Sodium and potassium concentration in the tissues of wild and domesticated representatives of the chicken order

Na and K content has been studied in tissues of the hazel grouse Bonasa bonasia, black grouse Lyrurus tetrix, capercaillie Tetrao urogallus, domestic hen Gallus domesticus and turkey hen Meleagris gallopavo. With respect to the increase in potassium and sodium content, the tissues investigated in wild species form the following sequence: major thoracal muscle (red), minor thoracal muscle (white), gastrocnemius muscle, left ventricle of the heart, stomach muscles, brain hemispheres, spinal cord. Domestic birds exhibit lower sodium level in stomach muscles. Potassium distribution in tissues of wild birds is more even than in domestic ones; in the latter potassium content of the heart is significantly lower than that of other muscles. The main bulk of muscles in wild birds contain more potassium and less sodium as compared to the muscle tissue of domestic ones. No interspecific differences were found in potassium and sodium content of white and red pectoral muscles.     

Helping patients to die--an ethical challenge to nursing care and to its institutional framework]

The objective of this study was to determine fluid-electrolyte changes in male Wistar rats during 90 days of hypokinesia (decreased motor activity) and 15 days posthypokinesia. The animals were divided into two groups: rats subjected to hypokinesia served as experimental animals and rats placed under vivarium conditions served as control animals. The hypokinetic effect was carried out by keeping the experimental rats in small individual cages which restricted all their movements without hindering food and water intake. Determination was made of body weight, fluid consumed and eliminated in urine, sodium and potassium excretion in urine, concentrations of sodium and potassium in urine, the hematocrit level and water content in blood, and plasma concentration of sodium and potassium. During the experimental period body weight, water intake, urinary sodium and potassium content, and water content in blood decreased significantly, while electrolyte excretion in urine, plasma electrolyte concentration, hematocrit content and fluid excretion in urine increased significantly in the hypokinetic animals when compared with the control animals. During the initial seven days of the postexperimental period, water intake increased significantly while hematocrit level, water content in blood, and electrolyte plasma concentration remained markedly higher, and the fluid electrolyte excretion and electrolyte concentration thereof in urine decreased significantly. However, all these changes reverted back to the control level by the end of the post-experimental period. It was concluded that prolonged hypokinesia (HK) and the initial stages of post hypokinesia are associated with significant sodium and potassium changes and water consumption and elimination disturbances.     

Effects of reserpine on water, cation, and norepinephrine contents of cardiovascular tissues of normotensive dogs

Six adult male mongrel dogs were treated orally with reserpine (0.03 mg/kg) for 6 weeks, after which time the arterial tissue content of water, cations (sodium, potassium, magnesium, and calcium), and norepinephrine was determined and compared with those of six untreated dogs. Reserpine administration resulted in sustained decreases in the mean arterial blood pressure and heart rate, and the arterial tissues of the treated dogs contained less potassium, calcium, and magnesium, the last-named being affected most, but the sodium remained the same. Arterial norepinephrine content was significantly decreased. There was a slight but significant increase in plasma magnesium, without any noticeable changes in other plasma cations. The reduction in the arterial magnesium by reserpine may help to regulate vascular tone and (or) vascular reactivity.     

Urine sodium, potassium and osmolality in two rat strains selected for their different ethanol preferences

Urine sodium, potassium and osmolality were investigated during water and ethanol diuresis in two rat strains, AA and ANA, which drink voluntarily different amounts of ethanol. At the start of each experiment the rats were in a positive water balance. During ethanol intoxication the AA strain excreted more urine than the ANA strain. In ethanol experiments the osmolality of the urine was higher in the AA strain than in the ANA strain. With ethanol amounts of 2.4 g/kg body weight and 4.8 g/kg of body weight, urinary sodium and potassium output was greater in AA rats than ANA rats. When only water was introduced urine volumes and the excretion of sodium and potassium during 180 min were greater in ANA males than in AA males.     

