The effect of the anions, phosphate and sulphate, on normal rates of excretion of potassium in dogs.

Small doses of (NH4)2HPO4 or KH2PO4 by stomach tube caused increase in plasma PO4 and PO4 excretion. Above a threshold of 0-8 mmol. 1(-1), increase of plasma PO4 by 0-5 mmol. 1(-1) caused PO4 excretion to increase by about 35 mumol. min.-1 After KH2PO4 this relationship was not altered by the concurrent increases in plasma K and K excretion. After doses of (NH4)2SO4 or K2SO4, excretion of SO4 was similarly related to plasma SO4 and was independent of plasma K and K excretion. An effect of PO4 on K excretion was observed after doses of (NH4)2HPO4, when increased excretion of PO4 was accompanied by increased excretion of K without change in plasma K. There was also increased excretion of NH4 and a small increase in Na excretion. The changes were similar to those produced by (NH4)2SO4 [O'Connor and Summerill, 1976]. KH2PO4 and K2SO4 produced increase in plasma K and increased excretion of K not significantly different from the changes produced by KCl or KHCO3 [Baylis and O'Connor, 1976]. After KH2PO2 or K2SO4, the urinary anion was PO4 or SO4, instead of Cl and HCO3. Any effect of anions on K excretion was much less than the effect of increase in plasma K. At low rates of excretion of K, increased urinary excretion of impermeant anion can determine increased excretion of K. However, the effect of anion is small in comparison with the effect of increase in plasma K.     

NaHCO(3) and KHCO(3) ingestion rapidly increases renal electrolyte excretion in humans.

This paper describes and quantifies acute responses of the kidneys in correcting plasma volume, acid-base, and ion disturbances resulting from NaHCO(3) and KHCO(3) ingestion. Renal excretion of ions and water was studied in five men after ingestion of 3.57 mmol/kg body mass of sodium bicarbonate (NaHCO(3)) and, in a separate trial, potassium bicarbonate (KHCO(3)). Subjects had a Foley catheter inserted into the bladder and indwelling catheters placed into an antecubital vein and a brachial artery. Blood and urine were sampled in the 30-min period before, the 60-min period during, and the 210-min period after ingestion of the solutions. NaHCO(3) ingestion resulted in a rapid, transient diuresis and natriuresis. Cumulative urine output was 44 +/- 11% of ingested volume, resulting in a 555 +/- 119 ml increase in total body water at the end of the experiment. The cumulative increase (above basal levels) in renal Na(+) excretion accounted for 24 +/- 2% of ingested Na(+). In the KHCO(3) trial, arterial plasma K(+) concentration rapidly increased from 4.25 +/- 0.10 to a peak of 7.17 +/- 0.13 meq/l 140 min after the beginning of ingestion. This increase resulted in a pronounced, transient diuresis, with cumulative urine output at 270 min similar to the volume ingested, natriuresis, and a pronounced kaliuresis that was maintained until the end of the experiment. Cumulative (above basal) renal K(+) excretion at 270 min accounted for 26 +/- 5% of ingested K(+). The kidneys were important in mediating rapid corrections of substantial portions of the fluid and electrolyte disturbances resulting from ingestion of KHCO(3) and NaHCO(3) solutions.     

The effects of exogenous extracellular carbonic anhydrase on CO2 excretion in rainbow trout (Oncorhynchus mykiss): role of plasma buffering capacity

