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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.
Endogenous Digitalis-Like Factors: Past Progress and Future Prospects
Published in Antonio Coca, Ricardo P. Garay, Ionic Transport in Hypertension: New Perspectives, 2019
The first suggestion that the putative natriuretic hormone could function as an inhibitor of Na,K-ATPase was in a preliminary report by Kramer et al.13 Subsequent work by Gonick and associates14 clearly demonstrated that Na,K-ATPase activity was inhibited in the kidneys of volume-expanded animals, and that extracts of kidneys from volume-expanded animals contained Na,K-ATPase inhibitory activity. This transport system is located in the distal renal tubule and collecting duct, and is responsible for a considerable fraction of total renal sodium reabsorption.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Fluid loss stimulates renal sodium reabsorption, but sodium can be reabsorbed only either with chloride, or in exchange for hydrogen and potassium ions (to maintain electroneutrality). Gastric juice has a high concentration of chloride and patients losing gastric secretions become hypochloraemic. This means that less sodium than normal can be reabsorbed with chloride.
Perspectives on the management of hypertension in Japan
Published in Expert Opinion on Pharmacotherapy, 2020
Tatsuya Maruhashi, Yasuki Kihara, Yukihito Higashi
A combination of increased salt sensitivity and high salt intake is one of the main causes of nocturnal hypertension. Not only daytime blood pressure but also nighttime blood pressure is elevated by high salt intake in patients with high salt sensitivity to excrete sodium from the kidney during night time based on the abnormal pressure-natriuresis [71]. Salt sensitivity is increased by impaired renal sodium excretion due to renal dysfunction and/or enhanced renal sodium reabsorption due to activated RAAS and hyperinsulinemia. Therefore, nocturnal hypertension is common in patients with chronic kidney disease, primary aldosteronism, diabetes mellitus, and metabolic syndrome [72–74]. In those high-risk patients, assessment of nighttime blood pressure should be performed for the assessment of cardiovascular risk and achievement of lower blood pressure control throughout 24 h.
Emerging therapeutic strategies for transplantation-induced acute kidney injury: protecting the organelles and the vascular bed
Published in Expert Opinion on Therapeutic Targets, 2019
Nicolas Melis, Raphael Thuillier, Clara Steichen, Sebastien Giraud, Yse Sauvageon, Jacques Kaminski, Thomas Pelé, Lionel Badet, Jean Pierre Richer, Jonatan Barrera-Chimal, Frédéric Jaisser, Michel Tauc, Thierry Hauet
Aldosterone (Aldo) is the main regulator of renal sodium reabsorption, controlling volume and blood pressure levels, through its classical actions on the epitheliums of the distal nephron. Aldo binds to the mineralocorticoid receptor (MR), a transcription factor of the nuclear receptor family present in the kidney and also in non-epithelial cells [88]. Inappropriate mineralocorticoid signaling has been shown to play an important role in the progression of cardiovascular and renal diseases. New extra-renal pathological effects of this hormone have been characterized, extending its deleterious actions to the cardiovascular system [89]. Clinical trials (RALES, EPHESUS, and EMPHASIS-HF) have demonstrated the benefits of administering low doses of MR antagonists to patients with systolic HF with or without myocardial infarction, resulting in improvement of survival rate and morbidity [90,91].
Decreased expression of Na+-H+ exchanger isoforms 1 and 3 in denervated spontaneously hypertensive rat kidney
Published in Clinical and Experimental Hypertension, 2019
Jianling Li, Qiaoling He, Qingjie Li, Rongjie Huang, Xiaoyan Wei, Xiaofeng Pan, Weifeng Wu
Previous studies have reported that basolateral NHE1 regulates apical NHE3 and HCO3− absorption in the renal medullary thick ascending limb, by controlling the organization of the actin cytoskeleton (36–39). In addition, although the direction of NHE1-dependent Na+ flux is opposite to Na+–K+ ATPase and Na+-HCO3− cotransporter-A (NBC1-A) mediated Na+ translocation, NHE1 may play a regulatory role in proximal tubule vectorial Na+ transport through functional interaction with these transporters (23). Sonalker et al. (13) reported that chronic noradrenaline infusions strongly upregulate the renal expression of renal sodium transporters NHE3, NBC-1 and bumetanide-sensitive Na–K–2Cl cotransporter (BSC-1). Moreover, renal denervation normalizes the protein expression of the proximal tubule NHE3, BSC-1 expression in the thick ascending limb and sodium chloride cotransporter (NCC) expression in the distal convoluted tubule of programmed rats (40). All of these studies, together with our results, suggest that the renal sympathetic nervous system may regulate renal sodium reabsorption in large part by affecting the expression of transport systems in the nephron. Renal denervation reduces blood pressure, and the mechanism for this effect is likely linked to the role of renal nerves in the regulation of sodium transport.