The purpose of this study was to investigate the influence of mixed NaCl-KCl salt on sodium intake and urinary excretion of sodium and potassium. In this study, 3-day food records for pre-experimental diet and 24-hr urine collected for 2-days, 6-day experimental diet food and 24-hr urine were used to evaluate the relationship between Na metabolism. In the experimental diet food, mixed NaCl-KCl salt was added. During the pre-experimental diet period, intakes of Na and K were 178.2 mEq and 56.4 mEq, respectively. The urinary excretion of Na and K in 24-hr were 139.6 mEq, 27.7 mEq, respectively and urinary Na/K ratio was 6.6. During the experimental diet period, intakes of Na and K were 130.2 mEq and 120.4 mEq, respectively. The urinary excretion of Na and K in 24-hr were 100.2 mEq, 37.1 mEq, respectively and urinary Na/K ratio was 2.8. According to this study, it is concluded that mixed NaCl-KCl salt diet decreased the intake of Na, and increased the intake of K.
Diet ; Metabolism ; Potassium* ; Sodium*

Na+/H+ antiporter plays an important role in mechanisms of the plant salt tolerance, it extrudes Na+ from cell energized by the proton gradient generated by the plasm membrane H(+)-ATPase and/or compartmentalizes Na+ in vacuole energized by the proton gradient generated by the vacuolar membrane H(+)-ATPase and H(+)-PPiase. This review mainly discusses the latest progress in the study of Na+/H+ antiporter in plant and yeast at molecular level.
Phylogeny ; Plants ; metabolism ; Salts ; metabolism ; Sodium ; metabolism ; Sodium-Hydrogen Exchangers ; classification ; metabolism ; Vacuoles ; physiology

No abstract available.
Animal ; Chlorides/metabolism* ; Endometrium/metabolism* ; Female ; Mice ; Sodium/metabolism*

The aim of the present paper was to study the role of sodium calcium exchanger (NCX) in the generation of action potentials (APs) in cardiomyocytes during early developmental stage (EDS). The precisely dated embryonic hearts of C57 mice were dissected and enzymatically dissociated to single cells. The changes of APs were recorded by whole-cell patch-clamp technique before and after administration of NCX specific blockers KB-R7943 (5 μmol/L) and SEA0400 (1 μmol/L). The results showed that, both KB-R7943 and SEA0400 had potent negative chronotropic effects on APs of pacemaker-like cells, while such effects were only observed in some ventricular-like cardiomyocytes. The negative chronotropic effect of KB-R7943 on ventricular-like cardiomyocytes was accompanied by shortening of AP duration (APD), whereas such an effect of SEA0400 was paralleled by decrease in velocity of diastolic depolarization (Vdd). From embryonic day 9.5 (E9.5) to E10.5, the negative chronotropic effects of KB-R7943 and SEA0400 on ventricular-like APs of embryonic cardiomyocytes gradually disappeared. These results suggest that, in the short-term development of early embryo, the function of NCX may experience developmental changes as evidenced by different roles of NCX in autorhythmicity and APs generation, indicating that NCX function varies with different conditions of cardiomyocytes.
Action Potentials ; Animals ; Calcium/metabolism* ; Mice ; Myocytes, Cardiac/metabolism* ; Sodium/metabolism* ; Sodium-Calcium Exchanger ; Thiourea/pharmacology*

Interaction of salinity (NaCl) and cadmium (Cd) on growth, mineral nutrients, Na and Cd accumulation in four barley genotypes differing in salt tolerance was studied in a hydroponic experiment. Cd, NaCl and their combined stresses reduced Ca and Mg concentrations in roots and shoots, K concentration in shoots, increased K and Cu concentrations in roots relative to control, but had non-significant effect on micronutrients Cu, Fe and Mn concentrations in shoot. The three stresses reduced accumulation of most tested nutrients in both roots and shoots, except NaCl and NaCl+Cd stresses for root K and shoot Cu accumulation in salt tolerant genotypes. The salt tolerant genotypes did not have higher nutrient concentration and accumulation than the sensitive ones when exposed to Cd and NaCl stresses. In conclusion, the affecting mechanism of Cd stress on nutrients was to some extent different from salinity stress, and the NaCl+Cd stress was not equal to additional Cd and NaCl stresses, probably due to the different valence and competitive site of Na(+) and Cd(2+). NaCl addition in the Cd-containing medium caused remarkable reductions in both Cd concentration and accumulation, with the extent of reduction being also dependent on genotypes. The salt-tolerant genotypes had lower Na concentration than sensitive ones.
Cadmium ; metabolism ; toxicity ; Chlorophyll ; metabolism ; Genotype ; Hordeum ; drug effects ; genetics ; metabolism ; Minerals ; metabolism ; Sodium ; metabolism ; Sodium Chloride

