Calcium paradox of aldosteronism and the role of the parathyroid glands

The hypercalciuria and hypermagnesuria that accompany aldosteronism contribute to a fall in plasma ionized extracellular Ca2+ and Mg2+ concentrations ([Ca2+]o and [Mg2+]o). Despite these losses and the decline in extracellular levels of these cations, total intracellular and cytosolic free Ca2+ concentration ([Ca2+]i) is increased and oxidative stress is induced. This involves diverse tissues, including peripheral blood mononuclear cells (PBMC) and plasma. The accompanying elevation in plasma parathyroid hormone (PTH) and reduction in bone mineral density caused by aldosterone (Aldo)-1% NaCl treatment (AldoST) led us to hypothesize that Ca2+ loading and altered redox state are due to secondary hyperparathyroidism (SHPT). Therefore, we studied the effects of total parathyroidectomy (PTx). In rats receiving AldoST, without or with a Ca2+-supplemented diet and/or PTx, we monitored urinary Ca2+ and Mg2+ excretion; plasma [Ca2+]o, [Mg2+]o, and PTH; PBMC [Ca2+]i and H2O2 production; plasma alpha1-antiproteinase activity; total Ca2+ and Mg2+ in bone, myocardium, and rectus femoris; and gp91(phox) labeling in the heart. We found that 1) the hypercalciuria and hypermagnesuria and decline (P < 0.05) in plasma [Ca2+]o and [Mg2+]o that occur with AldoST were not altered by the Ca2+-supplemented diet alone or with PTx; 2) the rise (P < 0.05) in plasma PTH with AldoST, with or without the Ca2+-supplemented diet, was prevented by PTx; 3) increased (P < 0.05) PBMC [Ca2+]i and H2O2 production, increased total Ca2+ in heart and skeletal muscle, and fall in bone Ca2+ and Mg2+ and plasma alpha1-antiproteinase activity with AldoST were abrogated (P < 0.05) by PTx; and 4) gp91(phox) activation in right and left ventricles at 4 wk of AldoST was attenuated by PTx. AldoST is accompanied by SHPT, with parathyroid gland-derived calcitropic hormones being responsible for Ca2+ overload in diverse tissues and induction of oxidative stress. SHPT plays a permissive role in the proinflammatory vascular phenotype.     

叶片淋洗对NaCl胁迫下玉米生长和矿质营养的影响

研究了叶片淋洗对NaCl胁迫下玉米生长和体内矿质营养含量的影响 .结果表明 ,无盐或低盐浓度下(0、5 0mmol·L-1) ,淋洗处理与对照的生物量没有差异 ,高盐浓度下 (10 0、2 0 0mmol·L-1) ,淋洗处理的生物量提高 ,pH3 .5淋洗液的淋洗效果好于 pH 7.0 .无盐胁迫时 ,淋洗处理的茎叶K含量高于对照 ,2 0 0mmol·L-1盐胁迫时则低于对照 ;在高盐胁迫时 ,淋洗处理的茎叶Na含量低于对照 ;无盐胁迫时 ,淋洗处理茎叶中Ca、Mg含量高于对照 .根系K、Na、Ca、Mg含量以及植株相对水分含量在淋洗和对照之间基本无明显差别 ,说明淋洗可以减轻中高度盐胁迫下玉米植株的受害程度 ,其原因与淋洗降低茎叶中Na含量有关 .     

The effect of aging on intestinal absorption and status of calcium, magnesium, zinc, and copper in rats: A stable isotope study

