In an attempt to obtain evidence in the mechanism of stone formation, the effectiveness of Amiloride. a K-sparing diuretic known to act on the distal nephron. on the kidney with oxamide-induced urolithiasis was investigated. Futhermore. the influence of stone formation on the distribution of intrarenal blood flow and the effect of Amiloride on them were also studied. Most prominent derangements of renal function observed during stone formation were decreases of both C(PAH) and C(cr) indicating the curtailment in renal hemodynamics. The oxamide-treated kidney also responded to Amiloride with typical natriuresis and antikaluresis. in the same fashion with normal kidneys. The experiments in which the intrarenal blood flow distribution was measured by PAH-extraction technique raveled that mainly the cortical blood flow was curtailed, whereas non-cortical blood flow (medullary flow) did not change during oxamide-stone formation. Amiloride did not influence the intrarenal b100d flow distribution both in normal and oxamide kidneys. These observations suggest that oxamide-stone formation was initiated not by tubular necrosis produced by the toxic action of oxalate on the tubules, but rather by mechanical obstruction of the tubules.
Amiloride* ; Hemodynamics ; Kidney* ; Natriuresis ; Necrosis ; Nephrons ; Renal Circulation ; Urolithiasis

Neuromyelitis optica spectrum disorder (NMOSD) may present with area postrema syndrome, which is characterized by intractable vomiting and hiccups. Hyponatremia is common in NMOSD and is mostly associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In contrast to SIADH, cerebral salt wasting syndrome (CSWS) causes hyponatremia, which is associated with severe natriuresis and extracellular volume depletion in patients with cerebral disease. To our knowledge, hyponatremia associated with CSWS has not been reported in a patient with NMOSD. Here, we describe a NMOSD presenting with hyponatremia, which may be caused by CSWS following area postrema syndrome.
Area Postrema ; Hiccup ; Humans ; Hyponatremia ; Inappropriate ADH Syndrome ; Natriuresis ; Neuromyelitis Optica* ; Vomiting ; Wasting Syndrome*

Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction with associated cerebral pathology. It is distinct from the syndrome of inappropriate antidiuretic hormone secretion, which is characterized by inappropriate retention of free water. We report a patient with a porencephalic cyst who developed cerebral salt wasting. His initial treatment was supplementation of water and salt, which did not improve natriuresis or volume contraction. Fludrocortisone administration effectively managed the cerebral salt wasting.
Adolescent ; Fludrocortisone/*therapeutic use ; Humans ; Hyponatremia/*drug therapy ; Male ; Natriuresis/physiology ; Sodium Chloride/therapeutic use

BACKGROUND: K+ channel opener has been considered as a vasorelaxing agent working through hyperpolarization of vascular smooth muscle cells. Renal tubules-proximal, thick ascending limb of Henle and cortical collecting duct-are the site of the diversity of the K+ channel. ATP-sensitive K+ channel has been observed in the apical membranes of the thick ascending limb of Henle and collecting duct, and basolateral membrane of the proximal tubule. It was also shown that K+ channel opener increased renal hemodynamics and elicited diuretic and natriuretic effects. METHODS: To clarify the renal effects of WAY120491, a K+ channel opener, experiments were performed in unanesthetized normotensive and renal hypertensive rabbits allowing unilateral renal arterial infusion of agent. RESULTS: Intrarenal arterial infusion (0.13, 0.32 and 0.64 microgram/kg/min) of WAY120491 increaased CPAH, CCr, urine volume, UNaV, UKV and CH2O. Renal hemodynamic effects and increments of urine volume and free water clearance were completely blocked by glibenclamide (8.2 g/kg/min), while increments of UNaV and FENa were not significantly affected. Renal hemodynamic and tubular effects of WAY120491 were not significantly different in two-kidney one clip Goldblatt hypertensive rabbits from sham-operated rabbits. CONCLUSIONS: These results suggest that WAY120491 elicits renal effects through ATP-sensitive K+ channel in the renal vasculatures and renal tubules and the renal effects of WAT120491 may not be altered in the hypertension.
Diuresis ; Extremities ; Glyburide ; Hemodynamics ; Hypertension ; Membranes ; Muscle, Smooth, Vascular ; Natriuresis ; Natriuretic Agents ; Rabbits* ; Water

