Plasma renin activity, total renin, active renin, and aldosterone were measured as well as urinary prostaglandin E2 and kallikrein in a group of patients with hyperkalemia (6.1-7.7 mEq per liter) and hyporeninemic hypoaldosteronism. Plasma renin activity and aldosterone were low and the response was markedly blunted to upright posture, and furosemide. The rise in cortisol but not aldosterone was normal following ACTH stimulation. Active renin was depressed; however, total renin was normal. Urine PGE was variable including some low values, but the mean of the group was normal (p greater than 0.1). Urine kallikrein excretion was markedly diminished and undetectable in most cases. Fludrocortisone normalized potassium but minimally increased kallikrein in the patients. The possibility exists that kallikrein deficiency in these patients may underlie the inability to generate active renin.
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http://dx.doi.org/10.1016/0161-4630(81)90116-6 | DOI Listing |
Front Cardiovasc Med
January 2025
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
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January 2025
Department of Cardiology, the 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect of VEGFR3 in salt-sensitive hypertension. However, the specific mechanism underlying the role of VEGFR3 in kidney during the overactivation of the renin-angiotensin-aldosterone system remains unclear.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Urology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita-city, 565-0871, Osaka, Japan.
Nocturnal polyuria is a major cause of nocturia, which affects quality of life. Aging-related decreases in nitric oxide production have been reported to contribute to salt-induced nocturnal polyuria. We posited that enhanced nitric oxide production from exercise could mitigate salt-induced nocturnal polyuria.
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Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, 11562 Cairo, Egypt.
Tau hyper-phosphorylation has been recognized as an essential contributor to neurodegeneration in Alzheimer's disease (AD) and related tauopathies. In the last decade, tau hyper-phosphorylation has gained considerable concern in AD therapeutic development. Tauopathies are manifested with a broad spectrum of symptoms, from dementia to cognitive decline and motor impairments.
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