Many investigators have reported changes in mineral status with age but conflicting observations were done concerning mineral absorption. This study was conducted to clarify the effect of aging on intestinal absorption and status of minerals, using a stable isotope approach. To do so, 40 rats of different ages: 9, 22, 44, and 88 weeks were fed with a semi-purified diet for a total of 30 days. At the beginning of the 4th week, the rats received a stable isotope solution containing (44)Ca, (25)Mg, (67)Zn, and (65)Cu. Individual feces and urine were then collected during 4 consecutive days in order to measure stable isotopes by inductively coupled plasma/mass spectrometry (ICP/MS) and blood and tissues were sampled for mineral status determination. Intestinal absorption of (44)Ca and (67)Zn considerably decreased with age, whereas intestinal (25)Mg absorption decreased only moderately and intestinal (65)Cu absorption was unaffected. Plasma and bone calcium (Ca) were not modified with age whereas urinary Ca excretion considerably increased. Plasma and erythrocyte magnesium (Mg) levels were unaffected with age whereas urinary Mg excretion and Mg bone level decreased. Plasma zinc (Zn) level decreased and bone Zn level increased with age whereas red blood cell and liver Zn level and urinary Zn excretion remained unchanged. Plasma Cu level increased with age whereas liver and bone Cu levels and urinary Cu excretion remained unchanged. These results show that the effect of aging on the intestinal mineral absorption and status differ largely according to the mineral considered. Further studies are required under different nutritional conditions to explore the underlying mechanisms during aging and to adjust a better nutrition of the elderly.     

盐胁迫下柚和橘幼苗体内矿质元素变化的比较研究

采用沙培法,对盐胁迫下坪山柚和福橘幼苗体内矿质元素的变化进行了研究。结果表明,随着NaCl浓度的增加,坪山柚和福橘幼苗根部及地上部Na^＋、Cl-含量增加,且相同浓度下,福橘比坪山柚高。40mmol／L NaCI胁迫下,坪山柚和福橘幼苗地上部的K^＋、Fe含量,根部的Ca^2＋、Mg^2＋、Zn含量显著下降,而根部Fe含量及地上部Zn含量显著增加。随NaCl浓度增大,坪山柚根部K^＋含量,地上部Ca^2＋、Mg^2＋含量变化不明显,而福橘根部、地上部上述离子含量在NaCl浓度≥160mmol／L时均显著下降。因此,根部K^＋含量,地上部Ca^2＋、Mg^2＋含量存在品种问差异,或许可作为耐盐性鉴定指标。NaCl胁迫降低坪山柚和福橘幼苗根部及地上部P、Mn含量,而Cu含量在较高浓度NaCl胁迫下显著增加。NaCl胁迫明显降低坪山柚和福橘幼苗地上部K^＋／Na^＋、Ca^2＋／Na^＋和Mg^2＋／Na^＋值,其中K^＋／Na^＋值的变化可考虑作为柑橘耐盐性鉴定的指标。     

Mg2+ and ATP effects on K+ activation of the Ca2+-transport ATPase of cardiac sarcoplasmic reticulum.

ATP and the divalent cations Mg2+ and Ca2+ regulated K+ stimulation of the Ca2+-transport ATPase of cardiac sarcoplasmic reticulum vesicles. Millimolar concentrations of total ATP increased the K+-stimulated ATPase activity of the Ca2+ pump by two mechanisms. First, ATP chelated free Mg2+ and, at low ionized Mg2+ concentrations, K+ was shown to be a potent activator of ATP hydrolysis. In the absence of K+ ionized Mg2+ activated the enzyme half-maximally at approximately 1 mM, whereas in the presence of K+ the concentration of ionized Mg2+ required for half-maximal activation was reduced at least 20-fold. Second MgATP apparently interacted directly with the enzyme at a low affinity nucleotide site to facilitate K+-stimulation. With a saturating concentration of ionized Mg2+, stimulation by K+ was 2-fold, but only when the MgATP concentration was greater than 2 mM. Hill plots showed that K+ increased the concentration of MgATP required for half-maximal enzymic activation approx. 3-fold. Activation of K+-stimulated ATPase activity by Ca2+ was maximal at an ionized Ca2+ concentration of approx. 1 microM. At very high concentrations of either Ca2+ or Mg2+, basal Ca2+-dependent ATPase activity persisted, but the enzymic response to K+ was completely inhibited. The results provide further evidence that the Ca2+-transport ATPase of cardiac sarcoplasmic reticulum has distinct sites for monovalent cations, which in turn interact allosterically with other regulatory sites on the enzyme.     

