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Biomedical subjects

H G Preuss

Publications and source records attributed to H G Preuss.

At least 109 records · Page 6Linked to original sources
PubMed1981

Evidence of activation of the renal glutamate dehydrogenase pathway in intact acidotic dogs.

To determine if activity of the renal glutamate dehydrogenase (GD) pathway changes during chronic acidosis in intact dogs, we assessed the deamination of glutamate formed within renal cells during glutamine and alanine infusions. Infusing glutamine into chronically acidotic, normal and acutely alkalotic dogs enhanced renal ammonia production; more was formed as glutamine loading increased. In 4 acidotic dogs, the ratio of ammonia produced to glutamine extracted by the kidneys during exogenous glutamine loading was 1.93 compared with 0.99 for 5 alkalotic dogs and 1.23 for 2 control dogs. Little glutamate and alanine were released into the renal vein in acidotic dogs, whereas over 50% of the exogenous glutamine extracted in acutely alkalotic dogs could be accounted for as glutamate and alanine released into the renal vein. Renal glutamate concentrations were not elevated in acidosis compared with alkalosis despite greater deamidation. When glutamine infusions increased renal ammoniagenesis in acutely alkalotic and control dogs to levels seen in chronically acidotic dogs receiving no exogenous glutamine, approximately 4 to 6 times more glutamate was released from the kidneys. Infusing alanine into 7 chronically acidotic dogs enhanced ammoniagenesis significantly (p less than 0.01), but lesser augmentation was seen in 3 control dogs and no augmentation was seen in 6 acutely alkalotic dogs. The increases were secondary to enhanced glutamate deamination, not secondary to any changes in glutamine extraction and/or transaminase activity. We conclude that the glutamate dehydrogenase pathway is more active in intact acidotic dogs than it is in control and alkalotic dogs.

Acidosis↗
PubMed1981

Effects of glipizide on water and electrolyte handling in water-loaded humans.

Renal handling of H2O, Na, and K during H2O diuresis was studied in the same healthy subjects on two occasions, after the administration of either 5 mg of the sulfonylurea, glipizide, or a placebo. Following glipizide, there was no significant overall change in creatinine clearance and the calculated rate of distal Na + K delivery (CH2O + C(Na + K)) in 9 individuals. However, the clearance of free water (CH2O) and the mean fraction of Na + K reabsorbed at the diluting site increased significantly from 8.5 +/- (SEM) 0.8 to 9.8 +/- (SEM) 0.8 ml/min/100 ml GFR (p less than 0.02) and from 55 +/- (SEM) 6 to 67 +/- (SEM) 7% (p less than 0.05), respectively. The mean rate of total Na and K excretion fell following glipizide (p less than 0.05). Our results, in conjunction with the results from similar type studies, suggest that ingestion of glipizide and other sulfonylureas that lack antidiuretic properties increase CH2O, at least in part, by augmenting ion reabsorption at the diluting sites of the nephron.

Adult↗
PubMed1981

Humoral regulation of renal growth. Evidence for and against the presence of a circulating renotropic factor.

The stimuli for compensatory renal growth following a decrease in functioning renal mass have interested a number of investigators. The existence of a humoral incitor and/or regulator of renal growth, renotropin, has been postulated; and three types of experiments have been performed to determine its existence. These include parabiotic, in vivo, and in vitro assays. In general, the three different methodologies support the existence of a renotropic factor (or factors) but further investigations are needed to clarify its precise roles in compensatory renal growth.

Adaptation, Physiological↗
PubMed1981

Correlation between glutamate deamination and glutamine deamidation in rat kidney mitochondria.

