Interaction of NaCl and behavioral stress on endogenous sodium pump ligands in rats

Our study investigated the hypothesis that the combination of a high NaCl diet and social isolation stress would increase systolic blood pressure (SBP) and endogenous sodium pump ligands (SPL), ouabainlike compound (OLC), and marinobufagenin (MBG). Excretion of MBG and OLC, SBP, and organ weights were studied in four groups (n = 8) of male Fisher 344 x Norwegian brown rats: controls, socially isolated (Iso), 4% NaCl diet (Salt), and the combination of Salt and Iso (Iso+Salt). In Salt, MBG excretion increased by 78% (P < 0.01), whereas SBP and OLC remained unchanged. In Iso, SBP and MBG did not change, but OLC peaked on day 1. In the Iso+Salt, SBP increased by 9 mmHg, MBG excretion increased (42.0 +/- 7.6 vs. 10.0 +/- 1.5 pmol/24 h, P < 0.01), whereas OLC peaked at day 1 (25.0 +/- 2.5 vs. 10.0 +/- 2.0 pmol/24 h, P < 0.01) and remained elevated. Heart and kidney weights were increased in Salt and Iso+Salt. Aortic weights were increased in Iso and Iso+Salt. Thus a high NaCl intake stimulates MBG excretion, whereas isolation stress stimulates OLC. The combination of Salt and Iso is accompanied by marked stimulation of both SPL.     

Salt intake and depletion increase circulating levels of endogenous ouabain in normal men

High-salt diets elevate circulating Na+ pump inhibitors, vascular resistance, and blood pressure. Ouabain induces a form of hypertension mediated via the alpha2-Na+ pump isoform and the calcium influx mode of the vascular sodium calcium exchanger (NCX). Whereas elevated levels of an endogenous ouabain (EO) and NCX have been implicated in salt-sensitive hypertension, acute changes in sodium balance do not affect plasma EO. This study investigated the impact of longer-term alterations in sodium balance on the circulating levels and renal clearance of EO in normal humans. Thirteen normal men consumed a normal diet, high-salt diet, and hydrochlorothiazide (HCTZ), each for 5-day periods to alter sodium balance. EO and other humoral and urinary variables were determined daily. On a normal diet, urinary sodium excretion (140 +/- 16 meq/day), plasma EO (0.43 +/- 0.08 nmol/l) and urinary EO excretion (1.04 +/- 0.13 nmol/day) were at steady state. On the 3rd day of a high-salt diet, urine sodium excretion (315 +/- 28 meq/day), plasma EO (5.8 +/- 2.2 nmol/l), and the urinary EO excretion (1.69 +/- 0.27 nmol/day) were significantly increased, while plasma renin activity and aldosterone levels were suppressed. The salt-evoked increase in plasma EO was greater in older individuals, in subjects whose baseline circulating EO was higher, and in those with low renal clearance. During HCTZ, body weight decreased and plasma renin activity, aldosterone, and EO (1.71 +/- 0.77 nmol/l) rose, while urinary EO excretion remained within the normal range (1.44 +/- 0.31 nmol/day). Blood pressure fell in one subject during HCTZ. HPLC of the plasma extracts showed one primary peak of EO immunoreactivity with a retention time equivalent to ouabain. High-salt diets and HCTZ raise plasma EO by stimulating EO secretion, and a J-shaped curve relates sodium balance and EO in healthy men. Under normal dietary conditions, approximately 98% of the filtered load of EO is reabsorbed by the kidney, and differences in the circulating levels of EO are strongly influenced by secretion and urinary excretion of EO. The dramatic impact of high-salt diets on plasma EO is consistent with its proposed role as a humoral vasoconstrictor that links salt intake with vascular function in hypertension.     

Influence of chronic alterations of salt intake and aging on the kinetic of red cell Na+ and K+ transport in Sprague-Dawley rats