Acute effect of hydrochlorothiazide on renal calcium and magnesium handling in postmenopausal women

A single 50 mg dose of hydrochlorothiazide (HCTZ) decreases the urinary excretion of calcium (U(Ca)V), clearance (C(Ca)) and fractional excretion (FE(Ca)) of calcium. This is accompanied by an increase of total calcium and ionized calcium (Ca2+) concentrations in the serum. On the other hand, HCTZ increases fractional excretion of magnesium (FE(Mg)) and decreases serum Mg2+ concentrations. Moreover, HCTZ decreases markedly clearance of phosphate (C(Pi)) and fractional excretion of phosphate (FE(Pi)) and increases serum phosphate (Pi) concentrations in healthy postmenopausal women. It is concluded that intrinsic renal cellular control promptly uncouples calcium and magnesium tubular reabsorption even without K+ depletion.     

Aglomerular kidney function when challenged with exogenous MgSO4 loading or environmental MgSO4 depletion

The goal of this study was to investigate the role of MgSO4 in aglomerular kidney function, independent of changes in NaCl. The renal handling of MgSO4 was manipulated by intravenous infusion of an isoosmotic solution containing 80 mmol/L MgSO4 or through exposure to an environment that was reduced in MgSO4 concentration by 90%. Intravenous infusion resulted in a transient increase in circulating Mg2+ and SO4 (2-) levels; however, the concentration of both divalent ions in the urine remained elevated throughout the entire infusion period. Infusion also resulted in a transient increase in urine flow rate and apparent glomerular filtration rate, measured using the glomerular filtration rate marker, [3H] PEG 4000. Exposure to MgSO4-depleted conditions resulted in a significant decrease in plasma and urine concentrations of Mg2+ and in the urine concentrations of SO4 (2-); correspondingly, urine flow rate was significantly depressed. The urinary excretion of both Mg2+ and SO4 (2-) demonstrated nonlinear saturation kinetics. The urinary excretion of Mg2+ was significantly correlated with plasma Mg2+ concentration (r=0.75, P=0.04) and yielded a Michealis constant (Km) of 1.67+/-1.43 mmol/L; P=0.26 and a maximal velocity (Vmax) of 117.4+/-47.0 micromol/kg/hr; P=0.046. The urinary excretion of SO4 (2-) was significantly correlated with plasma SO4 (2-) concentration (r=0.94, P<0.02) with a Km of 0.76+/-0.54; P=0.26 and a Vmax of 59.3+/-13.1; P=0.02.     

Increased formation of methylglyoxal and protein glycation, oxidation and nitrosation in triosephosphate isomerase deficiency

Triosephosphate isomerase deficiency is associated with the accumulation of dihydroxyacetonephosphate (DHAP) to abnormally high levels, congenital haemolytic anaemia and a clinical syndrome of progressive neuromuscular degeneration leading to infant mortality. DHAP degrades spontaneously to methylglyoxal (MG)--a potent precursor of advanced glycation endproducts (AGEs). MG is detoxified to D-lactate intracellularly by the glyoxalase system. We investigated the changes in MG metabolism and markers of protein glycation, oxidation and nitrosation in a Hungarian family with two germline identical brothers, compound heterozygotes for triosephosphate isomerase deficiency, one with clinical manifestations of chronic neurodegeneration and the other neurologically intact. The concentration of MG and activity of glyoxalase I in red blood cells (RBCs) were increased, and the concentrations of D-lactate in blood plasma and D-lactate urinary excretion were also increased markedly in the propositus. There were concomitant increases in MG-derived AGEs and the oxidative marker dityrosine in hemoglobin. Smaller and nonsignificant increases were found in the neurologically unaffected brother and parents. There was a marked increase (15-fold) in urinary excretion of the nitrosative stress marker 3-nitrotyrosine in the propositus. The increased derangement of MG metabolism and associated glycation, oxidative and nitrosative stress in the propositus may be linked to neurodegenerative process in triosephosphate isomerase deficiency.     