The buffering capacity (beta) of rainbow trout (Oncorhynchus mykiss) plasma was manipulated prior to intravascular injection of bovine carbonic anhydrase to test the idea that proton (H+) availability limits the catalysed dehydration of HCO3- within the extracellular compartment. An extracorporeal blood shunt was employed to continuously monitor blood gases in vivo in fish exhibiting normal plasma beta (-3.9+/-0.3 mmol 1(-1) pH unit(-1)), and in fish with experimentally (using N-[2-hydroxyethyl]piperazine-N'-[2-ethanesulfonic acid]) elevated plasma beta (-12.1+/-1.1 mmol 1(-1) pH unit(-1)). An injection of 5 mg kg(-1) carbonic anhydrase equally reduced (after 90 min) the arterial partial pressure of CO2 in trout with regular (-0.23+/-0.05 Torr) or high (-0.20+/-0.05 Torr) plasma beta; saline injection was without effect. Because ventilation and venous blood gases were unaffected by carbonic anhydrase, the effect of extracellular carbonic anhydrase in lowering arterial partial pressure of CO2 was likely caused solely by a specific enhancement of CO2 excretion owing to acceleration of HCO3- dehydration within the plasma. The lowering of arterial partial pressure of CO2 in trout after injection of exogenous carbonic anhydrase provides the first in vivo evidence that the accessibility of plasma HCO3- to red blood cell carbonic anhydrase constrains CO2 excretion under resting conditions. Because the velocity of red blood cell Cl-/HCO3- exchange governs HCO3- accessibility to red blood cell carbonic anhydrase, the present study also provides evidence that CO2 excretion at rest is limited by the relatively slow rate of Cl-/HCO3- exchange. The effect of carbonic anhydrase in lowering arterial partial pressure of CO2 was unrelated to plasma buffering capacity. While these data could suggest that H+ availability does not limit extracellular HCO3- dehydration in vivo at resting rates of CO2 excretion, it is more likely that the degree to which plasma beta was elevated in the present study was insufficient to drive a substantially increased component of HCO3- dehydration through the plasma.     

Kaliuretic response to potassium loading in amiloride-treated dogs.

To assess whether an intact mechanism of sodium transport in the distal nephron is a prerequisite for the development of a kaliuresis in response to an acute potassium load (0.4 M KCl, 1 ml/min), the effects of a simultaneous infusion of KCl and amiloride (1 mg/kg/h) were evaluated in anesthetized dogs. A major reduction in potassium excretion mainly due to a sharp decrease in urine K+ concentration to one tenth of control levels was found after amiloride. The simultaneous infusion of KCl and amiloride resulted in a rapid and major increase in kaliuresis that was accounted for mostly by the rise in urine K+ concentration. The increased kaliuresis after the acute potassium infusion was of similar magnitude when expressed as percent value of control to that previously reported in dogs not receiving amiloride; the absolute rates of K+ excretion, however, were only 2.7 and 7.3% (before and after KCl infusion, respectively) of the values in dogs not receiving amiloride. Our observations suggest that potassium infusion in the intact dog increases kaliuresis primarily as a result of a more favorable chemical gradient of this cation between blood and/or distal tubular cells and urine. Yet, when a chemical gradient is the only driving force of potassium secretion, as was the case in our amiloride-treated dogs, the absolute rate of kaliuresis is very modest. The presence of an unimpaired electrical profile and sodium transport mechanisms in the distal nephron, although not critical for the development of kaliuresis in response to a K+ load, accounts for a severalfold rise in renal potassium excretion above basal levels.     

Effect of acute reversal of experimentally-induced ketoacidosis with sodium bicarbonate on the plasma concentrations of phosphorus and potassium

To determine if ketoacidosis per se, or its reversal with NaHCO3, predisposes to hypophosphatemia, six conditioned dogs were infused for two hours with 3.0 mmol/kg body wt/hour of beta-hydroxybutyric acid, followed by 1.5 mmol/kg/hour of NaHCO3 for two hours. Acid infusion caused moderate decrements in blood pH and [HCO3], a 23 +/- 4% increase in plasma [P] (p less than 0.005), and a 15 +/- 3% decrease in plasma [K] (p less than 0.005). NaHCO3 administration returned blood pH and [HCO3] levels to or slightly greater than baseline. Plasma [P] decreased, but not below baseline, whereas plasma [K] remained below baseline, and underwent an additional small decline (p less than 0.01). We conclude that acute correction of experimental ketoacidosis with NaHCO3 reverses the characteristic hyperphosphatemia but does not induce hypophosphatemia. On the other hand, NaHCO3 administration appeared to contribute to the perpetuation of hypokalemia.     