Ninety weaned albino rats divided into three different dietary groups according to the amount of salt in their diet. Each diet consisted of a basic diet of vegetable origin to which was added a specific amount of NaCl. Diet I contained 0.51 mEq Na(0.03% NaCl), diet II 9.96mEq Na(0.58%NaCl), and diet III 24.60 mEq Na(1.45% NaCl) per 100 grams of diet. Each diet contained 14 mEq of potassium per 100 grame of diet. All rats grew satisfactorily, regardless the type of diet, until the age of 60 weeks. Both male and female rats were on the highest volume of water consumption in the first 10 weeks and in all groups the female rats consumed more water than males. No significant difference in the level of serum and osseous electrolytes was found. In animals receving the higher sodium diet the ratio of heart to kidney weight per kilogram of body weight was 6-8% higher than in the other groups. The frequency of occurence of a chromophobe adenoma seems to be influenced both by the rat strain and by the stress such as is found where a low sodium diet is given. In this study, animals on the highest sodium diet (24. 60 mEq Na: 1.45% NaCl) had a longer life span than the two other lower sodium diet groups.
Animals ; *Body Weight ; *Cereals ; Diet ; Potassium/*metabolism ; Rats ; Sodium/*metabolism

OBJECTIVETo determine whether the GABA-containing neurons in rat central nucleus of amygdala (CeA) can be activated by acute sodium deprivation.

METHODSAcute sodium depletion was induced by subcutaneous injection of furosemide in rats followed by 24 h of dietary sodium deprivation. The rats underwent 0.3 mol/L NaCl/distilled water two bottle choice test, and the activated neurons were labeled and identified with GABA/Fos-double labeling immunohistochemistry.

RESULTSThe rats with acute sodium depletion exhibited significantly more numerous c-fos-positive neurons and GABA/Fos double-labeled neurons in the CeA than the control group (P<0.01, P<0.05). Consumption of 0.3 mol/L NaCl significantly increased the number of c-fos and GABA/Fos double labeled neurons compared to the distilled water group (P<0.001, P<0.01).

CONCLUSIONGABAergic neurons in the CeA may play an inhibitory role in the regulation of sodium intake in rats with acute sodium depletion.

Amygdala ; cytology ; metabolism ; Animals ; GABAergic Neurons ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary ; metabolism ; Sodium, Dietary

Renal outer medullary potassium (ROMK) channel is an important K⁺ excretion channel in the body, and K⁺ secreted by the ROMK channels is most or all source of urinary potassium. Previous studies focused on the ROMK channels of thick ascending limb (TAL) and collecting duct (CD), while there were few studies on the involvement of ROMK channels of the late distal convoluted tubule (DCT2) in K⁺ excretion. The purpose of the present study was mainly to record the ROMK channels current in renal DCT2 and observe the effect of high potassium diet on the ROMK channels by using single channel and whole-cell patch-clamp techniques. The results showed that a small conductance channel current with a conductance of 39 pS could be recorded in the apical membrane of renal DCT2, and it could be blocked by Tertiapin-Q (TPNQ), a ROMK channel inhibitor. The high potassium diet significantly increased the probability of ROMK channel current occurrence in the apical membrane of renal DCT2, and enhanced the activity of ROMK channel, compared to normal potassium diet (P < 0.01). Western blot results also demonstrated that the high potassium diet significantly up-regulated the protein expression levels of ROMK channels and epithelial sodium channel (ENaC), and down-regulated the protein expression level of Na⁺-Cl^- cotransporter (NCC). Moreover, the high potassium diet significantly increased urinary potassium excretion. These results suggest that the high potassium diet may activate the ROMK channels in the apical membrane of renal DCT2 and increase the urinary potassium excretion by up-regulating the expression of renal ROMK channels.
Potassium Channels, Inwardly Rectifying/metabolism* ; Kidney Tubules, Distal/metabolism* ; Potassium/metabolism* ; Epithelial Sodium Channels/metabolism* ; Diet