Modifying sugarcane mineral levels through sodium chloride and mannitol exposure in temporary immersion bioreactors

Temporary immersion bioreactors (TIBs) have been shown to be useful for studying plant stress physiology and inducing chemical mutagenesis. This study describes the effects of exposure to NaCl (salt stress) and mannitol (osmotic stress) within TIB on sugarcane mineral levels in vitro. Shoots were exposed to concentration of NaCl (89.4 mM) and mannitol (123.1 mM) previously shown to result in a 50% reduction in multiplication rate for 30 d. Thereafter, shoot multiplication rate, shoot cluster fresh weight, and levels of selected minerals were measured. Using ICP-OES, the following minerals were quantified: Na, Ga, Mn, Cr, K, Zn, Ca, Li, Mg, Sr, Co, B, Fe, S, P, Al, Ba, and N. Both NaCl and mannitol decreased shoot multiplication by c. 53% and except for Al and Ba altered mineral levels significantly relative to the control: Na accumulation increased markedly (six-fold in NaCl treatment); levels of Ga, Mn, Cr, K, and Zn changed moderately; Ca, Li, Mg, Sr, Co, B, Fe, S, P, and N levels changed to a limited extent. In terms of the minerals that were most affected, Ga, Mn, K, and Zn levels declined under both stresses; Cr appears to be the only exception, having decreased under the salinity stress and increased under the osmotic stress. Our results suggest that both stresses not only affect growth in the same manner and degree but also appear to have similar effects on the physiological mechanisms that modulate mineral levels at the cellular level under stress conditions. Sugarcane growth inhibition appeared to be mainly due to turgor loss under mannitol-induced stress and the accumulation of Na ions under salt stress. Stress resistance in this species is most likely promoted by the retention of a “safe” water status, a high amount of K and Ca, and a low level of Na.

     

Effect of dietary calcium on renal prostaglandins.

The present study was designed to clarify the possible role of renal prostaglandins (PGs) on blood pressure (BP) regulation during calcium (Ca) restriction or supplementation. Twelve normotensive women with a mean age of 21.2 years participated in the study. After 1 week of normal Ca intake (mean +/- SE, 536 +/- 2 mg/day), a low-Ca diet (163 +/- 1 mg/day) was given for a further 1 week. Additional asparagine Ca (3 g as Ca/day) was also given to half of the subjects. BP, heart rate, and serum total and ionized Ca concentrations were measured at the end of each period. Levels of Ca, sodium, PGE2, 6-keto-PGF1 alpha and thromboxane (TX) B2 excreted into urine were also determined. The plasma level of ionized Ca was significantly increased without any change in total Ca in both groups. Low and high Ca intake decreased and increased urinary Ca excretion by 28% and 56%, respectively. BP was not altered after Ca deprivation or loading. However, urinary PGE2 excretion was significantly augmented from 668.9 +/- 68.1 to 959.7 +/- 183.1 ng/day by Ca loading, whereas Ca deprivation decreased PGE2 excretion (695.4 +/- 108.1 to 513.2 +/- 55.2 ng/day). No changes were observed in 6-keto-PGF1 alpha or TXB2 urinary excretion. These results suggest that renal PGE2 synthesis is stimulated or decreased by 1-week Ca loading or deprivation, indicating a possible antihypertensive role of renal PGE2 during high-Ca intake in hypertensives.     

A (Ca2+, Mg2+)-ATPase activity in plasma membrane fragments isolated from squid nerves

A (Ca2+, Mg2+)-ATPase activity and a (Ca2+, Mg2+)-dependent phosphorylation from ATP have been found in plasma membrane fragments from squid optical nerves under conditions where contamination by intracellular organelles is unlikely. The properties of this (Ca2+, Mg2+)-ATPase activity are almost identical to those of the ATP-dependent uncoupled Ca2+ efflux observed in dialyzed squid giant axons. This gives further support to the notion that the mechanism responsible for maintaining the low levels of ionized Ca concentration in nerves at rest is not a Na+-Ca2+ exchange system but an ATP-driven uncoupled Ca2+ pump.     