Intramitochondrial glutamate removal through deamination may regulate renal ammoniagenesis from glutamine. However, little information is available to determine if there is a strong association between glutamine deamidation and the removal within mitochondria of the glutamate subsequently formed after deamidation. Using rat renal mitochondria, we found that ammonia production, glutamate appearance, and amide nitrogen disappearance were near equal aerobically and anerobically, when no ADP-generating system was present. When an ADP-generating system was added (ATP alone, ATP+ malonate, or ATP+2,4 DNP), more ammonia was formed aerobically from glutamine. Additionally, less glutamate appeared even though more amide nitrogen disappeared. Intramitochondrial concentrations of glutamate decreased. When pyruvate and alpha-ketoglutarate were added to the system, ammoniagenesis, deamidation, and deamination decreased; while glutamate built up in both the medium and mitochondria. In our mitochondrial system, we found a significantly positive correlation between glutamate deamination and glutamine deamidation, between glutamate accumulation and intramitochondrial glutamate concentrations; and a significantly negative correlation between glutamate deamination and glutamate accumulation, between glutamine deamidation and intramitochondrial glutamate concentrations, and between glutamate deamination and glutamate accumulation. We conclude that there is a biochemical relationship between glutamine deamidation and deamination of the glutamate subsequently formed. We propose that increased deamination lowers mitochondrial concentrations of glutamate and increases deamidation. In contrast, slowing deamination increases mitochondrial concentrations of glutamate and decreases deamidation.

Adenosine Diphosphate↗
PubMed1981

Propranolol-associated hypoglycemia in patients on maintenance hemodialysis.

Propranolol is widely employed in hemodialysis patients for the control of renin-dependent hypertension. Infrequent reports have linked hypoglycemia and propranolol, especially in complex situations such as malnutrition, anesthesia, and excessive insulin use. Three patients on maintenance hemodialysis taking propranolol developed severe hypoglycemia resulting in cardiac arrest. The life-threatening hypoglycemia occurred without apparent precipitating cause and unaccompanied by the classical signs and symptoms of hypoglycemia. These three cases suggest that propranolol in a setting of chronic renal failure and dialysis may bring about severe hypoglycemia, a complication previously unsuspected.

Adult↗
PubMed1981

Early diagnosis of polycystic kidney disease.

Polycystic kidney disease is the most prevalent hereditary renal disorder, accounting for over 5 percent of patients on chronic hemodialysis. Early diagnosis can aid in family planning, and "preventive therapy" may prolong useful life and defer dialysis. Intravenous pyelography with nephrotomography has been the standard procedure for definitive diagnosis, but ultrasonography, radionuclide scanning and computerized tomography have become increasingly useful. Ultrasonography is particularly valuable because it is free of radiation hazards. Impaired urinary concentrating ability is a frequent early sign of the disorder.

Adult↗
PubMed1980

Autoradiographic studies of the rat renotropic system.

Rat sera, 10-30 h after unilateral nephrectomy (UNI), enhance 3H-thymidine ("3H-Tdr) incorporation into DNA of incubating renal tissue from control rats. Stimulation is even greater when extracts from remaining growing kidneys 20 h after UNI are combined with sera from rats after UNI. UNI extracts, i.e., extracts from the kidney remaining after uninephrectomy, are nonstimulatory alone. UNI sera and UNI sera plus UNI extracts could theoretically augment 3H-Tdr incorporation into renal DNA via dilutional means rather than enhanced DNA synthesis. To determine if our results were secondary to enhanced DNA synthesis, we performed our in vitro assay using the labelling of nuclei via autoradiography as another index. The addition of UNI sera compared to sera from sham-operated rats (SHAM) in seven paired experiments enhanced incorporation of 3H-Tdr into DNA by 30% (p less than 0.02) and the addition of both UNI sera and UNI extracts compared to SHAM sera and SHAM extracts enhanced incorporation by 48% (p less than 0.001). Unlike a dilutional effect, nuclear labelling also increased in these same seven experiments: UNI sera versus SHAM sera increased 25% (p less than 0.05) and UNI sera + UNI extracts versus SHAM sera + SHAM extracts increased 37% (p less than 0.01). We conclude that UNI sera and UNI sera + UNI extracts enhance 3H-Tdr incorporation into DNA by augmenting DNA synthesis, driving cells into the "S" phase. The use of 3H-Tdr incorporation into DNA in our assay does estimate DNA synthesis.

Animals↗
PubMed1980

Tubulointerstitial diseases.