Regional increase in extracellular potassium can be arrhythmogenic due to nonuniform muscle contraction in rat ventricular muscle

In the ischemic myocardium, extracellular potassium ([K(+)](o)) increases to ≥20 mmol/l. To determine how lethal arrhythmias occur during ischemia, we investigated whether the increased spatial pattern of [K(+)](o), i.e., a regional or a global increase, affects the incidence of arrhythmias. Force, sarcomere length, membrane potential, and nonuniform intracellular Ca(2+) ([Ca(2+)](i)) were measured in rat ventricular trabeculae. A "regional" or "global" increase in [K(+)](o) was produced by exposing a restricted region of muscle to a jet of 30 mmol/l KCl or by superfusing trabeculae with a solution containing 30 mmol/l KCl, respectively. The increase in [Ca(2+)](i) (Ca(CW)) during Ca(2+) waves was measured (24°C, 3.0 mmol/l [Ca(2+)](o)). A regional increase in [K(+)](o) caused nonuniform [Ca(2+)](i) and contraction. In the presence of isoproterenol, the regional increase in [K(+)](o) induced sustained arrhythmias in 10 of 14 trabeculae, whereas the global increase did not induce such arrhythmias. During sustained arrhythmias, Ca(2+) surged within the jet-exposed region. In the absence of isoproterenol, the regional increase in [K(+)](o) increased Ca(CW), whereas the global increase decreased it. This increase in Ca(CW) with the regional increase in [K(+)](o) was not suppressed by 100 μmol/l streptomycin, whereas it was suppressed by 1) a combination of 10 μmol/l cilnidipine and 3 μmol/l SEA0400; 2) 20 mmol/l 2,3-butanedione monoxime; and 3) 10 μmol/l blebbistatin. A regional but not a global increase in [K(+)](o) induces sustained arrhythmias, probably due to nonuniform excitation-contraction coupling. The same mechanism may underlie arrhythmias during ischemia.     

Compensation of respiratory alkalosis induced after acclimation to simulated altitude

Conscious intact rats previously acclimated for 3 wk to barometric pressure of 370-380 Torr (3WHx) were made alkalotic for 3 h by a decrease in inspired O2 fraction from 0.10 to 0.075 at ambient barometric pressure (730-740 Torr). Controls were normoxic littermates (Nx) in which inspired O2 fraction was lowered from approximately 0.21 to 0.10 for 3 h. Arterial PCO2 decreased progressively and similarly in both groups (65-70% of control at 15 min). Initially, arterial pH increased less in 3WHx (0.09 +/- 0.004 vs. 0.15 +/- 0.008). As hypocapnia continued, delta[HCO3-]/delta pH (mmol.l-1.pH) became more negative in Nx, from -15.2 +/- 2.5 at 15 min to -37.0 +/- 2.9 at 3 h, indicating nonrespiratory compensation of alkalosis. In 3WHx, delta[HCO3-]/delta pH did not change during alkalosis. Cumulative renal excretion of base (mueq/100 g) during alkalosis increased by 73.2 +/- 11.1 in Nx and 25.4 +/- 7.3 in 3WHx. This difference was mainly due to a larger increase in HCO3- excretion in Nx. The data suggest that the smaller compensation of hypocapnic alkalosis in 3WHx is partly due to the smaller increase in renal base excretion. Because base availability limits renal base excretion, the smaller renal response of 3WHx may be secondary to the low plasma HCO3- concentration that accompanies altitude acclimation.     

