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Publications and source records attributed to J Areas.

12 recordsLinked to original sources
PubMed1990

Influence of oat bran on sucrose-induced blood pressure elevations in SHR.

To determine whether oat fiber influences BP, we gave spontaneously hypertensive rats (SHR) a diet high in sucrose and low in protein (calories: sucrose 52%, protein 15%, fat 33%) or a diet low in sucrose and high in protein (calories: sucrose 13%, protein 52%, fat 35%). The amount of fat in these particular diets has not been shown to influence BP, so we modified the 2 diets by replacing fat with oat bran (10% w/w). Accordingly, we examined 4 groups of 5 rats consuming different diets: high sucrose, high sucrose + oat bran, low sucrose, and low sucrose + oat bran. Not unexpectedly, SHR consuming the diet high in sucrose had a significantly higher BP after 2 weeks than those consuming the diet low in sucrose. The significant difference in BP continued over the next 3 weeks. At the end of 6 week duration of study, we found the following BP: SHR ingesting the high sucrose diet, 217 mm Hg +/- 5 (SEM) vs SHR consuming the low sucrose diet, 187 mm Hg +/- 4 (SEM) p less than .0001]. SHR eating the low sucrose diet and consuming supplemental bran showed no significant change in BP after 6 weeks compared to SHR eating the basic diet alone, 188 mm Hg +/- 6 (SEM); however, 5 SHR consuming the high sucrose diet with added oat bran showed a significantly lower BP 200 mm Hg +/- 2 (SEM) than SHR ingesting the basic high sucrose diet devoid of oat bran [p less than .01]. We conclude that addition of oat bran to the diet can ameliorate sucrose-induced BP elevations in SHR.

Analysis of Variance↗
PubMed1990

Effect of sodium and potassium ingestion on renal growth in rats.

To determine whether differences in dietary Na and K intake influence renal growth and compensatory renal growth following unilateral nephrectomy (uni), rats were given 2 diets for 2 weeks which differed only in Na-K concentrations. Diet 1 (High Na, Low K) contained 1.0% Na, 0.36% K and diet 2 (Low Na, High K) contained 0.05% Na, 2.0% K. Half of the rats consuming diets 1 and 2 for 1 week received uni and the other half of sham operation (sham). The rats were followed for another week while consuming the experimental diets. Uni and sham rats on diet 1 showed significant increase in blood pressure (BP) (136 +/- 4 v 126 +/- 3 mm Hg, P less than .05). Uni itself did not alter blood pressure. Body weight and heart rate were unchanged by diet or operation. Kidney weight, renal RNA, protein, RNA/DNA, and protein/DNA increased significantly after uni but the differences were not affected by diet. Serum blood urea nitrogen (BUN) and creatinine were not markedly different among any group of rats suggesting no major renal damage. We conclude that dietary changes of Na-K which cause no obvious renal damage even though BP is elevated moderately do not influence renal growth or compensatory renal growth. Based on RNA, DNA and protein metabolism, the form of growth (hypertrophy or hyperplasia) is also not influenced by renal electrolyte handling.

Analysis of Variance↗
PubMed1988

Renotropic stimulation in rat kidney cell culture.

A circulating renotropic factor specific for renal cells has been described in rats. The addition of sera obtained from unilaterally nephrectomized (uni) rats 24h after operation compared to sham-operated (sham) rats augments 3H-thymidine incorporation into the DNA of incubating kidney slices approximately 10%-30%. Attempting to amplify the sensitivity of the assay for this renotropic agent, we replaced slices with primary rat kidney cultures. The assay system was based on one previously used for rabbits. The cultured cells were synchronized in their growth phase by a period of protein-free starvation. Compared to sera from sham rats, sera from uni rats showed significant stimulation of thymidine incorporation into DNA, 35.5% +/- 9.3 (SEM), p less than .0001, at 16 h; 63.3% +/- 10.0 (SEM), p less than .001, at 24 h; and 19.5% +/- 6.5 (SEM), p less than .01, at 48 h post operation. Accordingly, the maximal stimulation at 24 h was greater than that previously found using the kidney slice assay. Measurable renotropic activity occurred earlier and over a shorter duration than in rabbits. Stimulation was similar when a D-valine medium, relatively specific for renal epithelial cells, replaced DME medium. We conclude that growth synchronized, primary rat renal cells in culture verify the presence of a circulating renotropin arising 24 h post uni.

Animals↗
PubMed1988

The rabbit renotropic system.