Alkaloids and procyanidins of an Uncaria sp. from Peru

The direct and indirect effects of staphylococcal enterotoxins A and C on the flux of water, sodium, and potassium have been studied in paired Thiry Vella fistulae in dogs. Administration of toxin resulted in a significant decrease in absorption, both in the loop to which the toxin had been administered and its pair. This decrease in absorption was associated with a decrease in movement out of the lumen, movement into the lumen remaining relatively unchanged. The mechanism of action of staphylococcal enterotoxins is discussed, and comparisons made with other enterotoxins.     

Effects of dietary salt restriction on blood pressure and the renal vasoactive system in the congenitally bilateral hydronephrotic rat

We examined the responses on blood pressure when the renal vasoactive system such as renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system (KKS) was activated by dietary salt restriction in the congenitally bilateral hydronephrotic rat (BHN). In a low salt diet (LS)-normotensive and normal kidney control rats after 8 weeks from initiating dietary salt restriction, the plasma sodium concentration (PNa) was retained at a level similar to that in the normal diet (ND)-control rats, and plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein activity (UKA) were about 1.8-, 9.4-and 1.7-fold higher, respectively, than those in the ND-control rats. In addition, LS-control rats had a significantly (p < 0.001) high systolic blood pressure (163 +/- 2.0 mm Hg) compared with that (136 +/- 5.8) of ND-control rats. These results suggest that the activated renal vasoactive system acted for not only sodium retention but also for elevation of blood pressure in LS-control rats. In LS-BHN at week 8, PNa was also retained at a nearly normal level. However, the renal vasoactive system activation for sodium retention was higher than that of LS-control rats; that is, increase of PRA, PAC and UKA were about 3.8-, 24.7-and 10.0-fold, respectively, than in ND-BHN. The higher activation of RAAS, nevertheless, does not affect blood pressure in BHN; that is, both hypertension of BHN fed LS and ND developed similarly. These findings suggest that dietary salt restriction could markedly activate the renal vasoactive system for sodium retention without elevating blood pressure in BHN different from control rats.     

Treatment of impaction colics

The objective of this investigation was to determine electrolyte concentration in skeletal muscles and plasma of rats during 90 days of hypokinesia (decreased motor activity) and 15 days of posthypokinesia. The animals were divided into three groups: 1) supplemented hypokinetic rats (SHR), i.e., rats subjected to hypokinesia and taking daily an additional 9 ml water per 100 g body weight plus 6 ml isotonic sodium chloride per 100 g body weight; 2) unsupplemented hypokinetic rats (UHR), i.e., rats subjected to hypokinesia; 3) vivarium control rats (VCR), i.e., rats placed under ordinary vivarium conditions. Hypokinesia was effected by keeping SHR and UHR animals in small individual cages that restricted their movements in all directions without hindering food and water intake. Determinations were made of water and electrolyte (sodium potassium, calcium, magnesium) concentrations in muscle tissue; concentration of electrolytes (sodium, potassium, calcium, magnesium, phosphorus, chloride) in plasma; body weight; fluid consumed and eliminated in urine; whole blood, red blood cell and plasma volumes; hematocrit content and plasma protein concentration. During the hypokinetic period, electrolytes and water concentration in muscle tissue and plasma electrolyte concentration changes significantly in the UHR when compared with SHR and VCR while in comparing the SHR with the VCR these same variables had no significant changes. Body weight, water balance, volume of blood, red blood cell and plasma, hematocrit and plasma protein concentration in the UHR were also significantly different when compared with the VCR. No significant difference was seen in these parameters when the SHR and VCR were compared. During the initial seven days of the posthypokinetic period the changes in these same parameters remained significantly different in the UHR when compared with the SHR and VCR while changes were insignificant when the SHR and the VCR were compared. It was concluded that daily hyperhydration may be used to attenuate or normalize water and electrolyte concentrations in muscles and plasma of rats subjected to prolonged restriction of motor activity.     

