Enhanced supply of $Ca^{2+}$ as well as NO$_3$$^{[-10]}$ is known to restrict the uptake of the Na$^{+}$ and Cl$^{[-10]}$ ion and ameliorate growth under saline conditions. This test was conducted to investigate the ameliorating effects of Ca(NO$_3$)$_2$ or CaCl$_2$ on the growth and yield of NaCl-stressed tomato plants grown in plastic pot filled with soil. All treatments except for the control were supplied with 80 mM NaCl fur two weeks after transporting. The saline solutions with nutrient were supplemented with either 0, 10 or 20 mM Ca(NO$_3$)$_2$ and either 0, 10 or 20 mM CaCl$_2$ during harvesting time from two weeks after transporting. Ca(NO$_3$)$_2$ or CaCl$_2$ application enhanced the growth such as plant height, fresh weight, dry weight, fruit number, and fruit weight, and yield of NaCl-stressed tomato, and also their effects increased greater as concentration of supplemented Ca(NO$_3$)$_2$ or CaCl$_2$increased. Yield increased in 20 mM Ca(NO$_3$)$_2$ compared with the others except fur the control. Photosynthetic rate in Ca treatments was lower than that of the control, but higher than that of NaCl treatment. Leaf chlorophyll content was higher in Ca treatments compared with the others, especially in younger leaf, while that was not affected by concentration of supplemented Ca. Ca(NO$_3$)$_2$ or CaCl$_2$ supply increased the $K^{+}$ and $C^{2+}$ concentration of tomato plants, whereas the Na$^{+}$ transport to the leaves was inhibited. There was a strong increase in the $K^{+}$/Na$^{+}$ ratio in plants treated Ca(NO$_3$)$_2$, or CaCl$_2$. Cl$^{[-10]}$ content of plants was decreased by supplemental Ca(NO$_3$)$_2$ but Cl$^{[-10]}$ was increased in plants with CaCl$_2$compared with Ca(NO$_3$)$_2$. N concentration in plants of tomato increased with enhanced Ca(NO$_3$)$_2$ or CaCl$_2$supply, In conclusion, our study confirms the potential of Ca(NO$_3$)$_2$ or CaCl$_2$to alleviate NaCl-induced growth reductions in tomato.
Effects of Ca supplementation on blood pressure(BP) response to dietary Na level were studied in 15 normotensive healthy college women with family history of hypertension. All subjects, randomly divided into 3 groups, ate low Na diet(1816mg/day) prepared in the laboratory during the first 2 weeks and normal Na diet(4064mg/day) of their own home for the next 8 weeks. The one group received daily 1g Ca supplement at both low and normal Na diet periods, the second group took daily 1g Ca supplement only at normal a diet period, and the last group took placebo during both periods. Average Ca and energy intakes at the basal of and during the trial ranged 450-600mg and 1735-1878kcal, respectively. Systolic/diastolic BP was decreased by 9.2-9.8/4.4-4.5 mmHg during low Na diet period and was increased again during next normal Na diet period. However simultaneous Ca supplementation during both low and normal Na diet period suppressed the elevation of systolic/diastolic BP occurred at normal Na diet period. Ca supplementation only at normal Na diet peroid did not affect the BP elevation. The increase of serum Ca and Ca/Mg ratio and the decrease of serum Na and Na/K ratio might be related to the BP lowering effects of Ca supplementation. In conclusion, Ca supplement could attenuate BP elevation induced by increasing Na intake. The BP lowering effect of Ca supplementation was not appeared at low Na intake. Further studies were needed to make it certain. Low Na intake was also confirmed as an effective diet control for lowering blood pressure.