Calcium and zinc dyshomeostasis during isoproterenol-induced acute stressor state

Acute hyperadrenergic stressor states are accompanied by cation dyshomeostasis, together with the release of cardiac troponins predictive of necrosis. The signal-transducer-effector pathway accounting for this pathophysiological scenario remains unclear. We hypothesized that a dyshomeostasis of extra- and intracellular Ca2+ and Zn2+ occurs in rats in response to isoproterenol (Isop) including excessive intracellular Ca2+ accumulation (EICA) and mitochondrial [Ca2+]m-induced oxidative stress. Contemporaneously, the selective translocation of Ca2+ and Zn2+ to tissues contributes to their fallen plasma levels. Rats received a single subcutaneous injection of Isop (1 mg/kg body wt). Other groups of rats received pretreatment for 10 days with either carvedilol (C), a β-adrenergic receptor antagonist with mitochondrial Ca2+ uniporter-inhibiting properties, or quercetin (Q), a flavonoid with mitochondrial-targeted antioxidant properties, before Isop. We monitored temporal responses in the following: [Ca2+] and [Zn2+] in plasma, left ventricular (LV) apex, equator and base, skeletal muscle, liver, spleen, and peripheral blood mononuclear cells (PBMC), indices of oxidative stress and antioxidant defenses, mitochondrial permeability transition pore (mPTP) opening, and myocardial fibrosis. We found ionized hypocalcemia and hypozincemia attributable to their tissue translocation and also a heterogeneous distribution of these cations among tissues with a preferential Ca2+ accumulation in the LV apex, muscle, and PBMC, whereas Zn2+ declined except in liver, where it increased corresponding with upregulation of metallothionein, a Zn2+-binding protein. EICA was associated with a simultaneous increase in tissue 8-isoprostane and increased [Ca2+]m accompanied by a rise in H2O2 generation, mPTP opening, and scarring, each of which were prevented by either C or Q. Thus excessive [Ca2+]m, coupled with the induction of oxidative stress and increased mPTP opening, suggests that this signal-transducer-effector pathway is responsible for Isop-induced cardiomyocyte necrosis at the LV apex.     

Is hypercalcemic diet a possible antidote to oral contraceptive-induced hypertension?

Administration of oral contraceptive (OC) has been associated with body fluid retention and in high doses over a long period, promotes hypertension. This present investigation tests the hypothesis that the dietary calcium supplementation increases salt and water excretion in OC (norgestre/ethinylestradiol) treated 32 female albino rats randomly distributed into four (1-4) groups of 8 rats each: Control, OC-treated, OC-treated+ Calcium diet fed and Calcium diet fed only respectively. OC was administered to the appropriate groups by gavage. Experimental diet contained 2.5% calcium supplement. Plasma and urinary [Na+] [K+] were evaluated after 8 weeks of experimentation by flame photometry and plasma [Ca2+] by colorimetric method. OC-treatment induced a significant fall in urinary [Na+]. Water excretion was significantly reduced in these animals (control, 3.1±0.56 Vs OC-treated rats, 1.47±0.16). OC-treated rats had significantly higher plasma [K+] compared to control rats. Calcium supplementation induced increases in plasma [Na+], [K+] and augmented urinary Na+ excretion (OC-treated + Ca2+ diet Vs OC-treated only). Compared with the control rats, high Ca2+ diet fed rats exhibited significant increases in plasma [Na+] and [K+] accompanied by significant decreases in urinary H20 excretion. These results strongly suggest that high dietary Ca2+ supplementation increases salt and water excretion in OC-treated rats and potentially moderates fluid retention and blood pressure in these animals, and may be of clinical significance in OC-induced abnormal fluid retention and perhaps OC-induced hypertension.Keywords: Hypercalcemic-diet, Oral contraceptive, Plasma electrolytes, Hypertension, Female-albino-rats.     

Fructooligosaccharides enhance mineral apparent absorption and counteract the deleterious effects of phytic acid on mineral homeostasis in rats