The kinetics of Na+ and K+ (Rb)+ transport mediated by the Na(+)-K+ pump and Na(+)-K+ cotransport system (assessed as a function of Rb+o and Na+i) as well as the magnitude of cation leaks were determined in red cells of young male rats subjected to chronic salt deprivation or salt loading (0.1% and 8% NaCl diet). These salt intake alterations induced moderate kinetic changes of the Na(+)-K+ pump which did not result in significant changes of ouabain-sensitive (OS) Rb+ uptake or Na+ net extrusion at in vivo Na+i and K+o concentrations because a decreased affinity for Na+i in salt-loaded animals was compensated by an increased maximal transport rate. High furosemide-sensitive (FS) Rb+ uptake in red cells of salt-deprived rats was caused by an increase of both the maximal transport rate and the affinity for Rb+o. Cation leaks were also higher in salt-deprived than in salt-loaded rats. In three age groups of rats fed a 1% NaCl diet FS Rb+ uptake (but not FS Na+ net uptake) rose with age due to an increasing maximal transport rate whereas the affinity of the cotransport system for Rbo+ did not change. The age-dependent changes in the kinetics of the Na(+)-K+ pump resulted in a slight decrease of OS Rb+ uptake with age that was not paralleled by corresponding Na+ net extrusion. No major age-related changes of cation leaks were found. Thus some intrinsic properties of red cell transport systems can be altered by salt intake and aging.     

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03-0.75 mmol.kg(-1).day(-1) for 7 days. Acute NaCl administration increased PV (+6.3-8.9%) and plasma sodium concentration (~2%) and decreased plasma protein concentration (-6.4-8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.     

SGK1 as a determinant of kidney function and salt intake in response to mineralocorticoid excess

Mineralocorticoids modify salt balance by both stimulating salt intake and inhibiting salt loss. Renal salt retention is accomplished by upregulation of reabsorption, an effect partially mediated by serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored the contribution of SGK1 to the regulation of renal function, salt intake, and blood pressure during mineralocorticoid excess. DOCA/1% NaCl treatment increased blood pressure and creatinine clearance to a similar extent in SGK1-deficient sgk1(-/-) and wild-type sgk1(+/+) mice but led to more pronounced increase of proteinuria in sgk1(+/+) mice (by 474 +/- 89%) than in sgk1(-/-) mice (by 154 +/- 31%). DOCA/1% NaCl treatment led to significant increase of kidney weight (by 24%) and to hypokalemia (from 3.9 +/- 0.1 to 2.7 +/- 0.1 mmol/l) only in sgk1(+/+) mice. The treatment enhanced renal Na(+) excretion significantly more in sgk1(+/+) mice (from 3 +/- 1 to 134 +/- 32 micromol.24 h(-1).g body wt(-1)) than in sgk1(-/-) mice (from 4 +/- 1 to 49 +/- 8 micromol.24 h(-1).g body wt(-1)), pointing to SGK1-dependent stimulation of salt intake. With access to two drinking bottles containing 1% NaCl or water, DOCA treatment did not significantly affect water intake in either genotype but increased 1% NaCl intake in sgk1(+/+) mice (within 9 days from 3.5 +/- 0.9 to 16.5 +/- 2.4 ml/day) consistent with DOCA-induced salt appetite. This response was significantly attenuated in sgk1(-/-) mice (from 2.6 +/- 0.6 to 5.9 +/- 0.9 ml/day). Thus SGK1 contributes to the stimulation of salt intake, kidney growth, proteinuria, and renal K(+) excretion during mineralocorticoid excess.     

盐胁迫下水稻叶绿体中Na~ 、Cl~-积累导致叶片净光合速率下降

研究了 0～ 2 0 0mmol/L的NaCl胁迫下耐盐性不同的水稻品种Pokkali(耐盐 )和Peta(盐敏感 )根系、叶片和叶绿体中Na 、K 和Cl-含量的变化及其与叶片光合作用的关系。结果表明 :随着NaCl胁迫时间和浓度的增加 ,供试 2个品种在根、叶片和叶绿体中Na 、Cl-含量增加 ,K 含量下降。耐盐品种体内Na 、Cl-含量增加或K 含量减少的幅度小于盐敏感品种。在 2 0 0mmol/L的NaCl胁迫下盐敏感品种根、叶片和叶绿体中的Na /K 分别是耐盐品种的 2 0 8%、30 8%和 2 97%。与Na 相比 ,耐盐品种根系对K 的吸收和向叶片运输的选择性 (SK ,Na)较强。但在经过0、10 0和 2 0 0mmol/L的NaCl处理后 2个品种叶绿体中的Na /K 均高于叶片 (SK ,Na均小于 1)。盐胁迫下水稻叶绿体中Na 、Cl-含量和Na /K 与叶片净光合速率呈极显著负相关。     