Twenty two hypertensive and thirty normotensive in-patients were participated in this study to investigate the relationship between plasma renin activity and metabolism of Ca and Na, Prior to pharmacological treatments, renin activity, aldosterone and parathyroid hormone(PTH) levels were measured from the fasting blood samles. Twenty four hour urine samples were collected to analyze urinary levels of creatinine, Ca, Na and K. Habitual intake of Na and Ca were also measured for hypertensive and normotensive patients. Hypertensive subjects were classified into higher reinin hypertensive (HH), medium renin hypertensive(MH) and low renin hypertensive (LH) group according to their renin activities. PTH level of LH group was the highest among three hypertensive groups. It appeared that aldosterone levels of HH group were significantly higher than LH or MH groups(p<0.05). However there were no significan시 differences in aldosterone level between LH group and normotensive group. Habitual intake of Na and Ca were highest in LH group but lowest in HH group, however, they were not statistically different. Positive correlations of systolic blood pressure with PTH(r=0.2597) and aldosterone(r=0.26480existed(p<0.05). Urinary Ca level was positively correlated with urinary Na(r=0.5619), K(r=0.4533) and habitual Na intake(r=0.3253). Above results suggested the possible relationships among renin activity, habitual Ca intake and Na intake and suggested a further study on the interrelationship between the hormonal control of Ca and Na metabolism and blood pressure in hypertension.
Kim, Eui-Yong;Hwang, Sang-Ik;Earm, Yung-E;Sung, Ho-Kyung
The Korean Journal of Physiology
/
v.23
no.2
/
pp.291-299
/
1989
Na and Ca effects on contracture were studied in order to estimate Na/Ca exchange ratio in the isolated atrial muscle of the rabbit. All experiments were performed in tris-buffered Tyrode solution which was being aerated with 100% $O_2\;and\;kept\;at\;37^{circ}C$. To load intracellular $Na^+,\;10{-6}M$ ouabain or K-free solution were used. Contractures were induced by brier exposure of atrial muscle to Tyrode solution containing various concentrations of Ca or of Na. The results obtained were as follows: 1 ) Increasing the extracellular Ca concentration, the amplitude of contracture also increased and was maximum at 8 mM Ca-Tyrode solution. 2) The relationship between extracellular Ca concentrations and relative amplitude of the contractures showed hyperbolic pattern. By using Hill plot, the line has the slope of 1 12 which means the number of Ca binding sites of the carrier in the cell membrane. 3) The amplitude of the contracture was maximum in 0 mM Na-Tyrode solution and decreased in dose dependent manner when the Na concentration increased. 4) When the relationship between extracellular Na concentrations and the amplitude of contractures was expressed as dose-response curve, the curve showed sigmoid pattern. The line with the slope of 2.82 was obtained by using Hill plot. 5) From above all the results, it is suggested that exchange ratio of Na and Ca via Na/ca exchange system in the atrial muscle of rabbit could be 3:1 approximately.
$Na^+-Ca^{2+}$ exchange process in sarcolemmal vesicles isolated from mesenteric arteries of Wistar-Kyoto normotensive(WKY) and spontaneously hypertensive rats(SHR) was investigated. The sarcolemmal fractions isolated after homogenization and sucrose density gradient centrifugation were enriched with 5'-nucleotidase and ouabain sensitive, $K^+-dependent$ phosphatase activities. When the vesicles were loaded with $Na^+$, a time dependent $Ca^{2+}$ uptake was observed. However, very little $Ca^{2+}$ uptake was observed when the vesicles were loaded with $K^+$, or $Ca^{2+}$ uptake of the $Na^+-loaded$ vesicles was carried out in high sodium medium so that there was no sodium gradient. When the vesicles loaded with $Ca^{2+}$ by $Na^+-Ca^{2+}$ exchange were diluted into potassium medium containing EGTA, $Ca^{2+}$ was rapidly released from the vesicles. $Na^+-dependent\;Ca^{2+}$ uptake was increased in SHR compared to WKY, but passive efflux of preaccumulated $Ca^{2+}$ from the vesicles was decreased in SHR. The data indicate that the membrane vesicles of rat mesenteric arteries exhibit $Na^+-Ca^{2+}$ exchange activity. It is also suggested that changes of this process in vascular smooth muscle cell membrane of SHR may be involved in higher intracellular $Ca^{2+}$ concentration and higher basal tone in SHR.