PURPOSE: We observed excessive renal excretion of salt and water, without underlying renal diseases or definite causes, accompanied with severe hypotension in critically ill patients. This study investigates the clinical courses and characteristics of these patients. METHODS: We retrospectively analyzed 13 patients with polyuria of unknown origin, which persited equal to or longer than 3 days, among hypotensive patients, who were admitted to intensive care unit. RESULTS: The causes of hypotension included sepsis in 11 patients and adrenal insufficiceny in one patient. The cause of hyptension was unknown in one patient. Vassopressors were used in all patients, and hypotension persisted for 13.2+/-8.6 days. Polyuria persisted for 10.6+/-8.2 days, and the duration of polyuria was strongly correlated with that of hypotension (R=0.919, p<0.001). Low dose steroid was used in 8 patients for the treatment of hypotension, and hypotension improved in 3 patients within 2 days after steroid administration. Four patients died during the hosptialization, and the duration of hypotension in non-survivors was greater than that in survivors (21.2+/-9.7 days and 9.6+/-5.2 days respectively, p=0.020). CONCLUSION: In critically ill patients with severe hypotension, we observed 13 cases of inappropriate natriuresis and polyuria. These results suggest that the persistence of poyluria and hypotension might affect the prognosis of these patients, and adrenal insufficicieny might be associated with this appearance in some patients. Further studies are needed to establish causes and treatments for this appearance.
Adrenal Insufficiency ; Critical Illness ; Humans ; Hypotension ; Intensive Care Units ; Natriuresis ; Polyuria ; Prognosis ; Retrospective Studies ; Sepsis ; Survivors

Central tryptaminergic system has been shown to play an important role in the regulation of renal function: 5-HT-1 (5-hydroxytryptamine-1) receptors might seem to mediate the diuresis and natriuresis, whereas the 5-HT-2 and 5-HT-3 receptors mediate the antidiuretic and antinatriuretic effects. This study attempted to delineate the role of central 5-HT-1A subtype in the regulation of rabbit renal function by observing the renal effects of intracerebroventricularly(icv)-administered PAPP (p-aminophenylethyl-m-trifluoromethylphenyl piperazine, LY165163), a selective agonist of 5-HT-1A receptors. PAPP in doses ranging from 40 to 350 microgram/kg icv induced significantly diuresis, natriuresis, and kaliuresis, along with increased renal perfusion and glomerular filtration. Systemic blood pressure was also increased. Free water reabsorption (T-cH-2O), a measure of ADH (antidiuretic hormone) secretion, was increased also. Intravenous 350 microgram/kg of PAPP elicited antidiuresis and antinatriuresis together with decreased blood pressure, thus indicating that the effects of icv PAPP were brought about through the central mechanisms, not by direct peripheral effects of the drug on kidney. Ketanserin, a selective 5-HT-2 antagonist, 40 microgram/kg icv, did not affect the renal effects of the icv PAPP. Methysergide, a non-selective 5-HT-1 antagonist, also did not block the renal functional responses by the icv PAPP. NAN-190, a 5-HT-1A antagonist, also did not antagonized the renal action of the icv PAPP. However the increased free water reabsorption was abolished by both methysergide or ketanserin pretreatment. The increments of blood pressure by icv PAPP was blocked only by NAN-190 pretreatment. These observations suggest that the central 5-HT-1A receptor might be involved in the central regulation of rabbit renal function by exerting the diuretic and natriuretic influences.
Blood Pressure ; Diuresis ; Filtration ; Ketanserin ; Kidney ; Methysergide ; Natriuresis ; Perfusion ; Rabbits* ; Water