Daily variations of platelet aggregation in relation to blood and plasma serotonin in diabetes

INTRODUCTION: An increase in digitalis-like substances has been reported in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. We hypothesized that the role of saline and unilateral nephrectomy in DOCA hypertension may be due to stimulation of endogenous digitalis-like substances. METHODS: We investigated the effects of digoxin and DOCA alone and in combination in intact rats drinking water. Forty male Sprague-Dawley rats were used (body weight 223-298 g). RESULTS: Neither digoxin (40 micrograms/kg per day, by gavage, for 35 days, n = 10) nor DOCA (30 mg/kg twice a week, subcutaneously, for 5 weeks, n = 10) caused a consistent increase in blood pressure in intact rats drinking water. In contrast, combined digoxin and DOCA administration (n = 10) increased systolic blood pressure from day 18 of treatment onwards, to a maximum at day 34 compared with sham-treated rats (n = 10). There were no consistent changes in water intake, urine volume, urinary sodium or potassium excretion, or plasma sodium or potassium concentration with digoxin treatment. DOCA increased water intake and urine volume, and caused an initial decrease in urinary sodium excretion, but no change in urinary potassium excretion or plasma sodium concentration. Plasma potassium excretion was lower in DOCA- than sham-treated rats. CONCLUSION: Combined digoxin and DOCA administration in intact rats drinking water increased blood pressure significantly compared with either drug alone, raising the possibility that the mechanism by which nephrectomy and salt loading contribute to DOCA hypertension in the rat might be through stimulation of endogenous digitalis-like substances.     

Changes in renal metabolite profile and ammoniagenesis during acute and chronic metabolic acidosis in dog and rat

Acute metabolic acidosis was induced by an i.v. administration of hydrochloric acid to dogs and rats to decrease the plasma bicarbonate concentration from 22 to 12 mM in dogs and from 26 to 10 mM in rats. Chronic metabolic acidosis was also induced in dogs by ammonium chloride feeding for 5 days. Rats also were given ammonium chloride for 24 hours. The renal metabolite profile was determined on the freeze-clamped renal tissue before and after 100 min (dogs) or 30 to 240 min (rats) of acsute acidosis. Measurements on chronically acidotic dogs and rats with 24-hour acidosis were obtained also for comparison with acute acidosis. In both species, kidney glutamine, glutamate, and alpha-ketokglutarate concentrations decreased drastically following induction of acute or chronic acidosis, In the dog, or in the rat during the first 2 hours of acidosis, malate concentration was unchanged. Malate concentration fell significantly in the rat kidney only after 2 hours of acidosis without change in phosphoenolpyruvate (PEP) concentration. In chronically acidotic dogs, malate and oxaloacetate rose fivefold with no change in PEP concentration. Phosphoenolpyruvate carboxykinase (PEPCK) activity was not stimulated by chronic metabolic acidosis in the dog in contrast to the rat. Acute acidosis by hydrochloric acid increased net renal glutamine extraction in the rat but not in the dog. These data suggest that an increased metabolic flux occurs between alpha-ketoglutarate and malate in both rat and dog kidney during acute metabolic acidosis. In the rat, however, after 2 hours, PEPCK activation modifies the kidney metabolite profile. Intrarenal glutamine transport seems to be a rate-limiting factor for adaptation to acute acidosis in the dog but not in the rat kidney.     

Reduced hedonic behavior and altered cardiovascular function induced by mild sodium depletion in rats.

Interactions among sodium homeostasis, fatigue, mood, and cardiovascular regulation have been described previously. The present study investigates the effects of sodium deficiency on an index of mood (hypohedonia; Experiment 1), cardiovascular function (Experiment 2), and plasma electrolytes (Experiment 3) in rats. Following 48 hr of sodium depletion with a diuretic (furosemide) and a sodium deficient diet, rats displayed hypohedonia evidenced by reduced responding for rewarding electrical brain stimulation into the hypothalamus. Also, sodium depletion produced increased heart rate and reduced heart rate variability. Plasma sodium levels were lower in sodium-depleted rats versus control rats, whereas potassium levels were unchanged. Thus, mild sodium depletion produces hypohedonia and cardiovascular alterations, which has implications for understanding behavioral and cardiovascular consequences of sodium deficiency. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Potassium depletion modulates aldose reductase mRNA in rat renal inner medulla