This study was designed to investigate the effect of Ca supplementation of 1,000mg per day for 53 weeks on lipid, Na, and K metabolism and on blood pressure in postmenopausal women. The subjects were 12 healthy women aged from 60 to 70 years. They were divided into two groups : the placebo(control group) and the Ca supplemented(1,000 mg/day) group(Ca group). Metabolic studies were conducted twice in the 1st and the 53rd weeks. The results were as follows : Serum triglyceride, total cholesterol and LDL-choesterol levels tended to be decreased after the experiment. Serum VLDL-cholesterol lowering effect was observed with Ca supplementation(p<0.05), and also the significantly elevated HDL/(LDL+VLDL) ratio in Ca supplemented subjects whose average Na intake was as high as 4.9g per day. This phenomena was accompanied with increased Na retention and increased Na excretion in feces, but with decreased urinary Na in Ca supplemented group. However, considering much higher Na reteniton in the control group at the end of experiment(control va Ca ; 1272.3mg vs 732.9mg), Ca supplementation may have some beneficial effects on Na blance. Serum aldosterone level increased significantly in the Ca group after the exsperiment(p<0.05). With these normotensive subjects, there were no level increased significantly in the Ca group after the experiment(p<0.05). With these normotensive subjects, there were no pronounced effect of Ca supplementation on blood pressure, however, decrease in diastolic blood pressure were observed at the 14th week and end of the experiment(p<0.05). In summary, the Ca supplementation on postmenopausal Koran women appears to exert a desirables effect on blood lipid patterns related to the coronary heart diseases and to be beneficial in controlling diastolic blood pressure. Further studies with hypertensive or/and hyperlipidemic subjects are required to clarify the effect of Ca supplementation in Koreans.
The $Na^+$-and $K^+$-induced $Ca^{++}$ release was measured isotopically by Milipore filter technique in mitochondria isolated from rabbit ventricles. The release of $Ca^{++}$ from mitochondria could be induced by 1-3 mM of $Na^+$ added in incubating medium under the presence of 0.5mM EGTA to prevent the released $Ca^{++}$ from rebinding with mitochondrial membrane. The amount of $Ca^{++}$ released was increased by increasing the concentration of $Na^+$ added. 100mM $K^+$, in itself, did not induce the $Ca^{++}$ release from cardiac mitochondria, the $Na^+$-induced $Ca^{++}$ release, however, was potentiated by the presence of $K^+$. The potentiation of $Na^+$-induced $Ca^{++}$ release by $K^+$ was proportional to the $Na^+/K^+$ ratio presented in the incubating medium. Among the monovalent cations other than $Na^+$, the release of $Ca^{++}$ from cardiac mitochondria was shared only by $Li^+$. The $Na^+$-induced $Ca^{++}$ release could be also observed in the mitochondria isolated from liver and kidney. However, the $Na^+$ sensitivity was somewhat lower in liver and kidney mitochondria than in heart mitochondria. The release of $Ca^{++}$ induced by $Na^+$ in the mitochondria isolated from the experimentally produced failured heart was not different from that in the normal heart mitochondria, and was not directly modified by $10^{-6}{\sim}10^{-5}$ M of Ouabain. From the experiments, it was suggested that the $Ca^{++}$ released from mitochondria by $Na^+$ could be used in excitation-contraction coupling process to initiate the contraction of the cardiac myofibrils. Futhermore, it appeared that the phenomenon of $Ca^{++}$ release from cardiac mitochondria by $Na^+$ and $K^+$ might be related to the inotropic effect of digitalis glycoside which could bring about the increase of $Na^+$ or the reduction of $K^+$ intracellulary through the inhibition of $Na^+$, $K^+$-ATPase.