This group of disorders has a number of causes. Early in the course of the disease, tubular malfunction is out of proportion to glomerular disease. The early presentation may be inability to concentrate urine, salt wasting, distal or proximal renal tubular acidosis and/or Fanconi's syndrome. With early diagnosis and treatment, progression of the renal disorder can be prevented or at least delayed. One can easily discontinue the antibiotic or analgesic, remove the heavy metal, treat the electrolyte abnormality, lower the uric acid or remove the genitourinary tract obstruction.

Analgesics↗
PubMed1979

Acid excretion in young and adult Wistar Kyoto and spontaneously hypertensive rats.

Wistar Kyoto rats (WKy), the most widely accepted control for SH rats, show an inability to excrete acid appropriately when compared to another normotensive strain, SD. Coupled with the fact than KWy also develops 'sodium-sensitive' hypertension, this makes them a more complex control than realized. At very young ages (less than 10-week-old), neither SH nor WKy show any deficiency in acid excretion.

Aging↗
PubMed1979

Effects of fluorocitrate on renal ammoniagenesis and glutamine metabolism in the intact dog kidney.

Renal glutamine metabolism was studied in vivo following infusions of fluorocitrate into chronically acidotic and alkalotic dogs. Coincident with a dramatic rise in renal cortical citrate concentrations, there was a significant fall in tissue glutamate in both acid-base states. This was accompanied by a significant increase in total renal ammonia production. Glutamine metabolism and ammoningenesis in alkalotic dogs receiving fluorocitrate simulated that achieved in acidotic dogs. The simultaneous administration of alpha-ketoglutarate and fluorocitrate significantly diminished the fall in tissue glutamate and the rise in ammoniagenesis induced by fluorocitrate alone. These results are compatible with the hypothesis that ammonia production from glutamine is enhanced secondary to increased glutamate deamination. We postulate that this chain of events may be the consequence of impaired alpha-ketoglutarate production from citrate.

Acidosis↗
PubMed1979

Studies on the tissue specificity of a circulating renotropic factor.

In 1970, it was found that sera removed from rats 24 hr after unilateral nephrectomy stimulate the incorporation of 3H-Thymidine into the DNA of incubating rat renal cortex. The same sera did not influence isotope incorporation into the DNA of incubating liver, spleen, and lung tissue. Later, a substance was described in renal tissue that enhanced the action of the renotropic factor in sera. It was proposed that this tissue factor activated the circulating renotropic substance and that lack of this activator in other tissues was responsible for the specificity of the circulating renotropic substance to renal tissue. The present study suggests that this is the case as the addition of the renal tissue factor and sera from uninephrectomized rats can stimulate 3H-Thymidine incorporation into the DNA of rat liver slices.

Animals↗
PubMed1978

The regulations of renal ammoniagenesis in the rat by extracellular factors. I. The combined effects of acidosis and physiologic fuels.

Substrate oxidation by rat kidney slices regulates renal ammoniagenesis from glutamine. At concentrations close to those expected in plasma, lactate alone, or combined with other renal fuels, inhibits ammoniagenesis markedly; glucose and citrate decrease ammoniagenesis slightly. However, lactate, citrate, and glucose inhibit ammoniagenesis of kidney slices from acidotic rats less than ammoniagenesis of kidney slices from control rats. Lesser inhibition of ammoniagenesis is seen also when acidotic slices rather than control slices are incubated in the presence of all the tested substrates combined in the same medium. In addition to decreasing the ammoniagenesis of renal slices from control rats, the presence of lactate causes an augmented accumulation of glutamate. In contrast, adding lactate to acidotic slices does not increase glutamate accumulation nearly as much. When glutamate is substituted for glutamine in the medium, lactate still decreases ammonia production, but to a lesser extent with acidotic slices. Changes in medium pH from 7.0 to 7.8 have no, or only small, overall effects on net renal slice ammonia production from glutamine under any of the circumstances tested. We conclude that lactate alone and combined with other substrates decreases ammoniagenesis primarily at the glutamate dehydrogenase step and that slices from acidotic rats are relatively resistant to substrate mediated inhibition.

Acidosis↗