Accumulation of potassium by human red cells

1. A method is described for measuring the accumulation of K at 37°C. by washed human red cells in glucose-containing systems in which the pH is kept constant, the K content of the cells being compared with that of the cells of systems which contain no added glucose but which are otherwise treated similarly. 2. In systems containing added glucose, the accumulation of K begins shortly after the cells have been warmed to 37°C., proceeds to a maximum which is reached after about 10 hours, and then falls exponentially. The maximum rate of accumulation is found during the first 3 hours. In systems which contain no added glucose, the K content of the cells appears to decrease exponentially with time for about 18 to 24 hours; thereafter the K content of the cells may decrease rapidly and the systems may show considerable hemolysis. Sometimes a small accumulation effect is observed during the first 2 to 3 hours; this may be the result of the washed cells not having been completely freed of glucose. 3. The accumulation process proceeds at its maximum rate at pH 7.4 to 7.6, which is also the pH at which the K loss from the red cells is at a minimum in systems containing no added glucose. 4. When red cells are stored at 4°C. for increasing lengths of time, the storage is accompanied by increasing K loss and the maximum rate of accumulation observed when the cells are warmed to 37°C. at first becomes greater. If the storage at 4°C. is continued for more than 3 to 4 days, the rate of the accumulation which occurs at 37°C decreases again, the accumulation mechanism showing progressive deterioration with time even at low temperatures. This deterioration has a counterpart in the progressive deterioration (deduced from the analysis of the curves relating K content and time) of the accumulation mechanism with time at 37°C. 5. The accumulation of K occurs at a maximum rate when the concentration of glucose in the system is between 50 and 200 mg./100 ml. Its temperature coefficient over the range 27–37°C. is 2.4. In the presence of glucose and at pH 7.6, accumulation of K takes place from isotonic mixtures of KCl and LiCl or of KCl and CsCl only a little less actively than from mixtures of KCl and NaCl; i.e., the accumulation of K under optimum conditions seems to be an active process which is at least partly independent of the excretion of Na.     

Electrolyte composition changes of chronically K-depleted rats after K loading

The responses of whole body, skeletal muscle, and plasma to oral K loading were studied in K-depleted male rats. Potassium depletion was induced by feeding the rats a K-deficient diet for 4 wk and injecting deoxycorticosterone acetate during the first week. After 4 wk, the rats were growth retarded and hypokalemic (1.9 mmol/l plasma) and had low whole-body and muscle K content, 188 +/- 27 and 276 +/- 19 mmol/kg fat-free dried tissue (FFDT), respectively, compared with 296 +/- 10 and 454 +/- 13 mmol/kg FFDT for the control group. Sodium and water retention also occurred in the K-deficient group. After K depletion, the rats were divided into four groups and received either 0, 1, 2, or 3 intragastric doses of 10 mmol KCl/kg at 8-h intervals. The rats were killed 8 h after the last dose. Control rats were treated similarly. K-depleted and control rats responded differently to K loading. In the normal rats, plasma K remained at 5.0 +/- 0.5 mmol/l, muscle K increased to 502 +/- 24 mmol/kg, and muscle K/N ratio increased from 3.0 to 3.4 mmol/g. In the K-depleted rats, plasma K increased to 7.2 +/- 0.7 mmol/l, muscle K increased to 453 +/- 50 mmol/kg, and muscle K/N ratio increased from 1.8 to 3.1 mmol/g. These data indicate that the capacity of the muscles to accumulate K was impaired after severe K depletion and caused elevated plasma K levels when repletion was complete.     

Urinary kallikrein excretion after potassium adaptation in the rat

24-h urinary kallikrein excretion in male Sprague-Dawley rats was measured before and after 14 days with 100 mM potassium chloride as drinking fluid ad libitum. Urinary kallikrein excretion increased in K+-adaptation. The increase was greater when the rats were given distilled water rather than 100 mM sodium chloride to drink prior to the potassium chloride. The urinary potassium excretion increased in all rats studied. The urinary sodium excretion, urine volume and fluid intake increased significantly in rats that had distilled water to drink prior to the KCl. In marked contrast, when rats were offered NaCl prior to KCl, the urinary sodium excretion was unaffected while the urine volume and fluid intake decreased significantly. This study shows that prior NaCl intake abolishes the natriuretic and diuretic effects of KCl load and only suppresses the increase in urinary kallikrein excretion. This suggests that K+ secretory activity at the distal tubules is the major determinant of the release of renal kallikrein in the rat.     

