Adipose tissue lipolytic activity and urinary catecholamine excretion in cold-acclimated piglets

This study was designed to investigate the effect of chronic cold exposure (12 degrees C for 3 weeks) on catecholamine production and noradrenaline-induced lipolytic rate to further describe thermoregulatory mechanisms in 5- to 8-week-old pigs. Lipolytic activity in white adipose tissue was assessed in vitro while catecholamine production was estimated by measuring noradrenaline, adrenaline, and dopamine levels in 24-h urine samples. Animals were fed ad libitum and food intake was 20% greater in the cold. In control piglets maintained in a 23 degrees C environment, the addition of increasing amounts of noradrenaline (10(-6), 10(-5), 10(-4) M) stimulates lipolysis (p less than 0.05) and enhances the basal lipolytic rate (5.4 mu equiv. fatty acids.120 min-1.g-1 tissue) by 2.5-, 2.7-, and 3.9-fold, respectively. Three weeks of cold acclimation had no effect on basal lipolytic rate but increased significantly noradrenaline responsiveness: incubation of subcutaneous white fat in the presence of 10(-4) M noradrenaline does increase the basal lipolytic rate by sixfold. Noradrenaline effects were maximally activated by theophylline. Daily dopamine and noradrenaline excretions (3-10 micrograms/24 h) were increased significantly (up to eightfold) after 10 days of cold acclimation. By contrast, adrenaline excretion was quite low (0.6-1.6 micrograms/24 h) and showed no significant variation with time. It is likely that these hormonal and biochemical modifications play a prominent part in the mechanism of cold acclimation in the piglet. Their significance in the development of shivering and nonshivering thermogenesis is discussed in relation to the supply of energy substrates to the fatty acid utilizing tissues and to the possible uncoupling effect of free fatty acids.     

The mechanism of disorders of salivary catecholamine excretion in acute starvation in rats

Using standard HPLC method the authors estimated adrenaline and noradrenaline content in saliva and salivary gland tissue. In severe starvation A and NA content were diminished in 24 hours.     

Effect of hyperosmotic solutions on salt excretion and thirst in rats

We investigated urinary changes and thirst induced by infusion of hyperosmotic solutions in freely moving rats. Intracarotid infusions of 0.3 M NaCl (4 ml/20 min, split between both internal carotid arteries) caused a larger increase in excretion of Na(+) and K(+) than intravenous infusions, indicating that cephalic sensors were involved in the response to intracarotid infusions. Intravenous and intracarotid infusions of hyperosmotic glycerol or urea (300 mM in 150 mM NaCl) had little or no effect, suggesting the sensors were outside the blood-brain barrier (BBB). Intracarotid infusion of hypertonic mannitol (300 mM in 150 mM NaCl) was more effective than intravenous infusion, suggesting that cell volume rather than Na(+) concentration of the blood was critical. Similarly, intracarotid infusion (2 ml/20 min, split between both sides), but not intravenous infusion of hypertonic NaCl or mannitol caused thirst. Hyperosmotic glycerol, infused intravenously or into the carotid arteries, did not cause thirst. We conclude that both thirst and electrolyte excretion depend on a cell volume sensor that is located in the head, but outside the BBB.     

Hypertension and cardiovascular hypertrophy during chronic catecholamine infusion in rats

Chronic continuous infusion of norepinephrine (NE) or epinephrine (Epi) subcutaneously in rats resulted in a rapid elevation of systolic blood pressure (SBP) by 40 mm Hg. Pressure remained high for the duration of the infusion but rapidly returned to control levels after its termination. Pronounced hypertrophy of the thoracic aorta, abdominal aorta and heart was evident within 2 days of the initiation of NE infusion and a plateau was attained by 5 days of infusion. The activity of tissue ornithine decarboxylase (ODC), the rate limiting enzyme in polyamine biosynthesis, was elevated preceeding the onset of tissue hypertrophy, and returned to control levels coincidentally with the cessation of accelerated tissue growth. It is concluded that high blood pressure in this animal model of hypertension is dependent upon the continued presence of exogenous catecholamine, and that pronounced cardiovascular hypertrophy $\text{per}$$\text{se}$ is not sufficient to maintain the hypertension. The elevation and decline of vascular ODC activity is consistent with reports that in other tissues an elevation of ODC activity is an obligatory early event in hypertrophy.     

Lead increases urinary zinc excretion in rats

The major purpose of this study was to determine whether acute or chronic Pb exposure would increase urinary excretion of zinc in the rat. Four groups of unanesthetized rats were given 0, 0.03, 0.3, or 3 mg Pb (as acetate) kg intravenously, and urinary excretion of zinc, sodium, and potassium was monitored for 6 h. Only at the highest dose was urinary Zn excretion significantly elevated; there were no significant changes in sodium and potassium excretion at any dose. Two other groups of rats were studied for 9 weeks in metabolism cages before and during administration of either 500 ppm Pb (as acetate) or equimolar Na acetate in the drinking water. Two days after Pb treatment and continuing through day 35, Zn excretion was elevated in the Pb-exposed animals; beyond this day, zinc excretion became similar in the two groups. The difference in Zn excretion was not the result of lower water intake by the Pb-treated animals. At sacrifice (70 days after starting Pb exposure), Pb-exposed animals had lower Zn content of the plasma and testis, but there was no difference in kidney Zn. Plasma renin activity was significantly higher in Pb-exposed animals. We conclude that chronic Pb exposure in rats can result in some degree of decreased tissue zinc, which is, at least in part, secondary to increased urinary losses of zinc.     