The organic osmolytes present in renal inner medullary cells balance the extracellular hyperosmolality and protect the cell against the effects of high salts and urea. We previously demonstrated that a renal concentrating defect due to potassium depletion was associated with a decrease in organic osmolytes including sorbitol. However, we could not determine whether a reduction in medullary organic osmolyte would be cause or effect of urine concentration defect associated with potassium depletion. We focused on the synthesis of sorbitol catalyzed by the enzyme, aldose reductase. To clarify whether the treatment of potassium depletion would affect aldose reductase when extracellular tonicity, and medullary sodium or potassium was maintained at the level of control rats, we administered a hypertonic solution of NaCl or KCl to potassium-depleted rats and evaluated aldose reductase enzymatic activity and mRNA abundance as well as the medullary contents of organic osmolytes. Either infusion significantly reduced tissue sodium content in potassium-depleted rats. With KCl infusion protocol but not that of NaCl, sorbitol as well as aldose reductase mRNA abundance increased to the control level. Medullary contents of other organic osmolytes exhibited a pattern similar to sorbitol. Data suggested that aldose reductase mRNA abundance was reduced in potassium depletion irrespective of medullary sodium content. A decrease in sorbitol level may precede a urinary concentrating defect. Our finding constitutes the first demonstration of the relationship between a potassium deficiency and the abundance of aldose reductase mRNA, an osmoregulatory protein in the kidney.     

The effect of sodium nitroprusside on the membrane potential and mechanical tension of the smooth-muscle cells in the rat aorta

The rat aorta smooth muscles were contracted and depolarised with high potassium or phenylephrin solution which was followed by a relaxation and repolarisation after sodium nitroprusside administration. The latter effect was decreased az a combined action of phenylephrin and high potassium solution. Nitroprusside seems to act through a cGMP-dependent potassium transient activation of the smooth muscle cell membrane.     

Increased intracellular potassium and water contents in rat heart after alpha-1-adrenoceptor stimulation

Potassium accumulation in rat heart after alpha-1-adrenoceptor stimulation has previously been reported from indirect measurements. Here we present data on intracellular potassium content measured directly in the heart. Isolated rat hearts perfused in a non-recirculating system were exposed to alpha-1-adrenoceptor stimulation (5 x 10(-5) mol/l phenylephrine in the presence of 10(-6) mol/l timolol). 14C-Sucrose was used to estimate the extracellular space. From heart homogenates intracellular potassium, magnesium and cellular water contents were determined and the ion concentrations calculated accordingly. The intracellular magnesium content remained unchanged during all experimental conditions. alpha-1-Adrenoceptor stimulation evoked an increase in potassium content by 9% (4, 14; 95% confidence interval (CI), P = 0.0006). Due to an observed increase in intracellular water by 17% (9, 26; 95% CI, P = 0.0006), the potassium concentration apparently decreased by 8% (0.3, 15; 95% CI, P = 0.04). During partial inhibition of the Na+/K(+)-ATPase by 10(-5) mol/l ouabain, there was an increase in potassium content by 5% (1, 9; 95% CI, P = 0.008). There was, however, no significant increase in intracellular water in this situation. Calculated intracellular potassium concentration showed accordingly a slight increase. The effects upon potassium and water both in the absence and presence of ouabain were eliminated by the alpha-1-adrenoceptor blocker prazosin (10(-6) mol/l). alpha-1-Adrenoceptor stimulation apparently increased cellular dry weight by 10% (2, 18; 95% CI, P = 0.02). Changes in translocation of potassium and water must be considered as part of the alpha-1-adrenergic heart effects.     

The molecular markers of hemostatic activation on coronary artery disease

The male Otsuka Long-Evans Tokushima Fatty (OLETF) rat shows insulin resistance in skeletal muscle and visceral obesity. To obtain information on the mechanism of the insulin resistance in the diabetic rats, we examined the content of insulin-regulated glucose transporter (GLUT4) in skeletal muscles. The results indicate that the total content of the transporter is significantly decreased (P < 0.05) in muscles of the diabetic rats. Plasma membrane content of the GLUT4 protein in muscles of the diabetic rats was increased in the basal state as compared to control rats. Hyperinsulinemic clamps increased GLUT4 levels in the plasma membrane of control rats but failed to do so in the diabetic rats. The distribution of GLUT4 in OLETF rat is reminiscent of the characteristics of human non-insulin-dependent diabetes mellitus.     