The physiology of overwintering in a turtle that occupies multiple habitats,the common snapping turtle (Chelydra serpentina)

Common snapping turtles, Chelydra serpentina (Linnaeus), were submerged in anoxic and normoxic water at 3 degrees C. Periodic blood samples were taken, and PO(2), PCO(2), pH, [Na(+)], [K(+)], [Cl(-)], total Ca, total Mg, [lactate], [glucose], hematocrit, and osmolality were measured; weight gain was determined; and plasma [HCO(3)(-)] was calculated. Submergence in normoxic water caused a decrease in PCO(2) from 10.8 to 6.9 mmHg after 125 d, partially compensating a slight increase in lactate and allowing the turtles to maintain a constant pH. Submergence in anoxic water caused a rapid increase in lactate from 1.8 to 168.1 mmol/L after 100 d. Associated with the increased lactate were decreases in pH from 8.057 to 7.132 and in [HCO(3)(-)] from 51.5 to 4.9 mmol/L and increases in total Ca from 2.0 to 36.6 mmol/L, in total Mg from 1.8 to 12.1 mmol/L, and in [K(+)] from 3.08 to 8.45 mmol/L. We suggest that C. serpentina is tolerant of anoxic submergence and therefore is able to exploit habitats unavailable to some other species in northern latitudes.     

Oil formation from glucose with formic acid and cobalt catalyst in hot-compressed water

Liquefaction of glucose into oil was examined in hot-compressed water at 300 degrees C and 30 or 60 min in a tumbling batch reactor. The effects of alkali (KHCO(3)), a hydrogenating agent (HCO(2)H), and a cobalt catalyst (Co(3)O(4)) were studied. Also the combinations of these additives were investigated. HCO(2)H and KHCO(3) showed a positive effect on oil formation. Co(3)O(4) was found to be an advantageous additive as well, increasing the oil formation from glucose, but the stability of this catalyst under reaction conditions was quite low.     

Evidence for K+-dependent HCO3- utilization in the marine diatom Phaeodactylum tricornutum

Photosynthetic utilization of inorganic carbon in the marine diatom Phaeodactylum tricornutum was investigated by the pH drift experiment, measurement of K(1/2) values of dissolved inorganic carbon (DIC) with pH change, and comparison of the rate of photosynthesis with the rate of the theoretical CO(2) formation from uncatalyzed HCO(3)(-) conversion in the medium. The higher pH compensation point (10.3) and insensitivity of the photosynthetic rate to acetazolamide indicate that the alga has good capacity for direct HCO(3)(-) utilization. The photosynthetic rate reached 150 times the theoretical CO(2) supply rate at 100 micromol L(-1) DIC (pH 9.0) in the presence of 10 mmol L(-1) K(+) and 46 times that in the absence of K(+), indicating that for pH 9.4-grown P. tricornutum, HCO(3)(-) in the medium is taken up through K(+)-dependent and -independent HCO(3)(-) transporters. The K(1/2) (CO(2)) values at pH 8.2 were about 4 times higher than those at pH 9.0, whereas the K(1/2) (HCO(3)(-)) values at pH 8.2 were slightly lower than those at pH 9.0 whether without or with K(+), providing further evidence for the presence of the two HCO(3)(-) transport patterns in this alga. Photosynthetic rate and affinity for HCO(3)(-) in the presence of K(+), respectively, were about 2- and 7-fold higher than those in the absence of K(+), indicating that K(+)-dependent HCO(3)(-) transport is a predominant pattern of HCO(3)(-) cellular uptake in low DIC concentration. However, as P. tricornutum was cultured at pH 7.2 or 8.0, photosynthetic affinities to HCO(3)(-) were not affected by K(+), implying that K(+)-dependent HCO(3)(-) transport is induced when P. tricornutum is cultured at high alkaline pH.     

Role of substance P in water homeostasis.