盐胁迫下水稻叶绿体中Na+、Cl-积累导致叶片净光合速率下降

研究了0-200mmol/L的NaCl胁迫下耐盐性不同的水稻品种Pokkali(耐盐）和Peta(盐敏感）根系,叶片和叶绿体中Na^ ,K^ 和Cl^-含量的变化及其与叶片光合作用的关系。结果表明：随着NaCl胁迫时间和浓度的增加,供试2个品种在根,叶片和叶绿体中Na^ ,Cl^－含量增加,K^ 含量下降。耐盐品种体内Na^ ,Cl^－含量增加或K^ 含量减少的幅度小于盐敏感品种。在200mmol/L的NaCl胁迫下盐敏感品种根,叶片和叶绿体中的Na^ /K^ 分别是耐盐品种的208％,308％和297％。与Na^ 相比,耐盐品种根系对K^ 吸收和向叶片运输的选择性（SK,Na)较强。但在经过0,100和200mmol/L的NaCl处理后2个品种叶绿体中的Na^ /K^ 均高于叶片（SK,Na均小于1）。盐胁迫下水稻叶绿体中Na^ ,Cl^-含量和Na^ /K^ 与叶片净光合速度呈极显著负相关。     

Evidence for a raised concentration of a circulating sodium transport inhibitor in essential hypertension.

A cytochemical technique that measures the ability of plasma to stimulate guinea-pig renal glucose-6-phosphate dehydrogenase (G6PD) activity in vitro, which is a marker of its ability to inhibit Na+-K+-adenosine-triphosphatase (Na+-K+-ATPase), was used in 19 patients with essential hypertension and 23 normotensive, healthy subjects. The ability of plasma to stimulate G6PD was significantly greater in the hypertensive patients when they were taking their normal sodium diet than in the normotensive subjects, and was significantly correlated with blood pressure. The ability of plasma to stimulate G6PD was inversely correlated with plasma renin activity in the hypertensive patients and increased with age and sodium intake in the normotensive subjects. These results support the hypothesis that essential hypertension, and also perhaps the increase in blood pressure with age in communities that consume large quantities of salt, is in part due to an increase in a circulating concentration of an inhibitor of Na+-N+-ATPase.     

Blood pressure and red cell sodium transport changes following salt load in patients with glomerulonephritis

A group of 44 patients with chronic glomerulonephritis (GN) and 20 healthy subjects were investigated under the conditions of normal dietary NaCl intake and after one week of salt load with a daily addition of 5 g NaCl per os. After the salt load, the mean blood pressure increased significantly in 47% subjects (salt-sensitive) and their natriuretic response was accompanied by an increase of glomerular filtration rate. The rates of ouabain-sensitive (OST) and furosemide-sensitive transport (FST) were decreased in patients with chronic GN even before salt loading which did not change these values. The lower OST rate can be explained by a reduced affinity for internal Na+. A decreased affinity of the Na(+)-K+ cotransport system for internal Na+ was detected only in hypertensive GN patients. In our study, no relationship between salt-sensitivity and red cell sodium transport either in normotensive or in hypertensive GN patients was found.     

Chronic potassium supplementation of newborn dogs increases cortical Na,K-ATPase but not urinary potassium excretion

The distal nephron of the newborn dog cannot secrete an acute potassium load as efficiently as can that of the adult dog. Distal nephron potassium secretion is dependent upon basolateral Na,K-ATPase activity. Because Na,K-ATPase activity is lower in the immature than the mature distal nephron, it was hypothesized that lower Na,K-ATPase activity may be responsible for the lower potassium secretory capacity of the immature nephron. In the adult, chronic high dietary potassium intake increases renal tubular potassium secretory capacity by increasing Na/K pump abundance in distal nephron segments responsible for potassium secretion. Therefore, in order to test the above hypothesis, renal cortical and outer medullary Na,K-ATPase activity under Vmax conditions (a measure of pump abundance) and urinary potassium excretion during acute potassium loading were determined in 7 age-matched, litter mate pairs (chronically potassium supplemented versus control) newborn dogs. The potassium supplemented member of each pair received 6 mmol.day-1.kg-1 of KCl as a 150 mM solution for 7-21 days after birth and the control member received an equal volume of water for the same period of time. This protocol resulted in a doubling of renal cortical Vmax Na,K-ATPase activity in the potassium supplemented animals (from 369 +/- 186 to 718 +/- 286 nmol Pi liberated.h-1.micrograms DNA-1, P = 0.025). There was no significant change in outer medullary enzyme activity. Contrary to the above hypothesis, this increase in cortical enzyme activity was not associated with increased potassium excretion at baseline or during acute potassium loading.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiotonic steroids differentially affect intracellular Na+ and [Na+]i/[K+]i-independent signaling in C7-MDCK cells