Lipid oxidation. Part 3. Oxidation of egg phosphatidylethanolamine

The norepinephrine content of the whole brainstem and of its different parts and the epinephrine and norepinephrine (NE) content in the blood and adrenals in dogs and rats during ontogenesis were studied. The catecholamine (CA) level in the blood and different parts of the dog brainstem increased to the age of 20-30 days and then decreased. The NE value of the whole dog brainstem increased to the age of 9-30 days, and then decreased. The content of NE of the rat brainstem increased to the age of 120 days and then decreased. The amount of CA of the dog and rat adrenals increased progressively from birth to adulthood. The CA brain and adrenal level of dogs during postnatal ontogenesis was lower than in rats.     

Renal functional and organic changes induced by salt and prostaglandin inhibition in spontaneously hypertensive rats

The prolonged (3 months) effects of high sodium intake and sodium meclofenamate were studied in two groups of male spontaneously hypertensive rats. Group 1 (8 rats) received 1% NaCl in tap water ad libitum and served as control. Group 2 (8 rats) received, besides 1% NaCl in tap water, 50 micrograms/ml of sodium meclofenamate per rat daily. Renal metabolic, hemodynamic and histologic studies were done at the end of the study. The renal functional studies were performed in the unanesthetized, unrestrained state. Group 2 rats developed significantly higher arterial pressures, renal vascular resistance and histologic changes (p less than 0.005), larger left ventricular weights (p less than 0.05) and significantly lower effective renal plasma flow, renal blood flow (p less than 0.005) and glomerular filtration rate (p less than 0.05) than group 1 rats. There were no differences between the two groups of rats with respect to heart rate, hematocrit, right ventricular weight, body weight, fluid intake, urine output, sodium and potassium excretion and serum electrolytes. The results suggest that the combination of high sodium intake and prostaglandin synthesis inhibition exert a greater damaging effect on the arterial pressure and renal function of spontaneously hypertensive rats than salt alone.     

Effects of varying sodium intake on blood pressure and renin-angiotensin system in subtotally nephrectomized rats

In rats in which the renal mass had been reduced by 70 per cent, the effects of varying sodium intake on blood pressure, serum electrolytes, renin-angiotensin system, and some other parameters that were modified simultaneously were studied. Within 4 weeks, a high sodium diet (750 mEa. per kilogram) resulted in marked hypertension, whereas a standard sodium diet (150 mEq. per kilogram) elevated the blood pressure only slightly. A low sodium diet (less than 0.2 mEq. per kilogram) prevented the rise in blood pressure. In the hypertensive group, the hematocrit values were markedly decreased, indicating the expansion of extracellular and intravascular spaces. The compensatory renal hypertrophy was accelerated by the high sodium diet and retarded during restriction. During low sodium intake, the serum concentration of sodium was diminished and that of potassium elevated. During the high sodium diet, the sodium concentration was unchanged, but the potassium concentration was decreased. Subtotal nephrectomy diminished the plasma angiotensin II concentration, and the renin content of the kidney remnant was lower than that of the kidneys from control animals. Sodium restriction stimulated the renin angiotensin system markedly, whereas high sodium intake suppressed it. After subtotal nephrectomy, elevation of blood pressure, renal hypertrophy, and suppression of the renin-angiotensin system are closely related to sodium intake.     

Renal nerves are not involved in sodium and water retention during mechanical ventilation in awake dogs