Phytic acid (PA) and fructooligosaccharides (FOS) such as inulin are two food components that are able to modify mineral absorption negatively or positively. The influence of PA and FOS on the cecal and apparent mineral absorption as well as on the mineral status (plasma, hepatic, and bone) were investigated in four groups of rats fed one of the experimental diets: a fiber-free (FF) diet, a FF diet containing 7 g/kg PA (FF + PA), a diet containing 100 g/kg inulin (FOS), or a FOS diet containing 7 g/kg PA (FOS + PA). The cecal enlargement together with the acidification of cecal pH in rats adapted to FOS diets led to an improved Ca and Mg cecal absorption. Mineral apparent absorption was significantly enhanced by FOS ingestion (Ca, +20%; Mg, +50%; Fe, +23%; Cu, +45%), whereas PA decreased this factor only for trace elements (Fe, -48%; Zn, -62%; Cu, -31%). These inhibitory effects of a FF + PA diet have repercussions on blood (Mg, -15%; Fe, -12%; transferrin saturation -31%), liver (Mg, -18%; Fe, -42%; Zn, -25%), and bone (Zn, -25%) variables. However, the introduction of FOS into a PA diet counteracted these observed deleterious effects by stimulating bacterial hydrolysis of PA (+60% in rats adapted to FOS + PA compared to those fed the FF + PA diet) and by improving cecal absorption of minerals.     

High Sodium-Induced Oxidative Stress and Poor Anticrystallization Defense Aggravate Calcium Oxalate Crystal Formation in Rat Hyperoxaluric Kidneys

Enhanced sodium excretion is associated with intrarenal oxidative stress. The present study evaluated whether oxidative stress caused by high sodium (HS) may be involved in calcium oxalate crystal formation. Male rats were fed a sodium-depleted diet. Normal-sodium and HS diets were achieved by providing drinking water containing 0.3% and 3% NaCl, respectively. Rats were fed a sodium-depleted diet with 5% hydroxyl-L-proline (HP) for 7 and 42 days to induce hyperoxaluria and/or calcium oxalate deposition. Compared to normal sodium, HS slightly increased calcium excretion despite diuresis; however, the result did not reach statistical significance. HS did not affect the hyperoxaluria, hypocalciuria or supersaturation caused by HP; however, it increased calcium oxalate crystal deposition soon after 7 days of co-treatment. Massive calcium oxalate formation and calcium crystal excretion in HS+HP rats were seen after 42 days of treatment. HP-mediated hypocitraturia was further exacerbated by HS. Moreover, HS aggravated HP-induced renal injury and tubular damage via increased apoptosis and oxidative stress. Increased urinary malondialdehyde excretion, in situ superoxide production, NAD(P)H oxidase and xanthine oxidase expression and activity, and decreased antioxidant enzyme expression or activity in the HS+HP kidney indicated exaggerated oxidative stress. Interestingly, this redox imbalance was associated with reduced renal osteopontin and Tamm-Horsfall protein expression (via increased excretion) and sodium-dependent dicarboxylate cotransporter NaDC-1 upregulation. Collectively, our results demonstrate that a HS diet induces massive crystal formation in the hyperoxaluric kidney; this is not due to increased urinary calcium excretion but is related to oxidative injury and loss of anticrystallization defense.     

Synergy between angiotensin and aldosterone in evoking sodium appetite in baboons

The synergy between ANG II and aldosterone (Aldo) in the induction of salt appetite, extensively studied in rats, has been tested in baboons. ANG II was infused intracerebroventricularly at 0.5 or 1.0 microg/h; Aldo was infused subcutaneously at 20 microg/h. Separate infusions over 7 days had no significant effect on the daily intake of 300 mM NaCl. Concurrent infusions, however, increased daily NaCl intake approximately 10-fold and daily water intake approximately 2.5-fold. In addition, the combined infusions caused 1) a reduction in daily food intake, 2) changes in blood composition indicative of increased vasopressin release, and 3) changes of urinary excretion rates of cortisol and Aldo indicative of increased ACTH release. Arterial blood pressure, measured in two baboons, rose during concurrent ANG II and Aldo treatment. These results indicate a potent synergy between central ANG II and peripheral Aldo in stimulating salt appetite in baboons. At the same time, other ANG II-specific brain mechanisms concerned with water intake, food intake, vasopressin release, ACTH release, and blood pressure regulation appear to have been activated by the same type of synergy. These central enhancement processes have never been previously demonstrated in primates.     