The effect of the naturally occurring peptide substance P on release of antidiuretic hormone (ADH) was studied in anesthetized dogs. Intravenous infusions of substance P in doses of 0.5, 5.0, and 50 ng/kg/min increased plasma concentrations of ADH in a dose-related fashion. At the two low doses, this increase occured in the absence of changes in urine volume, sodium excretion, free water clearance, and urinary cyclic AMP excretion. In addition, when substance P was administered in a concentration of 0.5 ng/kg/min, plasma levels of ADH were increased even though blood pressure did not change, suggesting that substance P may release antidiuretic hormone by a direct mechanism. Intrarenal infusions at a rate of 0.5 and 5 ng/kg/min caused dose-related decreases in free water clearance and significant increases in urinary cyclic AMP excretion. These data suggest that substabce P may play an important role in the regulation of water balance.     

Effect of potassium concentration and ouabain on the renal adaptation to potassium depletion in isolated perfused rat kidney

Renal adaptation for potassium (K) conservation has been demonstrated in isolated perfused kidneys from rats within 3 days of K depletion and appears to be independent of aldosterone and sodium excretion. This study was designed to investigate whether the renal adaptation for K conservation is independent of ambient [K] and renal tissue levels of K and whether ouabain may have effects on K excretion, which are in contrast to the effects on K excretion in normal animals. In the first study, rats K depleted for 3 days received 2500 mu equiv. KCI intraperitoneally, while other K-depleted rats and a group of control diet animals received intraperitoneal H2O alone to determine whether simple restoration of K deficits would reverse the renal adaptation for K conservation. Intraperitoneal KCI increased plasma [K] and kidney tissue K significantly within 3 h in the K-repleted group compared with the K-depleted rats. Isolated Kidneys were perfused from the three groups of rats 3 h after intraperitoneal injection. Despite K repletion in vivo, perfused kidneys from the K-repleted group still had significantly decreased K excretion (1.28 +/- 0.085 mu equiv./min) compared with controls (2.05 +/- 0.291 mu equiv./min), and K excretion was still not different from the K-depleted group (0.57 +/- 0.134 mu equiv./min). However, fractional K excretion by the kidneys from K-repleted rats was increased above K-depleted kidneys (0.48 +/- 0.051 vs. 0.18 +/- 0.034, p less than 0.01). Despite the increased renal tissue K in K-repleted kidneys at the start of perfusion (285 +/- 5.1 vs. 257 +/- 5.4 mu equiv./g), by the end of the perfusion tissue K in perfused kidneys was identical in all three groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantification and kinetics of purine catabolism in Dalmatian dogs at low and high purine intakes

1. In eight Dalmatian dogs low and high purine intakes resulted in plasma urate levels from 25 to 185 mumol/l. 2. The relationship between purine intake and excretion of uric acid and allantoin per day was described by linear regression equations. 3. The elimination of endogenous purines was 1.8 mmol/day for urate and 1.7 mmol/day for allantoin. Exogenous purines increased renal excretion by 0.57 mmol/mmol. 4. Kinetic measurements with [2(-14)C]uric acid infused continuously into each of two dogs on low and high purine revealed increases of plasma pool (urate + allantoin) of 3.3 fold and entry rate of 4.0 fold. Conversion of urate into allantoin increased from 20 to 36%. 5. Renal elimination of catabolites increased 3.3 fold and exhalation rate of purine-CO2 379 fold. Extra-renal elimination at high purine intake was quantitatively similar to humans and closely related to pool size.     

Quantitative relationship between plasma potassium levels and QT interval in beagle dogs

The aim of the current study was to establish the quantitative relationship between plasma potassium concentrations and the QT interval of the electrocardiogram in dogs. Furosemide, a potent diuretic, was given at increasing doses (5-60 mg/kg) to five male and five female beagle dogs. Electrocardiogram (ECG) was recorded three times each day, simultaneous to blood sampling for measurement of plasma potassium. Furosemide treatment produced a clear hypokalaemia, which was associated with an increase in QT and corrected QT intervals (QTc) duration. On average, the slopes of the negative linear correlation between potassium plasma levels and QT or QTc were steeper in females than in males. These results show that a decrease in potassium plasma level may explain a concomitant increase in QT duration in a toxicity study in dogs, in particular if potassium values are decreased below 3.3 mmol/L. Correction of QT interval for K+ plasma level has, therefore, been established separately for males and females. A global formula correcting QT for K+ and heart rate simultaneously was established. Hypokalaemia was also associated with changes in the morphology of the T wave recorded in CV5RL, in particular, with a flattening and/or a notching of the wave (appearance of a second peak), biphasic aspect or inversion of polarity. These changes are probably related to an increased heterogeneity of repolarization between different populations of cardiomyocytes. In conclusion, hypokalaemia is quantitatively associated with an increase in QT and QTc duration in dogs. The relationship is apparently stronger for females than for males. A formula may be used to correct QT for potassium plasma level.     

