OBJECTIVESome of the phenolic compounds detected in the soil of commercially cultivated American ginseng could inhibit the seed germination and seedling growth of American ginseng. In this paper we studied the root exudation of American ginseng induced by deficiency of nitrogen, phosphorus and potassium on the content of phenolic compounds.

METHODTwo years old American ginsengs were cultured in hydroponic culture with different nutrient solution. The culture solution was collected after 14 days. The exudations of different polarities in the culture solution were enriched by the amberlite XAD4 and XAD7. The content of the total phenolic acids in the exudation was analyzed by Folin-Ciocalteu colorimetry; the contents of vanillic acid, p-coumaric acid and trans-cinnamic acid were detected and quantified by HPLC.

RESULTBoth in the situation of nitrogen and potassium deficiency, the concentration of total phenolic compounds increased significantly in the exudation of American ginseng comparing with the complete nutrient solution (P < 0.05) , while decreased significantly under phosphorus deficient conditions (P < 0.05). The contents of the 3 autotoxic phenolic acids decreased significantly under nitrogen, phosphorus and potassium deficient conditions (P < 0.05).

CONCLUSIONThe contents of total phenolic compounds and the 3 autotoxic phenolics in the root exudation of American ginseng altered variously in the deficiency of nitrogen, phosphorus and potassium.

Coumaric Acids ; analysis ; Hydroxybenzoates ; analysis ; Nitrogen ; deficiency ; Panax ; chemistry ; metabolism ; Phosphorus ; deficiency ; Plant Exudates ; chemistry ; Plant Roots ; chemistry ; metabolism ; Potassium ; chemistry ; Propionates ; Soil ; chemistry ; Vanillic Acid ; analysis

BACKGROUND AND OBJECTIVES: Previous studies reported that sodium and potassium play an important role in the pathogenesis of hypertension. Recently attention has been directed towards a possible role of the divalent cations such as calcium, and magnesium. Plasma renin activity is also known to be related to divalent cations heterogeneously. This study investigated the relationships between serum magnesium and ionized calcium and plasma renin activity. MATERIALS AND METHODS: The subjects consisted of 27 essential hypertensive patients and 25 normotensive controls. Criteria for hypertensive group in this study were systolic blood pressure> or =140mmHg or a diastolic blood pressure > or =90mmHg (JNC-VI, 1997). Inclusion criteria were normal urinalysis, no history of systemic illness, no intake of antihypertensive drugs, and no recent intake of any other medication. We took magnesium-loading test for a reliable method of assessing possible magnesium deficiency. RESULTS: There was no significant difference between two groups in serum Magnesium concentration and other electrolytes and plasma renin activity. There was significantly higher rate in hypertensives than in normotensives in magnesium retention(hypertensive vs. normotensive: 63.56+/-12.21% vs. 38.43+/-11.53%, P<0.001). There was significant differences in ionized calcium between high-renin and low-or normo-renin hypertensives(P<0.001). Plasma renin activity was correlated positively with serum ionized calcium in hypertensives(r=.8147; P<0.001). CONCLUSION: These results suggest that plasma renin activity is a factor that can influence on serum ionized calcium in high-renin hypertensives.
Antihypertensive Agents ; Blood Pressure ; Calcium* ; Cations, Divalent ; Electrolytes ; Humans ; Hypertension ; Magnesium Deficiency ; Magnesium* ; Plasma* ; Potassium ; Renin* ; Sodium ; Urinalysis

BACKGROUND AND OBJECTIVES: Previous studies reported that sodium and potassium play an important role in the pathogenesis of hypertension. Recently attention has been directed towards a possible role of the divalent cations such as calcium, and magnesium. Plasma renin activity is also known to be related to divalent cations heterogeneously. This study investigated the relationships between serum magnesium and ionized calcium and plasma renin activity. MATERIALS AND METHODS: The subjects consisted of 27 essential hypertensive patients and 25 normotensive controls. Criteria for hypertensive group in this study were systolic blood pressure> or =140mmHg or a diastolic blood pressure > or =90mmHg (JNC-VI, 1997). Inclusion criteria were normal urinalysis, no history of systemic illness, no intake of antihypertensive drugs, and no recent intake of any other medication. We took magnesium-loading test for a reliable method of assessing possible magnesium deficiency. RESULTS: There was no significant difference between two groups in serum Magnesium concentration and other electrolytes and plasma renin activity. There was significantly higher rate in hypertensives than in normotensives in magnesium retention(hypertensive vs. normotensive: 63.56+/-12.21% vs. 38.43+/-11.53%, P<0.001). There was significant differences in ionized calcium between high-renin and low-or normo-renin hypertensives(P<0.001). Plasma renin activity was correlated positively with serum ionized calcium in hypertensives(r=.8147; P<0.001). CONCLUSION: These results suggest that plasma renin activity is a factor that can influence on serum ionized calcium in high-renin hypertensives.
Antihypertensive Agents ; Blood Pressure ; Calcium* ; Cations, Divalent ; Electrolytes ; Humans ; Hypertension ; Magnesium Deficiency ; Magnesium* ; Plasma* ; Potassium ; Renin* ; Sodium ; Urinalysis