Elevated levels of a specific renal growth factor, renotropin, have been associated with spontaneous hypertension. To examine this association more closely, we have undertaken the development of a better assay system to characterize and purify renotropin. Sera from rabbits prior to operation (control) and at a specified time after unilateral nephrectomy (uni) were examined for renotropic activity. Comparing the effects of uni to control sera in the same rabbit, significant stimulation of 3H-thymidine incorporation into the DNA of primary rabbit kidney cultures incubated in D-valine medium to eliminate fibroblast growth was noted: at 3 days postoperatively 73% (n = 13), at 7 days 103% (n = 39), at 10 days 130% (n = 31), at 21 days 101% (n = 24), at 42 days 89% (n = 13). All values were at least P less than 0.01. The stimulatory properties were dose-dependent but reached a plateau at high serum concentrations. Comparing CPM/mg protein in uni/control in different concentrations of sera 7 days postoperatively, uni versus control were 67/44 at 5% v/v, 139/72 at 10% v/v, 261/161 at 20% v/v, and 243/136 at 40% v/v. The renotropic effect of uni sera remained after dialysis in incubation medium and after sera were heated in boiling water for 5 minutes. Renal extracts obtained from growing kidneys 7 days postnephrectomy augmented renotropic activity. Atrial natriuretic factor, ouabain, PGF2 alpha, PGE1, and cAMP did not possess renotropic activity. We conclude that the primary rabbit kidney culture assay for renotropin is highly sensitive and will be an important tool to comprehend the role of renotropin in the pathogenesis of hypertension.

Animals↗
PubMed1988

Presence of a serum vasoconstrictive factor following unilateral nephrectomy.

Experimental hypertension is often associated with decreased renal mass and/or impediments to normal renal compensatory growth. This has led to the hypothesis that the renal growth factor (renotropin) is also a vasoconstrictor responsible for elevated blood pressure. Unilateral nephrectomy (uni) is the most popular mechanism to investigate compensatory renal growth. Accordingly, we examined the vasoconstrictive potential of rat sera following uni in order to compare it with serum renotropic activity. Compared to sham-operated (sham) rat sera, uni sera obtained at 24 hours after operation, a point in time when renotropic activity is highest, stimulated the constriction of isolated rat aortic rings significantly more than sham sera, and in a dose-dependent fashion. By paired analysis, the differences in constriction between uni and sham sera were significant at all doses examined. Unlike those obtained at 24 hours, uni sera did not show this response 48 hours, 1 week and 2 weeks after operation, simulating the temporal course of renotropin found in sera after uni. The uni serum factor was not influenced by dialysis suggesting that its molecular weight exceeds 6,000 daltons and that the vasoconstrictive response was not due to electrolyte differences between uni and sham sera. Vasoconstrictive activity was retained after serum passage through Affi-gel blue to remove albumin and after serum was heated in boiling water for 5 minutes. We conclude that a heat resistant serum vasoconstrictive factor with a molecular weight greater than 6,000 daltons arises shortly after uni but disappears once the remaining kidney begins to undergo a physiological compensatory growth response.

Animals↗
PubMed1987

Renal ammoniagenesis following glutamine loading in intact dogs during acute metabolic acid-base perturbations.

Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 mumol min-1 100 ml-1 GFR vs 148 mumol min-1 100 ml-1 GFR: P less than 0.001) and glutamine extraction (111.8 mumol min-1 100 ml-1 GFR vs 90.9 mumol min-1 100 ml-1 GFR: P less than 0.02). The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid-base perturbations. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.

Acid-Base Imbalance↗
PubMed1987

Effects of sera from uninephrectomized rats on renal slices: PAH and TEA uptake and QO2.

We followed the effects of sera from unilaterally nephrectomized (uninephectomized) rats compared to sham-operated rats on 3H-p-aminohippurate (3H-PAH) and 14C-tetraethylammonium (14C-TEA) uptake and oxygen consumption (QO2) in incubating rat kidney slices. These studies were based on the assumption that a circulating renotropic substance might also influence various transport mechanisms. Sera were obtained at various times postoperation; the height of renotropic activity occurs 17-24 h after kidney extirpation. Sera removed 17-24 h postuninephrectomy significantly decreased both 3H-PAH and 14C-TEA uptake in incubating kidney slices. Similar to the inability to show significant renotropic activity after 36 h, sera obtained 48, 96, and 168 h postuninephrectomy had no significant influence on 3H-PAH and 14C-TEA uptake. Addition of sera (10% v/v) generally depressed QO2. However, sera obtained from uninephrectomized rats compared to sera from sham-operated rats had relatively more depressive effects on QO2 in renal tissue after 30 min of incubation (p less than 0.01). No significant differences in QO2 were seen when the uninephrectomized and sham-operated sera were added to the tissue immediately or after 60 min of incubation in the sera. These serum studies on 3H-PAH and 14C-TEA uptake simulate in many respects ones performed previously with serum from spontaneously hypertensive and salt-loaded rats and suggest the presence of a common circulating factor.