Sodium excretory response to acute salt loading and induction of adrenal-regeneration hypertension in fischer 344 rats

Previous studies have shown Fischer 344 rats to be extremely resistant, if not immune to the development of salt hypertension. This is true even under the severe experimental conditions that overcome the very low susceptability of other strains such as the Long-Evans. These studies were confirmatory and also showed that the resistance could not be attributed to the ability of Fischer 344 rats to excrete salt more effectively than hypertension-prone SPD animals. Fischer 344 rats are normally susceptible to adrenal-regeneration, and not resistant to hypertension as such. Certain attributes and characteristics of strains showing resistance to salt hypertension are compared and contrasted.     

Influence of salt on glycaemic response to carbohydrate loading.

The effect of dietary salt on glycaemic responses to different test meals was investigated. Eight healthy male volunteers ate four test meals on consecutive mornings and in random order; the meals were 50 g carbohydrate taken as a 20% glucose solution or as boiled macaroni with and without supplementation with 6 g salt. In contrast with other reports, no significant differences in peak plasma glucose concentrations or areas under the plasma glucose curves could be established. These findings do not support a beneficial effect of salt restriction on glycaemic control in diabetes.     

The effect of protein and salt loading on urinary concentrating ability in four chromosomal species of Spalax ehrenbergi

Urinary concentrating ability was tested under protein and salt load in the four chromosomal species of subterranean mole-rats ( Spalax ehrenbergi superspecies) found in Israel. Protein stress induced by a diet of soyabeans supplemented by agar gel, demonstrated a significant increase in urinary osmolarity (UO). In the species living in the driest and warmest region (2n = 60). UO (1423·101 mOsmol/kg) was significantly (P<0·05) higher than in the other three species (2n = 52. 1172·31 mOsmol/kg; 2n = 54, 1160·116 mOsmol kg; and 2n = 58, 1216·145 mOsmol/kg). Upon salt loading this diet with 0·3 mol NaCl, UO increased significantly. However, when the salt load was increased to 0·45 mol NaCl, UO decreased significantly in all but one species (2n = 60) which maintained UO at 1522·65 mOsmol/kg. A decline in UO was attributed to diuresis resulting from a significant increase in urine and sodium excretion. The kidney, of only the xeric ranging species (2n = 60), demonstrated the ability to produce a hyperosmotic urine, in spite of the high salt load. These results might explain the restricted distribution of S. ehrenbergi: the only species (2n = 60) found in an environment rich in succulents and halophyte plants (steppe). This species appears to push speciation and adaptive radiation to the southern limit of its superspecies.     

Reduced urinary excretion of sulfated polysaccharides in diabetic rats

The aim of the present study was to further understand the changes in renal filtration that occur in the early stages of diabetes mellitus. Diabetes was induced in male Wistar rats by a single injection of streptozotocin. Glycemia, body weight, 24-h urine volume and urinary excretion of creatinine, protein and glycosaminoglycans were measured 10 and 30 days after diabetes induction. All the diabetic animals used in the present study were hyperglycemic, did not gain weight, and presented proteinuria and creatinine hyperfiltration. In contrast, the glycosaminoglycan excretion decreased. Dextran sulfates of different molecular weights (6.0 to 11.5 kDa) were administered to the diabetic rats, and to age-matched, sham-treated controls. Most of the dextran sulfate was excreted during the first 24 h, and the amounts excreted in the urine were inversely proportional to the dextran sulfate molecular weight for all groups. Nevertheless, diabetic rats excreted less and accumulated more dextran sulfate in kidney and liver, as compared to controls. These differences, which were observed only for the dextran sulfates of higher molecular weights (>7 kDa), increased with the duration of diabetes. Our findings suggest differential renal processing mechanisms for proteins and sulfated polysaccharides, with the possible involvement of kidney cells.     

Diet-induced nephrocalcinosis and urinary excretion of albumin in female rats

This study was carried out to test the hypothesis that diet-induced nephrocalcinosis causes enhanced loss of albumin in urine, irrespective of the composition of the nephrocalcinogenic diet. Female rats were fed various purified diets for 28 days. There was a control diet (0.5% Ca, 0.04% Mg, 0.4% P, 15.1% protein, wt/wt), a low Mg (0.01% Mg), a high protein (30.2% protein) and a high P diet (0.6% P). The low Mg and high P diet induced nephrocalcinosis as demonstrated histologically and by markedly increased concentrations of kidney Ca. In rats fed the high protein diet, nephrocalcinosis was essentially absent. Group mean values of urinary excretion of albumin and plasma concentrations of urea were increased in rats fed either the low Mg or high P diet. The high protein diet did not affect urinary albumin but caused lysozymuria which was not seen in the other groups. Plasma urea was increased in rats fed the high protein diet. In individual rats, the concentration of Ca in kidney and urinary albumin excretion were positively correlated. It is suggested that nephrocalcinosis in female rats induced by either low Mg or high P intake causes kidney damage which in turn leads to increased concentrations of albumin in urine and urea in plasma.