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At least 811 records · Page 45Linked to original sources
PubMed1999

MRI changes during water loading in patients with polydipsia and intermittent hyponatremia.

OBJECTIVE: Patients with polydipsia and intermittent hyponatremia have greater ventricle-brain ratios (VBRs) than matched patients without polydipsia and intermittent hyponatremia and normal subjects. Unlike previous studies, this study controlled for the impact of water loading when examining the volume of intracranial structures. METHOD: Under controlled conditions, eight male schizophrenic patients with polydipsia and intermittent hyponatremia were first assigned to either normal fluid intake or oral water loading and then the alternative condition the following day. Magnetic resonance imaging (MRI) volumetric measurements were made with the use of a standardized protocol. RESULTS: During water loading, total VBR and lateral ventricle volume significantly decreased by 13.1% and 12.6%, respectively. A strong association between change in serum sodium concentration and change in VBR was noted across conditions. CONCLUSIONS: These findings indicate that 1) water loading does not account for the diminished brain volume observed in patients with polydipsia and intermittent hyponatremia in previous studies, and 2) hyponatremia can significantly alter brain morphology on MRI.

Adult↗
PubMed2002

Hyponatremia in distance runners: fluid and sodium balance during exercise.

Since its first description in 1985, two opposing theories have evolved to explain the etiology of symptomatic hyponatremia of exercise. The first holds that the condition occurs only in athletes who lose both water and sodium during exercise, and fail to fully replace their sodium losses. The second theory holds that the symptomatic form of this condition occurs in athletes who generate a whole body fluid overload as a result of an excessive fluid intake during prolonged exercise. It is argued that the promotion of the idea that athletes should drink as much as possible during exercise has produced, rather than prevented, the recent increase in the incidence of this condition. A series of case reports and laboratory studies reported in the past 2 years have established that it is a whole body fluid overload, resulting from sustained high rates of fluid intake, that causes the symptomatic hyponatremia of exercise. There is no evidence that, in the absence of fluid overload, the usual sodium deficits generated during exercise can cause this condition. These findings confirm that the potentially fatal condition of symptomatic hyponatremia would be eliminated from sport immediately if all athletes were advised of the dangers of ingesting as much fluid as possible during any exercise that lasts more than 4 hours.

Female↗
PubMed2003

Hydration: issues for the 21st century.

Historically, hydration research reflected critical issues of the day. War, illness, surviving a shipwreck or time in the dessert, supplying fall-out shelters, and space exploration drove hydration research in the first half of the 20th century. The fitness revolution of the 1970s spurred research on dehydration in physically active people and athletes. The 1990s introduced the "fluid/disease relationship." What will be the driving force behind hydration research in the 21st century? Where are the gaps in our knowledge? This review provides an overview of issues pertinent to determining future directions in hydration research.

Dehydration↗
PubMed2002

Adenosine type 1 receptor antagonists in fluid retaining disorders.

Adenosine is a vasoactive hormone whose action is mediated through at least four receptors. The most prevalent receptors are type 1, which promote vasoconstriction, and type 2, comprised of 2 subtypes (a,b) that promote vasodilation. In the kidney, type 1 receptors located on preglomerular vessels and in the tubule are involved in the regulation of glomerular filtration. Whole body fluid balance is strongly dependent on the ability of the kidney to maintain stable glomerular filtration. Several antagonists to adenosine type 1 receptors have been developed. These agents generate excess fluid (diuresis) and sodium (natriuresis) excretion in control animals and animal models of fluid retention, as well as in normal and oedematous humans. In both animals and humans, these effects are generally achieved without major changes in glomerular filtration. Animal studies have confirmed the location of adenosine type 1 receptors in relevant tissue sites in the kidney. More highly selective antagonists for adenosine type 1 receptors are regularly developed, improving their use in fluid retaining disorders. Clinical trials with these agents have commenced for the treatment of hypertension, renal failure and congestive heart failure, all disorders that include varying levels of fluid retention. The clinical trial results have been mixed. The early results with congestive heart failure suggest great promise for these agents, whereas trials in hypertension and renal failure have been equivocal.

Animals↗
PubMed2005

Cellular effects of guanylin and uroguanylin.

Ingestion of a salty meal induces secretion of guanylin (GN) and uroguanylin (UGN) into the intestinal lumen, where they inhibit Na+ absorption and induce Cl-, HCO3-, and water secretion. Simultaneously, these hormones stimulate renal electrolyte excretion by inducing natriuresis, kaliuresis, and diuresis. GN and UGN therefore participate in the prevention of hypernatremia and hypervolemia after salty meals. The signaling pathway of GN and UGN in the intestine is well known. They activate enterocytes via guanylate cyclase C (GC-C), which leads to cGMP-dependent inhibition of Na+/H+ exchange and activation of the cystic fibrosis transmembrane regulator. In GC-C-deficient mice, GN and UGN still produce renal natriuresis, kaliuresis, and diuresis, suggesting different signaling pathways in the kidney compared with the intestine. Signaling pathways for GN and UGN in the kidney differ along the various nephron segments. In proximal tubule cells, a cGMP- and GC-C-dependent signaling was demonstrated for both peptides. In addition, UGN activates a pertussis toxin-sensitive G-protein-coupled receptor. A similar dual signaling pathway is also known for atrial natriuretic peptide. Recently, a cGMP-independent signaling pathway for GN and UGN was also shown in principal cells of the human and mouse cortical collecting duct. Because GN and UGN activate different signaling pathways in specific organs and even within the kidney, this review focuses on more recent findings on cellular effects and signaling mechanisms of these peptides and their pathophysiologic implications in the intestine and the kidney.

Animals↗
PubMed1999

"Loss prevention".

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Diagnostic Tests, Routine↗
PubMed1999

"Loss prevention".

Explore the source record for details and available documents.

Diagnostic Tests, Routine↗