Extracellular Ca²+ alleviates NaCl-induced stomatal opening through a pathway involving H₂O₂-blocked Na+ influx in Vicia guard cells

To gain further insights into the function of extracellular Ca2+ in alleviating salt stress, Vicia faba guard cell protoplasts (GCPs) were patch-clamped in a whole-cell configuration. The results showed that 100 mM NaCl clearly induced Na+ influx across the plasma membrane in GCPs and promoted stomatal opening. Extracellular Ca2+ at 10 mM efficiently blocked Na+ influx and inhibited stomatal opening, which was partially abolished by La3+ (an inhibitor of plasma membrane Ca2+ channel) or catalase (CAT, a H?O? scavenger), respectively. These results suggest that the plasma membrane Ca2+ channels and H?O? possibly mediate extracellular Ca2+-blocked Na+ influx in GCPs. Furthermore, extracellular Ca2+ activated the plasma membrane Ca2+ channels under NaCl stress, which was partially abolished by CAT. These results, taken together, indicate that hydrogen peroxide (H?O?) likely regulates Na+ uptake by activating plasma membrane Ca2+ channels in GCPs. In accordance with this hypothesis, H?O? could mimic extracellular Ca2+ to activate Ca2+ channels and block Na+ influx in guard cells. A single-cell analysis of cytosolic free Ca2+ ([Ca2+](cyt)) using Fluo 3-AM revealed that extracellular Ca2+ induced the accumulation of cytosolic Ca2+ under NaCl stress, but had few effects on the accumulation of cytosolic Ca2+ under non-NaCl conditions. All of these results, together with our previous studies showing that extracellular Ca2+ induced the generation of H?O? in GCPs during NaCl stress, indicate that extracellular Ca2+ alleviates salt stress, likely by activating the H?O?-dependent plasma membrane Ca2+ channels, and the increase in cytosolic Ca2+ appears to block Na+ influx across the plasma membrane in Vicia guard cells, leading to stomatal closure and reduction of water loss.     

Enhancement of (Ca2+ + Mg2+)-ATPase activity of human erythrocyte membranes by hemolysis in isosmotic imidazole buffer. II. Dependence on calcium and a cytoplasmic activator.

1. Activity of the (Ca2+ + Mg2+)-ATPase of erythrocyte membrane may be enhanced by a cytoplasmic protein activator. The presence of Ca2+ is necessary for the ionic strength-dependent interaction between the erythrocyte membrane and the activator. This is true no matter the purity of activator (unfractionated hemolysis supernatant or partially purified activator) or the major source of ionic strength (imidazole or NaCl). 2. When the endogenous activator enhances (Ca2+ + Mg2+)-ATPase activity of the erythrocyte membrane, there is a physical association between activator and membrane. This association is not disrupted by a decrease in ionic strength to 0.005 but is reversed by exposure to 5 mM ethyleneglycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid. 3. Activator binding necessary for enhancement of (Ca2+ + Mg2+)-ATPase activity may occur during preparation of membranes or during incubation for assay of ATPase.     

盐胁迫下构树幼苗各器官中K+、Ca2+、Na+和Cl-含量分布及吸收特征

将当年生构树幼苗置于含有不同浓度（04、1、2、3、4 g·kg^-1）NaCl的土壤中,研究其生物量积累、叶片细胞质膜透性和K⁺、Ca²⁺、Na⁺、Cl^-等离子的吸收、分布及运输,并观察盐害症状.结果表明：构树幼苗的叶片质膜透性随着NaCl浓度的增加和胁迫时间的延长而升高,根冠比随NaCl浓度的升高而增加,大于3 g·kg^-1的土壤盐胁迫对构树叶片的质膜透性及植株的生物量积累影响显著.构树幼苗各器官中Na⁺和Cl^-含量随土壤NaCl浓度升高而显著增加,K⁺和Ca²⁺则随之降低,叶片各离子含量均明显高于根和茎.说明盐胁迫影响根系对K⁺和Ca²⁺的吸收,并抑制了它们向地上部分的选择性运输,使叶和茎的K⁺和Ca²⁺含量下降.构树通过吸收积累Na⁺和Cl^-抵御土壤盐分带来的渗透胁迫,但过量的Na⁺和Cl^-积累会造成单盐毒害.作为抗盐性较高的非盐生植物,构树地上部分的拒盐作用不显著.