Recently, we reported that ouabain kills renal epithelial and vascular endothelial cells independently of elevation of the [Na(+)](i)/[K(+)](i) ratio. These observations raised the possibility of finding cardiotonic steroids (CTS) that inhibit the Na(+),K(+) pump without attenuating cell survival and vice versa. To test this hypothesis, we compared CTS action on Na(+),K(+) pump, [Na(+)](i) content, and survival of Madin-Darby canine kidney cells. At a concentration of 1 microM, ouabain and other tested cardenolides, as well as bufadienolides such as bufalin, cinobufagin, cinobufotalin, and telobufotoxin, led to approximately 10-fold inhibition of the Na(+),K(+) pump, a 2-3-fold decrease in staining with dimethylthiazol-diphenyltetrazolium (MTT), and massive death indicated by detachment of approximately 80% of cells and caspase-3 activation. In contrast, Na(+),K(+) pump inhibition and elevation of [Na(+)](i) seen in the presence of 3 microM marinobufagenin (MBG) and marinobufotoxin did not affect MTT staining and cell survival. Inhibition of the Na(+),Rb(+) pump in K(+)-free medium was not accompanied by a decline of MTT staining and cell detachment but increased sensitivity to CTS. In K(+)-free medium, half-maximal inhibition of (86)Rb influx was observed in the presence of 0.04 microM ouabain and 0.1 microM MBG, whereas half-maximal detachment and decline of MTT staining were detected at 0.03 and 0.004 microM of ouabain versus 10 and 3 microM of MBG, respectively. Both ouabain binding and ouabain-induced [Na(+)](i),[K(+)](i)-independent signaling were suppressed in the presence of MBG. Thus, our results show that CTS exhibit distinctly different potency in Na(+),K(+) pump inhibition and triggering of [Na(+)](i)/[K(+)](i)-independent signaling, including cell death.     

Gastrointestinal osmoreceptors and renal sodium excretion in humans

The hypothesis that natriuresis can be induced by stimulation of gastrointestinal osmoreceptors was tested in eight supine subjects on constant sodium intake (150 mmol NaCl/day). A sodium load equivalent to the amount contained in 10% of measured extracellular volume was administered by a nasogastric tube as isotonic or hypertonic saline (850 mM). In additional experiments, salt loading was replaced by oral water loading (3.5% of total body water). Plasma sodium concentration increased after hypertonic saline (+3.1 +/- 0.7 mM), decreased after water loading (-3.8 +/- 0.8 mM), and remained unchanged after isotonic saline. Oncotic pressure decreased by 9.4 +/- 1.2, 3.7 +/- 1.2, and 10.7 +/- 1.3%, respectively. Isotonic saline induced an increase in renal sodium excretion (104 +/- 15 to 406 +/- 39 micromol/min) that was larger than seen with hypertonic saline (85 +/- 15 to 325 +/- 39 micromol/min) and water loading (88 +/- 11 to 304 +/- 28 micromol/min). Plasma ANG II decreased to 22 +/- 6, 35 +/- 6, and 47 +/- 5% of baseline after isotonic saline, hypertonic saline, and water loading, respectively. Plasma atrial natriuretic peptide (ANP) concentrations and urinary excretion rates of endothelin-1 were unchanged. In conclusion, stimulation of osmoreceptors by intragastric infusion of hypertonic saline is not an important natriuretic stimulus in sodium-replete subjects. The natriuresis after intragastric salt loading was independent of ANP but can be explained by inhibition of the renin-angiotensin system.     

Influence of silicon on microdistribution of mineral ions in roots of salt-stressed barley as associated with salt tolerance in plants

Two contrasting barley (Hordeum vulgare L.) cultivars: Kepin No.7 (salt sensitive), and Jian 4 (salt tolerant) were grown hydroponically to investigate the microdistribution of mineral ions in roots as affected by silicon (Si) with respect to salt tolerance. The experiment was undertaken consisting of two treatments with 3 replicates: (i) 120 mmol · L-1 NaCl alone (referred to as Si-NaCl+), (ii) 120 mmol·L-1 NaCl + 1.0 mmol · L-1 Si (as potassium silicate) (referred to as Si+NaCl+). Plant root tips were harvested for microanalysis using an energy dispersive X-ray microanalyzer (EDX) 30 d after transplanting. Higher Cl and Na X-ray peaks were recorded in the root epidermal, cortical and stelar cells of roots for the treatment Si-NaCl+ with the majorities of Na and Cl being accumulated in epidermal and cortical cells, while relatively low K peaks were observed regardless of the barley cultivars used. By contrast, considerably higher K peaks were detected in the epidermal, cortical and stelar cells of th     