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/1.73m2, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.
Acidosis ; Aldosterone ; Arrhythmias, Cardiac ; Calcium Gluconate ; Constipation ; Diagnosis, Differential ; Dialysis ; Fatigue ; Furosemide ; Glomerular Filtration Rate ; Gluconates ; Hyperaldosteronism ; Hyperkalemia ; Hypertension ; Hypoaldosteronism ; Hypokalemia ; Hypotension ; Ileus ; Insulin ; Paresthesia ; Plasma ; Potassium ; Potassium Deficiency ; Renal Insufficiency ; Renin ; Rhabdomyolysis ; Seizures ; Vomiting

The potassium depletion has remarkable and opposite effect on kidney and body growth and has affected the expression of the several ion transporters. Previously, Ahn et al. have reported that HK alpha 1 and 2 subunit gene were upregulated in the hypokalemic rat kidney. To clone the unreported genes expressed in potassium deficiency, differential display PCR-based cloning strategy was used in normal and potassium-depleted rat kidney and a novel gene was isolated. Sequence analysis with blast search program identified a cDNA clone encoding an isoform of kidney sodium bicarbonate cotransporter-1. The tissue and cellular expression pattern of this gene were investigated with Northern analyses and in situ hybridization histochemistry (ISH) in normal and hypokalemic rats. This novel transcript was highly expressed in kidney and brain and at lower levels in distal colon, urinary bladder, and heart but not in salivary gland, stomach, liver, and lung in normal rat. In potassium-depleted rat, this transcript was upregulated in kidney, brain, and distal colon. By ISH, cellular distribution of this gene was highly expressed in S3 segment of proximal tubule, distal convoluted tubule, and cortical collecting duct of kidney and lower third of intestinal glands of distal colon but at lower levels in cortical and medullary thick ascending limb and medullary collecting duct of kidney and middle third of intestinal glands of distal colon. From these results, this candidate gene may play an important role in HCO3-transport by these organs during potassium depletion.
Animals ; Brain ; Clone Cells* ; Cloning, Organism* ; Colon ; DNA, Complementary ; Extremities ; Heart ; Hypokalemia ; In Situ Hybridization ; Intestinal Mucosa ; Ion Transport ; Kidney ; Liver ; Lung ; Potassium ; Potassium Deficiency ; Rats* ; Salivary Glands ; Sequence Analysis ; Sodium Bicarbonate ; Sodium-Bicarbonate Symporters* ; Stomach ; Urinary Bladder

OBJECTIVES: There are many interesting reports suggesting that magnesium(Mg) deficiency is deleterious in patients with congestive heart failure (CHF). It is paradoxical that the most important cause of Mg deficiency in these persons is maybe use of therapeutics including diuretics. Authors investigated the trend of serum and 24 hour urine Mg with other relating electrolytes in Mg homeostasis prospectively, in the management of CHF. And we assessd the effects of medications and many variables in .CHF on serum Mg, and the usefulness of serum Mg representing the body content. METHODS: Fifty three patients who were diagnosed as CHF by clinical finding and echocardiogaphy were prescribed conventional doses of diuretics as furosemide 40mg and spironolactone 50mg daily, with or without angiotensin converting enzyme(ACE) inhibitor and digitalis. And then, serial serum and 24 hour urine Mg, sodium, potassium and calcium were obtained at admission, 2nd day, 5th day, and discharge. RESULTS: The patients group with chronic CHF, which was defined as long-term use of diuretics over 6 months, showed higher prevalence of low level of serum Mg concentration than the group with acute one(11 of 28, 39% vs. 2 of 25. 8%, P< 0.01). Of those two groups, the latter showed upward trend of serum Mg from admission to discharge, but the former showed no change. In 24 hour urine Mg excretion, the amount of the patients with CHF was larger than that of control group. In the chronic CHF group, the effect of digitalis on decreasing serum Mg was evident. Serum Mg of acute CHF group correlated with serum BUN(r=0.5609). Whereas, that of chronic group with ejection fraction(r=-0.4742) and plasma renin activity(r=-0.3791), with serum potassium(r=0.4673) and creatinine(0.5846). Serum Mg may be useful indicator of Mg homeostasis, especially in chronic CHF patients. CONCLUSION: Because patients with chronic CHF were prone to deficiency of Mg in the management, maintaining the adequate serum Mg through long- term replacement seems very important in decreasing the morbidity and mortality of these persons.
Angiotensins ; Calcium ; Digitalis ; Diuretics ; Electrolytes ; Estrogens, Conjugated (USP)* ; Furosemide ; Heart Failure* ; Homeostasis ; Humans ; Magnesium Deficiency ; Magnesium* ; Mortality ; Plasma ; Potassium ; Prevalence ; Prospective Studies ; Renin ; Sodium ; Spironolactone