The pathophysiology of hypertension, which affects over 1 billion individuals worldwide, involves the integration of the actions of multiple organ systems, including the kidney. The kidney, which governs sodium excretion via several mechanisms including pressure natriuresis and the actions of renal sodium transporters, is central to long term blood pressure regulation and the salt sensitivity of blood pressure. The impact of renal sodium handling and the salt sensitivity of blood pressure in health and hypertension is a critical public health issue owing to the excess of dietary salt consumed globally and the significant percentage of the global population exhibiting salt sensitivity. This review highlights recent advances that have provided new insight into the renal handling of sodium and the salt sensitivity of blood pressure, with a focus on genetic, inflammatory, dietary, sympathetic nervous system and oxidative stress mechanisms that influence renal sodium excretion. Increased understanding of the multiple integrated mechanisms that regulate the renal handling of sodium and the salt sensitivity of blood pressure has the potential to identify novel therapeutic targets and refine dietary guidelines designed to treat and prevent hypertension.
Blood Pressure ; Genetics ; Hypertension ; Inflammation ; Kidney ; Natriuresis ; Nutrition Policy ; Oxidative Stress ; Public Health ; Sodium* ; Sympathetic Nervous System

Hypertension is a polygenic and multifactorial disease and is intimately related to salt homeostasis. Four important vasoactive peptide systems participate in regulating blood pressure and salt homeostasis. Their interplay is indispensible in many physiologic and pathologic conditions. While the renin-angiotensin and the endothelin systems raise blood pressure by inducing vasoconstriction and sodium retention (or excretion), the kallikrein-kinin and the natriuretic peptide systems reduce blood pressure by eliciting vasodilatation and natriuresis. Gene targeting as well as transgenesis have provided us a lot of information on the biological functions of the genes of these systems. Animal models from these technologies are discussed in relation to blood pressure regulation.
Angiotensins ; Animals* ; Blood Pressure* ; Endothelins ; Gene Targeting ; Gene Transfer Techniques ; Homeostasis ; Hypertension ; Models, Animal* ; Natriuresis ; Sodium ; Vasoconstriction ; Vasodilation

Hyponatremia in patients with central nervous system disorders is suggestive of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and volume restriction is recommended for its correction. However, if volume depletion is present in a situation otherwise compatible with SIADH, cerebral salt wasting syndrome (CSWS) should be considered as the cause of the hyponatremia to avoid hypovolemic shock that may be induced by the standard management of SIADH, i.e. volume restriction. We present a case of a 17-year-old male patient with CSWS associated with tuberculous meningitis. The clinical feature of the patient comprised hyponatremia, excessive natriuresis, polyuria, and hypovolemia. Following the administration of saline and fludrocortisone, natriuresis and polyuria were decreased, and the hyponatremia improved
Adolescent ; Central Nervous System Diseases ; Fludrocortisone ; Humans ; Hyponatremia ; Hypovolemia ; Inappropriate ADH Syndrome ; Male ; Natriuresis ; Polyuria ; Shock ; Tuberculosis, Meningeal* ; Wasting Syndrome*

The central nervous system (CNS) has important roles in the regulation of sodium and water homeostasis, so the risk of hyponatremia is increased for patients with neurological disorders. Cerebral salt wasting (CSW) is a syndrome that is characterized by hyponatremia and extracellular volume contraction, and these problems are caused by natriuresis and the concomitant polyuria in patient with intracranial disease. It is critical to differentiate CSW from syndrome of inappropriate secretion of antidiuretic hormone (SIADH) for patients with hyponatremia and after they experience cerebral insults. This is because fluid restriction is the treatment of choice for SIADH and administration of isotonic or hypertonic saline is important for treating CSW. We report here on a case of CSW following trassphenoidal surgery for pituitary tumor in a 67-year-old man with nonfunctioning pituitary macroadenoma. Hyposmotic hyponatremia, increased urine output and signs of dehydration developed postoperatively, and the patient was managed by water and salt supplementation.
Aged ; Central Nervous System ; Dehydration ; Homeostasis ; Humans ; Hyponatremia ; Inappropriate ADH Syndrome ; Natriuresis ; Nervous System Diseases ; Pituitary Neoplasms ; Polyuria ; Sodium