NaCl和Na2CO3胁迫对桑树幼苗生长和光合特性的影响

以1年生“青龙桑”幼苗为试验材料,研究了中性盐(NaCl)和碱性盐(Na2CO3)胁迫下桑树幼苗的生长和叶片光合特性.结果表明:盐胁迫明显降低了桑树幼苗的株高、叶片数、生物量和叶片的光合能力.随着Na+浓度的增加,桑树叶片的气孔导度、蒸腾速率、净光合速率、实际光化学效率、电子传递速率和光化学猝灭系数明显降低,过剩光能以非光化学猝灭形式耗散的比例增加,桑树叶片的光能转化效率和光合能力下降.在Na+浓度＜150 mmol·L-1时,桑树幼苗的光合能力和生长受到的抑制较小,通过增加根冠比进一步适应盐胁迫,但这种保护机制随着盐浓度的增加逐渐降低.在Na2CO3胁迫下,＞50 mmol·L-1 Na+浓度对桑树的生长和光合能力表现出较强的抑制作用,并随Na+浓度的增加,抑制程度加大.在NaCl＜ 150mmol·L-1时,桑树的光合能力主要依赖植株形态和光合代谢双重途径适应中性盐逆境,而在NaC1浓度＞150 mmol·L-1和碱性盐胁迫下,其主要依赖光合代谢来适应逆境.     

盐胁迫对豌豆根液泡膜H^＋—ATPase活性及含量的影响

为了阐明液泡膜H^ -ATPase在盐胁迫下的作用和适应性调节机制,对豌豆（Pisum sativum L.）植株进行不同盐浓度和不同盐胁迫时间（1－3d）的处理后,分别测定液泡膜H^ -ATPase的H^ 转运活性、水解性和蛋白含量（A亚基）的变化。结果表明,100mmol/L和200mmol/L NaCl 处理1dH^ -ATPase的水解活性没有变化,而250mmol/L NaCl处理1d引起水解活性降低约25％。100mmol/L NaCl处理2d内水解活性没有变化,而第3天活性下降约20％。但是上述盐胁迫均能提高液泡膜H^ -ATPase的质子转运活性,说明盐胁迫后H^ -ATPase的水解活性和质子转运活性的变化不成比例,盐胁迫可能导致偶联比率的改变。Western blot研究发现,上述盐胁迫对液泡膜H^ -ATPase（A亚基）的含量基本无影响,仅100mmol/L NaCl处理3d后A亚基的量略有下降,这些结果证明,盐胁迫能刺激提高豌豆根液泡膜H^ -ATPase的H^ 泵效率,且泵效率的提高是源于偶联比率的改变,而不是由于ATP水解活性的提高和蛋白含量的增加。     

Lymph osmolality and rehydration from NaCl solutions by toads, Bufo marinus

Toads, Bufo marinus, allowed to maintain an ad libitum state of hydration were dehydrated by 10 15% of their standard weight and allowed to rehydrate from either deionized water or from 10 or 50 mmol l(-1) NaCl solutions. Toads rehydrating from the dilute salt solutions recovered a larger fraction of their standard weight than did toads rehydrating from deionized water despite there being a reduced osmotic gradient. Amiloride did not reduce water gain from these solutions. Water uptake from 100 mmol l(-1) sucrose and 50 mmol l(-1) Na gluconate was reduced relative to deionized water by a fraction predicted from the osmotic gradient. Thus, the presence of both Na+ and Cl- are required for the augmentation of water gain from dilute salt solutions. Toads allowed to rehydrate from 120 mmol l(-1) NaCl for 180 min recovered nearly as much water as toads rehydrating from deionized water for 120 min and the lymph osmolality was not reduced relative to the dehydrated condition. The recovery of water from the salt solution was greater than that predicted from the reduced osmotic gradient and amiloride partially inhibited the rehydration from 120 mmol l(-1) NaCl. Solute coupled water transport can therefore be demonstrated in living animals but only from a NaCl solution that is nearly isoosmotic with the lymph. The mechanism for enhanced water gain from dilute salt solutions remains unresolved.     