deficiency has been observed widespread amongst heart failure (HF) patients, which could have harmful effects on their health condition. This study aims to investigate the effect of vitamin D supplements on blood pressure (BP) and physical activity of HF patients. Thirty-nine systolic HF patients with low ejection fraction (EF) < 50% and class III of New York Heart Association functional classification were randomly divided into 2 groups including intervention and placebo to enroll in an 8 weeks double-blind clinical trial. During the trial 6-minute walk test (6MWT), 25-hydroxyvitamin D (25[OH]D) level, BP, sodium and potassium intakes were assessed. The mean 25(OH)D level increased to 28.9 ± 11.7 ng/mL (p < 0.001) in the intervention group. There was a poor but non-significant reduction in systolic BP (−0.033 ± 4.71 mmHg, p = 0.531) in the intervention group. The BP also did not change in the placebo group at the end of the trial. A negligible decrease of 6MWT was observed in the intervention group (−6.6 ± 29.2 m) compared to the placebo (−14.1 ± 40.5 m). However, differences between the 2 groups were not statistically significant (p = 0.325). The results solely showed a slight positive correlation between 25(OH)D level and 6MWT. No significant improvements in BP and 6MWT were observed after vitamin D3 supplementation.TRIAL REGISTRATION: Iranian Registry of Clinical Trials Identifier: IRCT2016102113678N13]]>
Blood Pressure ; Cholecalciferol ; Classification ; Endothelial Cells ; Exercise Test ; Exercise Tolerance ; Heart Failure ; Heart ; Humans ; Motor Activity ; Myocytes, Cardiac ; Potassium ; Sodium ; Vitamin D ; Vitamin D Deficiency ; Vitamins

Voltage-gated K+ (Kv) channels have been considered to be a regulator of membrane potential and neuronal excitability. Recently, accumulated evidence has indicated that several Kv channel subtypes contribute to the control of cell proliferation in various types of cells and are worth noting as potential emerging molecular targets of cancer therapy. In the present study, we investigated the effects of the Kv1.1-specific blocker, dendrotoxin-kappa (DTX-kappa), on tumor formation induced by the human lung adenocarcinoma cell line A549 in a xenograft model. Kv1.1 mRNA and protein was expressed in A549 cells and the blockade of Kv1.1 by DTX-kappa, reduced tumor formation in nude mice. Furthermore, treatment with DTX-kappa significantly increased protein expression of p21Waf1/Cip1, p27Kip1, and p15INK4B and significantly decreased protein expression of cyclin D3 in tumor tissues compared to the control. These results suggest that DTX-kappa has anti-tumor effects in A549 cells through the pathway governing G1-S transition.
Adenocarcinoma/drug therapy/genetics/pathology ; Animals ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Elapid Venoms/*pharmacology ; Elapidae ; Humans ; Kv1.1 Potassium Channel/*antagonists & inhibitors/deficiency/genetics/metabolism ; Lung Neoplasms/*drug therapy/genetics/pathology ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Potassium Channel Blockers/*pharmacology ; RNA, Messenger/genetics ; Transplantation, Heterologous

Hyperoxic ventilation induces detrimental effects on the respiratory system, and ambient oxygen may be harmful unless compensated by physiological anti-oxidants, such as vitamin C. Here we investigate the changes in electrolyte transport of airway epithelium in mice exposed to normobaric hyperoxia and in gulonolacton oxidase knock-out (gulo[-/-]) mice without vitamin C (Vit-C) supplementation. Short-circuit current (Isc) of tracheal epithelium was measured using Ussing chamber technique. After confirming amiloride-sensitive Na+ absorption (DeltaIsc,amil), cAMP-dependent Cl- secretion (DeltaIsc,forsk) was induced by forskolin. To evaluate Ca2+-dependent Cl- secretion, ATP was applied to the luminal side (DeltaIsc,ATP). In mice exposed to 98% PO2 for 36 hr, DeltaIsc,forsk decreased, DeltaIsc,amil and DeltaIsc,ATP was not affected. In gulo(-/-) mice, both DeltaIsc,forsk and DeltaIsc,ATP decreased from three weeks after Vit-C deprivation, while both were unchanged with Vit-C supplementation. At the fourth week, tissue resistance and all electrolyte transport activities were decreased. An immunofluorescence study showed that the expression of cystic fibrosis conductance regulator (CFTR) was decreased in gulo(-/-) mice, whereas the expression of KCNQ1 K+ channel was preserved. Taken together, the CFTR-mediated Cl- secretion of airway epithelium is susceptible to oxidative stress, which suggests that supplementation of the antioxidant might be beneficial for the maintenance of airway surface liquid.
Animals ; Ascorbic Acid Deficiency/*metabolism ; Biological Transport/drug effects ; Chlorides/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/antagonists & inhibitors/drug ; Forskolin/pharmacology ; Hyperbaric Oxygenation ; Hyperoxia/*physiopathology ; Ion Transport/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Mice, Knockout/metabolism ; Mice, Transgenic ; Microscopy, Fluorescence ; Oxidative Stress ; Oxygen/adverse effects/pharmacology ; Potassium Channels/metabolism ; Respiratory Mucosa/drug effects/*metabolism/secretion ; Sodium ; Sugar Acids/metabolism