提高胞外钾引起的蛙骨骼肌咖啡因挛缩增强

用蛙胫前肌小束为材料, 研究了提高胞外钾[K+]O对咖啡因挛缩的作用.[K+]O从2 mmol/L提高到10或25 mmol/L, 由3 mmol/L咖啡因引起的挛缩明显增强.以PKC/PC (PKC和PC分别为在高钾和正常钾条件下的咖啡因挛缩)表示的咖啡因挛缩增强, 依赖[K+]O和高钾作用时间.随着10 mmol/L [K+]O作用时间延长, 直至10 min, 增强逐渐增加.但是, 25 mmol/L [K+]O作用1 min时增强达到最大, 然后下降到对照.PKC/PC变化时程不能用高钾引起的去极化解释, 而与由相似[K+]O引起的胞浆自由钙变化时程相符.提示, 至少在蛙骨骼肌, 高钾引起的咖啡因挛缩增强主要是由胞浆自由钙升高引起的.     

Metabolism of D(-)lactic acid in rats given high intragastral doses

In rats given D[u-14C]-labelled DL-lactate with 3.8-13.4 mmol D-lactate per kg 0.75 by stomach tube, the exhalation of CO2 produced from and the renal excretion of D-lactate and metabolites were measured. Exhalation of D-lactate-C accounted for 45-30% of the dosage given with a decreasing proportion at higher doses. The renal excretion of D-lactate averaged 0.9% and that of metabolites from D-lactate 2.4% of the doses given. The fraction of unrecovered D-lactate accounted for about 54-68% of the doses given and increased with doses. The time course of D-lactate oxidation indicated a maximum rate of about 1.5 mmol C per kg 0.75 in 1 hr which was reached at 1 hr after infusion at the earliest and extended up to 8 hr if high doses were given.     

Hormonal regulation of renal sodium and water excretion during normotensive sodium loading in conscious dogs

Saline was infused intravenously for 90 min to normal, sodium-replete conscious dogs at three different rates (6, 20, and 30 micromol x kg(-1) x min(-1)) as hypertonic solutions (HyperLoad-6, HyperLoad-20, and HyperLoad-30, respectively) or as isotonic solutions (IsoLoad-6, IsoLoad-20, and IsoLoad-30, respectively). Mean arterial blood pressure did not change with any infusion of 6 or 20 micromol x kg(-1) x min(-1). During HyperLoad-6, plasma vasopressin increased by 30%, although the increase in plasma osmolality (1.0 mosmol/kg) was insignificant. During HyperLoad-20, plasma ANG II decreased from 14+/-2 to 7+/-2 pg/ml and sodium excretion increased markedly (2.3+/-0.8 to 19+/-8 micromol/min), whereas glomerular filtration rate (GFR) remained constant. IsoLoad-20 decreased plasma ANG II similarly (13+/-3 to 7+/-1 pg/ml) concomitant with an increase in GFR and a smaller increase in sodium excretion (1.9+/-1.0 to 11+/-6 micromol/min). HyperLoad-30 and IsoLoad-30 increased mean arterial blood pressure by 6-7 mm Hg and decreased plasma ANG II to approximately 6 pg/ml, whereas sodium excretion increased to approximately 60 micromol/min. The data demonstrate that, during slow sodium loading, the rate of excretion of sodium may increase 10-fold without changes in mean arterial blood pressure and GFR and suggest that the increase may be mediated by a decrease in plasma ANG II. Furthermore, the vasopressin system may respond to changes in plasma osmolality undetectable by conventional osmometry.