Virtually all of the dietary potassium intake is absorbed in the intestine, over 90% of which is excreted by the kidneys regarded as the most important organ of potassium excretion in the body. The renal excretion of potassium results primarily from the secretion of potassium by the principal cells in the aldosterone-sensitive distal nephron (ASDN), which is coupled to the reabsorption of Na⁺ by the epithelial Na⁺ channel (ENaC) located at the apical membrane of principal cells. When Na⁺ is transferred from the lumen into the cell by ENaC, the negativity in the lumen is relatively increased. K⁺ efflux, H⁺ efflux, and Cl^- influx are the 3 pathways that respond to Na⁺ influx, that is, all these 3 pathways are coupled to Na⁺ influx. In general, Na⁺ influx is equal to the sum of K⁺ efflux, H⁺ efflux, and Cl^- influx. Therefore, any alteration in Na⁺ influx, H⁺ efflux, or Cl^- influx can affect K⁺ efflux, thereby affecting the renal K⁺ excretion. Firstly, Na⁺ influx is affected by the expression level of ENaC, which is mainly regulated by the aldosterone-mineralocorticoid receptor (MR) pathway. ENaC gain-of-function mutations (Liddle syndrome, also known as pseudohyperaldosteronism), MR gain-of-function mutations (Geller syndrome), increased aldosterone levels (primary/secondary hyperaldosteronism), and increased cortisol (Cushing syndrome) or deoxycorticosterone (hypercortisolism) which also activate MR, can lead to up-regulation of ENaC expression, and increased Na⁺ reabsorption, K⁺ excretion, as well as H⁺ excretion, clinically manifested as hypertension, hypokalemia and alkalosis. Conversely, ENaC inactivating mutations (pseudohypoaldosteronism type 1b), MR inactivating mutations (pseudohypoaldosteronism type 1a), or decreased aldosterone levels (hypoaldosteronism) can cause decreased reabsorption of Na⁺ and decreased excretion of both K⁺ and H⁺, clinically manifested as hypotension, hyperkalemia, and acidosis. The ENaC inhibitors amiloride and Triamterene can cause manifestations resembling pseudohypoaldosteronism type 1b; MR antagonist spironolactone causes manifestations similar to pseudohypoaldosteronism type 1a. Secondly, Na⁺ influx is regulated by the distal delivery of water and sodium. Therefore, when loss-of-function mutations in Na⁺-K⁺-2Cl^- cotransporter (NKCC) expressed in the thick ascending limb of the loop and in Na⁺-Cl^- cotransporter (NCC) expressed in the distal convoluted tubule (Bartter syndrome and Gitelman syndrome, respectively) occur, the distal delivery of water and sodium increases, followed by an increase in the reabsorption of Na⁺ by ENaC at the collecting duct, as well as increased excretion of K⁺ and H⁺, clinically manifested as hypokalemia and alkalosis. Loop diuretics acting as NKCC inhibitors and thiazide diuretics acting as NCC inhibitors can cause manifestations resembling Bartter syndrome and Gitelman syndrome, respectively. Conversely, when the distal delivery of water and sodium is reduced (e.g., Gordon syndrome, also known as pseudohypoaldosteronism type 2), it is manifested as hypertension, hyperkalemia, and acidosis. Finally, when the distal delivery of non-chloride anions increases (e.g., proximal renal tubular acidosis and congenital chloride-losing diarrhea), the influx of Cl^- in the collecting duct decreases; or when the excretion of hydrogen ions by collecting duct intercalated cells is impaired (e.g., distal renal tubular acidosis), the efflux of H⁺ decreases. Both above conditions can lead to increased K⁺ secretion and hypokalemia. In this review, we focus on the regulatory mechanisms of renal potassium excretion and the corresponding diseases arising from dysregulation.
Humans ; Bartter Syndrome/metabolism* ; Pseudohypoaldosteronism/metabolism* ; Potassium/metabolism* ; Aldosterone/metabolism* ; Hypokalemia/metabolism* ; Gitelman Syndrome/metabolism* ; Hyperkalemia/metabolism* ; Clinical Relevance ; Epithelial Sodium Channels/metabolism* ; Kidney Tubules, Distal/metabolism* ; Sodium/metabolism* ; Hypertension ; Alkalosis/metabolism* ; Water/metabolism* ; Kidney/metabolism*

Humans ; Sodium-Calcium Exchanger ; Carrier Proteins ; Pain ; Calcium/metabolism*