BACKGROUND: The role of renal nerves during positive end-expiratory pressure ventilation (PEEP) has only been investigated in surgically stressed, anesthetized, unilaterally denervated dogs. Anesthesia, sedation, and surgical stress, however, decrease urine volume and sodium excretion and increase renal sympathetic nerve activity independent of PEEP. This study investigated in awake dogs the participation of renal nerves in mediating volume and water retention during PEEP. METHODS: Eight tracheotomized, trained, awake dogs were used. The protocol consisted of 60 min of spontaneous breathing at a continuous positive airway pressure of 4 cm H2O, followed by 120 min of controlled mechanical ventilation with a mean PEEP of 15-17 cm H2O (PEEP), and 60 min of continuous positive airway pressure. Two protocols were performed on intact dogs, in which volume expansion had (hypervolemic; electrolyte solution, 0.5 ml x kg(-1) x min(-1)) and had not (normovolemic) been instituted. This was repeated on the same dogs 2 or 3 weeks after bilateral renal denervation. RESULTS: Hypervolemic dogs excreted more sodium and water than did normovolemic dogs. There was no difference between intact and renal-denervated dogs. Arterial pressure did not decrease when continuous positive airway pressure was switched to PEEP. Plasma renin activity, aldosterone, and antidiuretic hormone concentrations were greater in normovolemic dogs. The PEEP increased aldosterone and antidiuretic hormone concentrations only in normovolemic dogs. CONCLUSIONS: In conscious dogs, renal nerves have no appreciable contribution to sodium and water retention during PEEP. Retention in normovolemic dogs seems to be primarily caused by an activation of the renin-angiotensin system and an increase in the antidiuretic hormone. Excretion rates depended on the volume status of the dogs.     

Chronic immobilization stress reduces sodium intake and renal excretion in rats

The influence of chronic exposure to immobilization (IMO) on sodium appetite as well as sodium and potassium renal excretion in adult male Wistar rats was studied. The animals were individually housed and all variables under observation were measured in metabolic cages the first, seventh, and thirteenth days once the experiment had started. Half of the rats had access to water, and the remainder of the rats had access to both water and saline solution (1.5% NaCl). IMO reduced the intake of saline solution. Renal water, sodium, and potassium excretion in those IMO rats having access to saline were lower than in control rats. The effects of IMO were very similar during all observation days; therefore no evidence of adaptation to repeated stress was found. The present data indicate the following: (i) IMO stress reduced sodium appetite, probably as a secondary effect to the deficit in sodium renal excretion; (ii) IMO caused antidiuresis and antikaliuresis, only in those rats taking saline solution; (iii) no adaptation to repeated IMO stress was found in any of the tested variables. The reduction of sodium appetite observed in stressed rats might be a homeostatic mechanism to maintain sodium balance after impairment of renal sodium excretion caused by stress.     

Evaluation of the carcinogenic effect of ceramic fibers in experiments on rats and mice

The metabolism of toborinone, (+/-)-6-[3-(3,4-dimethoxybenzylamino)-2-hydroxypropoxy]-2(1H)-quin - olinone, a novel inotropic agent, was studied in rats and dogs after intravenous administration. Chemical structures of the 13 metabolites were characterized by direct-probe FAB/MS and field desorption/MS, LC/FAB/MS, and various NMR measurements. After intravenous dosing of 10 mg/kg [14C]toborinone, fecal and urinary recoveries of the 14C dose were approximately 70% and 26-30%, respectively, in both rats and dogs. The predominant component of radioactivity was the unchanged toborinone in every biological specimen in rats and dogs. Although unchanged toborinone was predominantly observed, toborinone underwent extensive conjugations with glucuronic acid, sulfate, and glutathione, either directly or following phase I reaction. Metabolites resulting from oxidative N-C cleavage were minor both in number and in quantity in every biological specimen in rats and dogs. In rats, toborinone underwent O-demethylation to form M-7 and successive phase it reaction to yield the glucuronide M-1 and the sulfoconjugate M-2, and deconjugation to yield M-7, which was a primary metabolite accounted for 35.67% of the radioactivity excreted in the feces by 48 hr. Conjugates M-1 and M-2 were the major metabolites in rat plasma. In dogs, toborinone was metabolized via mercapturic acid pathway to yield the primary metabolites, cysteine conjugates M-10 and M-11 that accounted for 19.10% and 6.70% of the radioactivity excreted in the feces by 48 hr and that were detected species specifically in dogs. The glutathione conjugate M-13, which was isolated from in vitro incubations using dog liver, led us to consider a possible mercapturic acid pathway from the parent compound to M-10. Metabolites in dog plasma and those in urine in both rats and dogs were minor in quantity. The metabolic pathways of toborinone in rats and dogs are proposed herein.