. This is accompanied by a decrease of activity of the renin-angiotensin system in kidneys. Subsequent progression of diabetes resulted in impairments of physiologically determined correlations between the components of these systems. Development of experimental diabetes for 30 days was accompanied by sign of a decrease of the adrenal glucocorticoid function regardless of stable impairments of carbohydrate metabolism. Under these conditions increased adrenal and hepatic 11beta-hydroxysteroid dehydrogenase activity may be responsible for maintenance of elevated levels of the main glucocorticoid in blood and tissues. Factor analysis revealed impairments in intersystem relationships between the adrenocortical and renin-angiotensin systems in experimental diabetes thus suggesting disintegration of regulatory systems.
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http://dx.doi.org/10.18097/pbmc20135902183 | DOI Listing |
Endocr Metab Immune Disord Drug Targets
January 2025
Department of Internal Medicine, Division of Nephrology and Hypertension, Faculty of Medicine, Dr. Cipto Mangunkusumo Hospital, Universitas Indonesia, Jakarta, Indonesia.
Chronic kidney disease (CKD) is a major complication of type 2 diabetes mellitus (T2D), which often leads to diabetic kidney disease (DKD). Traditional therapies, including renin- angiotensin-aldosterone system inhibitors and sodium-glucose cotransporter-2 inhibitors, are effective in slowing CKD progression. However, these approaches are insufficient to comprehensively inhibit mineralocorticoid receptor (MR) overactivation in the kidneys, which remains a significant driver of inflammation, fibrosis, and oxidative stress.
View Article and Find Full Text PDFJ Food Sci
January 2025
Faculty of Food Science and Engineering, Kunming University of Science and Technology, Kunming, China.
Hypertension is a major risk factor for many cardiovascular diseases, which can lead to kidney and heart disease, stroke, and premature death. Inhibiting angiotensin-converting enzyme (ACE) activity is an effective method to relieve hypertension. Previously, we screened an active peptide KYPHVF (KF6) from Boletus griseus-Hypomyces chrysospermus with excellent ACE inhibitory activity.
View Article and Find Full Text PDFBackground: The renin angiotensin system (RAS) has been proposed as a potential modifier of the development of Alzheimer's disease (AD). However, prospective studies of RAS are sparse especially among cognitively normal individuals with type 2 diabetes mellitus (T2DM) and other vascular risk factors. We aimed to determine whether plasma levels or activity of the RAS marker ACE-1 predicts cognitive decline over an 8-year period in this population.
View Article and Find Full Text PDFEur J Heart Fail
January 2025
Division of Cardiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Aims: Guidelines recommend immediate initiation of all four class I guideline-directed medical therapies, renin-angiotensin system inhibitors (RASI) or angiotensin receptor-neprilysin inhibitors (ARNI), beta-blockers, mineralocorticoid receptor antagonists (MRA) and sodium-glucose cotransporter 2 inhibitors (SGLT2i) following the diagnosis of heart failure (HF) with reduced ejection fraction (HFrEF). The extent to which this occurs in new-onset HFrEF is unclear. We assessed guideline-recommended therapies during the first year following a HFrEF diagnosis.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Nova Southeastern University, Fort Lauderdale, FL, USA.
Background: Cerebral amyloid angiopathy (CAA), the accumulation of amyloid proteins in the cerebral vasculature, increases the risk of stroke and vascular cognitive impairment and dementia (VCID). Not only is there no treatment for CAA, but the condition is also highly comorbid with Alzheimer's disease (AD), and its presence may serve as a contraindication to treating patients with anti-amyloid therapies due to an increased risk of hemorrhage and edema. Therefore, it is crucial to identify novel treatments for individuals with CAA.
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