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Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Adrenocortical hormones are produced by the adrenal cortex of suprarenal glands and consist of glucocorticoids and mineralocorticoids. Glucocorticoid is a steroid hormone produced by the suprarenal or adrenal gland and known particularly for its anti-inflammatory and immunosuppressive actions. Cortisol is the principal glucocorticoid in many species, including humans. Mineralocorticoids stimulate the retention of sodium in the extracellular body fluids. The most potent mineralocorticoid of all species is aldosterone.
Endocrine diseases and pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
The other major adrenal cortical steroid hormone, aldosterone, is a mineralocorticoid promoting renal sodium reabsorption and potassium excretion, and maintenance of extracellular fluid volume and blood pressure. Although ACTH stimulates aldosterone secretion, the primary regulation of aldosterone secretion is via the renin–angiotensin signal pathway. Decreased delivery of sodium to glomeruli via afferent arterioles in the nephron stimulates renin secretion by juxtaglomerular cells. Renin in turn activates the angiotensin-converting enzyme, resulting to conversion of inactive angiotensin-1 to active angiotensin-2 in the lung; angiotensin-2 is the major stimulant of aldosterone synthesis and secretion by the adrenal. Aldosterone in turn promotes renal sodium conservation and extracellular fluid volume expansion, resulting in rising arterial pressure and increasing delivery of water and sodium to the proximal nephron. Renin secretion is inhibited by increased sodium delivery to the afferent renal arteriole, thereby completing the feedback loop of the renin–angiotensin–aldosterone axis.
Adrenocortical Disease
Published in T.M. Craft, P.M. Upton, Key Topics In Anaesthesia, 2021
The adrenal cortex produces glucocorticoid, mineralocorticoid and sex hormones (mainly testosterone). Cortisol, the principal glucocorticoid, modulates stress and inflammatory responses. It is a potent stimulator of gluconeogenesis and antagonizes insulin. Aldosterone is the principal mineralocorticoid. It causes increased sodium reabsorption, and potassium and hydrogen ion loss at the distal renal tubule. Adrenal androgen production increases markedly at puberty, declining with age thereafter. Androstenedione is converted by the liver to testosterone in the male and oestrogen in the female. Cortisol and androgen production are under diurnal pituitary control (adrenocorticotrophic hormone — ACTH). Aldosterone is released in response to angiotensin II, produced following renal renin release and subsequent pulmonary angiotensin I conversion.
‘Drink clean, safe water and/or other fluids through-out the day even if you do not feel thirsty’: a food-based dietary guideline for the elderly in South Africa
Published in South African Journal of Clinical Nutrition, 2021
Upasana Mukherjee, Carin Napier, Wilna Oldewage-Theron
The most important hormones in the maintenance of body fluid levels are part of the renin-angiotensin system. In response to extracellular fluid loss, rennin is secreted and it increases water uptake and retention by the kidneys. Renin also stimulates the secretion of angiotensin, which induces thirst sensations through the hypothalamus of the brain. With the progression of age, the rennin function is lowered and the kidneys lose the ability to concentrate urine. Angiotensin stimulation of thirst may also be impaired as studies on rats reported that adding angiotensin stimulants in drinks does not increase thirst in the elderly as it would normally do in younger animals.13,27 The second important set of hormones regulating water balance are part of the arginine vasopressin system. Vasopressin is called the antidiuretic hormone because of its potent ability to increase fluid retention in the kidneys. Aldosterone is a mineralocorticoid that primarily regulates sodium balance in the kidneys by stimulating sodium reabsorption and potassium excretion. Both secretion and sensitivity of the hormone is reduced due to ageing.13,27,52
Effects of eplerenone on cerebral aldosterone levels and brain lesions in spontaneously hypertensive rats
Published in Clinical and Experimental Hypertension, 2020
Xue Wang, Yuhai Zhu, Shuanglin Wang, Zhuoqun Wang, Haonan Sun, Yujie He, Wei Yao
ACEI and ARB are widely used in clinical practice. Not only do they control BP, but they also protect organs (21). However, the efficacy of both types of drugs is limited because of issues such as aldosterone-breakthrough (22). Aldosterone has BP-independent effects that promote organ damage (23). Therefore, drugs blocking the mineralocorticoid receptors are relevant and have been increasingly used to treat patients. Kosmala et al. revealed that the addition of spironolactone (25 mg/day) to standard angiotensin II inhibition lowered left ventricular mass (LVM) and decreased levels of fibrotic markers in patients with metabolic syndrome (24). Other studies have shown that 50 mg or 200 mg eplerenone can reduce LVM in patients with resistant hypertension (25,26). ACEI and ARB treatment can also protect the brain. These drugs can ameliorate cognitive impairment induced by chronic restraint stress and are associated with cortical effects that have been correlated with reduced lesion volume and conservation of the hippocampus (27–29). However, research regarding the protective effects of eplerenone on the brain has been rare.
New pharmacotherapy for heart failure with reduced ejection fraction
Published in Expert Review of Cardiovascular Therapy, 2020
Sara Sotirakos, Peter Wheen, James Spiers, Richard Armstrong
Furthermore, MRAs can also be used [1]. Aldosterone is a mineralocorticoid produced by the adrenal glands which promotes the reabsorption of sodium and excretion of potassium in the collecting ducts within the kidney [7]. It does this by upregulating the synthesis of sodium channels and sodium-potassium ATPase via its DNA-binding receptor [7]. The result is higher levels of water reabsorption, higher blood volume, and thus higher blood pressure [7]. Therefore, an antagonist is a suitable target for HFrEF as it will aid in the reduction of fluid overload in patients experiencing symptomatic congestive HF [1]. Aldosterone also has a role in cardiac remodeling and fibrosis to which an MRA would attenuate these effects [8]. Conversely, dapagliflozin targets fluid reabsorption by the blocking of SGLT2, described further in section 1.2.3.