The $Na^+-and\;K^+-induced\;Ca^{++}$ release was measured isotopically by millipore filter technique in pig heart mitochondria. With EGTA-quenching technique, the characteristics of mitochondrial $Ca^{++}-pool$ and the sources of $Ca^{++}$ released from mitochondria by $Na^+\;or\;K^+$ were analyzed. The mitochondrial $Ca^{++}-pool$ could be distinctly divided into two components: internal and external ones which were represented either by uptake through inner membrane, or by energy independent passive binding to external surface of mitochondria, respectively. In energized mitochondria, a large portion of $Ca^{++}$was transported into internal pool with little external binding, while in de-enerigzed state, a large portion of transported $Ca^{++}$ existed in the external pool with limited amount of $Ca^{++}$ in the internal pool which was possibly transported through the $Ca^{++}-carrier$ present in the inner membrane. $Na^+$ induced the $Ca^{++}$ release from both internal pool and external pool and external binding pool of mitochondria. In contrast, $K^+$ did not affect $Ca^{++}$ of the internal pool, but, displaced $Ca^{++}$ bound to external surface of the mitochondria. When the $Ca^{++}-reuptake$ was blocked by EGTA, the $Ca^{++}$ release from the internal pool by $Na^+$ was rapid; the rate of $Ca^{++}-efflux$ appeared to be a function of $[Na^+]^2$ and about 8mM $Na^+$ was required to elicit half-maximal velocity of $Ca^{++}-efflux$. So it was revealed that $Ca^{++}-efflux$ velocity was particulary sensitive to small changes of the $Na^+$ concentration in physiological range. Energy independent $Ca^{++}-binding$ sites of mitochondrial external surface showed unique characteristics. The total number of external $Ca^{++}-binding$ sites of pig heart mitochondria was 29 nmoles per mg protein and the dissociation constant(Kd) was $34{\mu}M$. The $Ca^{++}-binding$ to the external sites seemed to be competitively inhibited by $Na^+\;and\;K^+$; the inhibition constant(Ki) were 9.7 mM and 7.1 mM respectively. Considering the intracellular ion concentrations and large proportion of $Ca^{++}$ uptake in energized mitochondria, the external $Ca^{++}-binding$ pool of the mitochondria did not seem to play a significant role on the regulation of intracellular free $Ca^{++}$ concentration. From this experiment, it was suggested that a small change of intracellular free $Na^+$ concentration might play a role on regulation of free $Ca^{++}$ concentration in cardiac cell by influencing $Ca^{++}-efflux$ from the internal pool of mitochondria.
The aim of this study was to investigate the interrelationship among urinary excretion dietary habit of Na, Ca intake and hormonal factors in 22 hypertensive and 30 normotensive hospitalized patients. The results were summarized as follows : 1. Urinary excretion of Na in normotensive patients was not significantly different from that of hypertensive patients, while Ca excretion(as expressed on the basis of mg of creatinine) was significantly higher in hypertensive patients. 2. Habitual dietary intake of Na, Ca in hypertensive patients were not significantly different from those of normotensive patients. 3. There were no significant differences in mean plasma renin activity, aldosterone and parathyroid hormone(PTH) level between two groups. However, systolic pressure significantly correlated with PTH(r=0.2597) and aldosterone level(r=0.24648)(P<0.05). In this study blood pressure did not show any significant relationship between urinary Na excretion and habitual dietary Na intake of Na. It is speculated that individual difference of Na sensitivity might result in heterogenous blood pressure response to dietary Na intake. Higher Ca excretion in hypertensive subjects suggested a future study on the interrelationship between Ca metabolism and aldosterone system in hypertension.
The interaction of $NpO^+_2$ with $Cl^-$ was studied using visible-near-infrared spectroscopy in $NaCl-Ca-Cl_2-NaClO_4$, $NaCl-NaClO_4$, and $CaCl_2-NaClO_4$ solutions with ionic strength (I) of 6M. The spectra of $NpO^+_2$ around 980 nm varied with $Cl^-$ concentration in the $NaCl-CaCl_2-NaClO_4$ and $NaCl-NaClO_4$ solutions at [$Cl^-$] ${\geq}3.5M$, but not in the $CaCl_2-NaClO_4$ solution. Assuming the 1:1 interaction between $NpO^+_2$ and $Cl^-$, the apparent equilibrium constants at I = 6M were evaluated. The presence of $Ca^{2+}$ was found to destabilize overall interaction between $NpO^+_2$ and $Cl^-$. The observations were consistent with the density functional theory calculation.
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