Aminohippuric Acids↗
PubMed1987

Renal ammonia production from the nitrogens of glutamine in intact acidotic dogs before and after bicarbonate infusions.

Renal ammonia is produced from the amide nitrogen of glutamine, approximately 33-50%. The remainder derives from the amino nitrogen of glutamine and other non amide sources, probably the amino nitrogens of other amino acids. We investigated the acute effects of acid-base perturbations on ammonia production from amide and non amide nitrogen sources to determine how they interrelate. Infusions of glutamine were given to some intact dogs to vary the renal load. Following an acute alkali challenge to dogs in metabolic acidosis, ammoniagenesis from the amide nitrogens decreased significantly when the presentation of glutamine to the kidney was normal or relatively low, but changed less or even increased when the glutamine load was relatively high. In contrast, ammonia from the non amide sources consistently decreased during acute alkalotic challenge at any glutamine load-high or low. Since decreased glutamine deamination leading to glutamate accumulation is generally associated with decreased deamidation in dogs with normal plasma glutamine concentrations, we explain the discrepancy of deamidation at high glutamine loads to an unmasking of a separate effect on the glutaminase (phosphate-dependent) pathway by the acute acid-base changes. Accordingly, our results indicate more than one influence from acute acid-base changes in vivo on renal ammonia formation, one stimulatory and other inhibitory. Nevertheless, the influence of glutamate removal predominates over the other effect on the phosphate-dependent glutaminase pathway at physiological concentrations of glutamine in the intact dog.

Acidosis↗
PubMed1987

Substrate oxidation in kidney slices from acidotic and alkalotic rats: role in ammoniagenic adaptation.

The enhanced renal ammoniagenesis that occurs during acidosis may depend on oxidative processes. To determine this, oxygen consumption (Qo2) of renal slices from acidotic rats (medium pH 7.0) and alkalotic rats (medium pH 7.8) in the presence of 4 different substrates (glutamine, lactate, acetate and 2-oxoglutarate) was investigated. Incremental addition of any oxidizable substrate tested to the incubation medium increased Qo2 until a maximal rate was approached (approximately 17-58% above baseline). Comparing acidotic to alkalotic slices, Qo2 was significantly less at low concentrations of lactate and acetate before maximal Qo2 occurred. In contrast, Qo2 was relatively higher at low concentrations of 2-oxoglutarate and glutamine with acidotic compared to alkalotic slices. Accordingly, acid-base perturbations produce different patterns of Qo2 depending on the substrate and its concentration. These observations coupled with others are consistent with the hypothesis that a relative block in the oxidation of lactate and acetate during acidosis provides more NAD+ for glutamine oxidation and participates in acidotic regulation of renal glutamine metabolism.

Acetates↗
PubMed1986

Effects of diets high in refined carbohydrates on renal ammonium excretion in rats.

Ammonium excretion was investigated in spontaneously hypertensive rats (SHR) and normotensive control rats (WKY) ingesting different diets. SHR and WKY on low protein-high sucrose diets surprisingly showed the same ammonium excretion as rats ingesting a higher protein-lower sucrose diet. This was unexpected, because ammonium excretion correlates positively with protein intake. The relatively high ammonium excretion despite low protein intake (approximately 40% of control) was not associated with acidosis, hypokalemia, hypocalcemia, and/or hypomagnesemia. In a follow-up study, where diets were high in refined carbohydrates (sucrose, glucose, and starch) but more equal in protein content compared with a diet high in carbohydrates of a more complex form (grains), ammonium excretion increased significantly. When we examined the factors known to influence ammonium excretion, the only significant positive correlations found were between norepinephrine, epinephrine, dopamine, and ammonium excretion. These correlations still remained significant when only the data from the rats on the diets high in refined carbohydrates, i.e., rats on the same dietary intake of minerals and proteins, were compared. In vitro, we corroborated that catecholamines significantly increased ammoniagenesis from kidney slices. Our data show that diets high in refined carbohydrates augment both ammonium and catecholamine excretion and suggest that these two events may be interrelated.

Ammonia↗
PubMed1984

In vitro correlation of glutamine and glutamate renal ammoniagenesis during adaptation.

Renal slices from 191 rats in various states of acid-base balance were investigated for their ability to produce ammonia from both glutamine and glutamate. Under a variety of conditions, in three different type studies, a significantly similar correlation existed between ammonia adaptation from glutamine and glutamate. This relationship was maintained during acute and chronic acidosis and during alkalotic inhibition of renal ammoniagenesis. We conclude from our findings that ammonia adaptation in rats secondary to acute and chronic acidosis is similar, although incomplete during acute acidosis. Our results further support the hypothesis that the rate of glutamate deamination is a major mechanism for overall renal ammonia adaptation in rats during acid-base changes.

Acid-Base Equilibrium↗