Disease relevance of sodium chloride

• To evaluate the behavior of active kallikrein excretion in salt-sensitive and salt-resistant hypertensive patients during changes in sodium-chloride (NaCl) intake, 61 male, nonobese, nondiabetic outpatients affected by uncomplicated essential hypertension were given a diet that contained 140 mmol NaCl per day for 2 wk [1].
• Sodium-chloride-induced protection in nephrotoxic acute renal failure: independence from renin [2].
• Strong ion difference (SID), strong ion gap, sodium-chloride effect, and the urinary SID were calculated [3].

High impact information on sodium chloride

• Electroneutral Na-(K)-Cl cotransporters are present in most cell types, where they play an important role in both sodium-chloride absorption and secretion and cell volume regulation [4].
• We have isolated cDNAs encoding the two major electroneutral sodium-chloride transporters present in the mammalian kidney, the bumetanide-sensitive Na(+)-K(+)-Cl- symporter and thiazide-sensitive Na(+)-Cl- cotransporter, and have characterized their functional activity in Xenopus laevis oocytes [5].
• To date, molecular genetic analyses have determined that mutations in the gene encoding the thiazide-sensitive sodium-chloride (Na-Cl) cotransporter underlie the pathogenesis of the Gitelman variant [6].
• Within the kidney, WNKs probably regulate the surface expression of several proteins involved in ion transport, including the sodium-chloride cotransporter (NCCT) and the potassium channel renal outer medullary potassium channel (ROMK), based on co-expression studies in Xenopus oocytes [7].
• Salt taste is detected only when above salivary sodium-chloride concentrations; thus saliva influences salt taste threshold levels [8].

Chemical compound and disease context of sodium chloride

• Renal factors assumed to be operative in juvenile hypertension are involving either volume control (by renal regulation of sodium-chloride and water balance) or vasoactive substances like the kallikrein-kinin, the renin-angiotensin and the prostaglandin system and other less well defined hormones [9].

Biological context of sodium chloride

• This study describes the biodiversity of the indigenous microbial community in the sodium-chloride water brines (cryopegs) derived from ancient marine sediments and sandwiched within permafrost 100-120,000 years ago after the Arctic Ocean regression [10].
• The sodium-chloride cotransport system would effect the uphill transport of chloride against its electrochemical potential gradient at the luminal membrane of the cell [11].
• The data presented here reveal that although B. calamita seems to be yet another exception to the rule of larval strict ammoniotelism, the tadpoles are not able to use urea as an osmolyte and rely on sodium-chloride balance instead [12].
• The predominant inhibition was in the ouabain-sensitive component of oxygen consumption, which suggests that BZDs inhibit active sodium-chloride transport in the TALH [13].
• As a result, a single nucleotide polymorphism in exon 23 of the solute carrier family 12 (sodium-chloride cotransporter) member 3 gene was found to be strongly associated with diabetic nephropathy [14].

Anatomical context of sodium chloride

• Coupled sodium-chloride influx across brush border of flounder intestine [15].
• Sodium-chloride sensitive receptors located in hepatic portal vein of the rat [16].
• Gitelman syndrome: genetic and expression analysis of the thiazide-sensitive sodium-chloride transporter in blood cells [17].
• Sodium-chloride transport in the medullary thick ascending limb of Henle's loop: evidence for a sodium-chloride cotransport system in plasma membrane vesicles [11].
• Integration of the mature protein occurs in the absence of stroma, into sodium-chloride-washed, and trypsin-treated thylakoid membranes [18].

Associations of sodium chloride with other chemical compounds

• We therefore wanted to determine if: 1) adenosine modulates furosemide-induced renin release and 2) sodium-chloride reabsorption at the macula densa is essential for adenosine actions [19].
• These studies indicate that the sodium-chloride cotransport system described previously in the rectal gland is in fact a sodium-potassium chloride cotransport system [20].
• We have previously shown that glutamate-induced neurotoxicity is mediated by a sodium-chloride component and a calcium component in our cerebellar granule cell culture [21].

Gene context of sodium chloride

• The majority of patients with Gitelman syndrome carry inactivating mutations in the SLC12A3 gene encoding the sodium-chloride cotransporter located in the distal convoluted tubule [22].
• Functional studies point to a defect in the distal renal tubule in the thiazide-sensitive, electroneutral sodium-chloride co-transporter (TSC) [23].

Analytical, diagnostic and therapeutic context of sodium chloride

• Antisense oligonucleotides to the sodium-chloride cotransporter specifically inhibited the chlorothiazide-induced depolarization and rise of intracellular calcium and reduced immunofluorescence staining for the sodium-chloride cotransporter protein in UMR-106 cells [24].

References