NaCl胁迫下野生和栽培大豆幼苗体内离子的再转运

采用NaCl根际处理和叶面饲喂^22Na方法,研究了野生大豆(Glycine soja)——耐盐的BB52、盐敏感的N23232和栽培大豆(Glycine max)——较耐盐的Lee68幼苗在盐胁迫及解除过程中对Na^ 、Cl^-的吸收和再转运。结果表明,在NaCl根际处理12h过程中,BB52和Lee68幼苗根对Na^ 、Cl^-吸收和向茎、叶的运输逐渐增加,10h时趋于稳定,Na^ 、Cl^-含量高低顺序是根＞茎＞叶。但N23232的Na^ 、Cl^-含量则是茎＞根＞叶。在用NaCl对根处理10h后再解除NaCl处理的0～36h内,BB52吸收的Na^ 、Cl^-较多地留于根部或转运至根茎过渡区,叶中较少。N23232吸收的Na^ 较多地转运至茎部,而Cl^-含量在幼苗各部分无差异。叶片饲喂^22Na 10h后,BB52吸收^22Na较N23232多,并较多地向根部运输。从离子再转运角度讨论了BB52的耐盐性。     

NaCl胁迫对高粱根、叶鞘和叶片液泡膜ATP酶和焦磷酸酶活性的影响

NaCl胁迫初期 ,Na 主要在根和叶鞘中积累。相应地 ,根和叶鞘液泡膜ATP酶和焦磷酸酶水解活性、依赖ATP和PPi的质子泵活性及Na /H 逆向转运活性均明显增加 ,根和叶鞘的生长没有受到抑制。NaCl胁迫后期 ,Na 开始向地上部分运输并在叶片中积累。此时 ,叶片液泡膜质子泵和Na /H 逆向转运活性开始增加 ,根和叶鞘的Na/K比增加 ,其液泡膜ATP酶和焦磷酸酶水解活性、质子泵活性和Na /H 逆向转运活性下降。相应地 ,根和叶鞘的生长也下降。当保温介质中Na/K比超过 1时 ,液泡膜微囊ATP酶和焦磷酸酶活性均随Na/K比的增加而下降。表明非盐生植物液泡膜质子泵在盐胁迫的初期对Na 在液泡内的积累及其耐盐性起重要作用     

盐胁迫对空心莲子草生长和光合作用的影响

用NaCl浓度为0(对照)、50、100、150、200、250、300、350mmol/L处理空心莲子草[Alternantheraphiloxeroides(Mart.)Griseb]。结果表明:盐胁迫下,植株鲜重、干重和根冠比都下降,含水量和肉质化程度先略高于对照,而后逐渐下降;根、茎和叶中Na 含量呈上升趋势,而K 含量呈下降趋势,且在同一浓度的盐处理下,叶的Na 和K 含量最高,茎的次之,根的最低;游离氨基酸(free amino acid,FAA)逐渐减少,脯氨酸(proline,Pro)含量先略低于对照,而后则急剧上升,可溶性糖含量(soluble sugar,SS)的变化正相反;净光合速率(net photosynthetic rate,Pn)、气孔导度(stomatal conductance,Gs)和蒸腾速率(transpirationrate,Tr)呈下降趋势,胞间CO2浓度(intercellular CO2concentration,Ci)呈上升趋势;膜稳定性呈下降趋势。因此,空心莲子草是一种盐生植物,且最适盐浓度较低;Na 主要积累在地上部的茎和叶中。推测它有可能向盐渍土壤蔓延。     

Effects of Salt Stress on the Activity and the Amount of Tonoplast H+-ATPase from Pea Roots

To study the function and adaptive mechanism of tonoplast H+ATPase under salt stress, pea ( Pisum sativum L.) seedlings were treated with different concentrations of salt （100-250 mmol/L NaCl） and with 100 mmol/L NaCl for different days (1-3 d). The ATP hydrolytic activity and the proton transport activity and the changes of the amount of tonoplast H+ ATPase (subunit A) were measured. ATP hydrolytic activity of H+ATPase prepared from plants treated with 250 mmol/L NaCl was reduced by about 25% compared to that of control plants, but that of stressed plants treated with 100 mmol/L and 200 mmol/L NaCl was unchanged. The activity from plants treated with 100 mmol/L NaCl for up to 3 d was lower than that of control plants by 20%. But the proton transport activity was increased under the same salt stresses as above. These results showed that the changes of the hydrolytic activity and the proton transport activity were not in proportion and salt stress may cause the change of the coupling ratio of H+ transport activity to ATP hydrolysis. The protein amount kept unchanged and reduced a little only when pea was treated with 100 mmol/L NaCl for 3 d. These results indicated that salinity stimulated the increase of the pump efficiency of the V-ATPase from pea roots, which was due to the change of the coupling ratio, but not due to the increase of ATP hydrolysis and the amount of V-ATPase.