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Biomedical subjects

H G Preuss

Publications and source records attributed to H G Preuss.

At least 91 records · Page 5Linked to original sources
PubMed1986

Refined carbohydrate increases blood pressure and catecholamine excretion in SHR and WKY.

In spontaneously hypertensive (SHR) and normotensive (WKY) rats fed different diets, blood pressure (BP) increased significantly in both strains when the carbohydrate (CHO) source was from refined rather than from natural ingredients. This BP increase was observed whether sucrose, glucose, or starch was the principal CHO. Urinary excretion of norepinephrine, dopamine, and, to some extent, epinephrine also increased, while myocardial concentrations were unaffected. Despite a comparable elevation of catecholamine excretion in both SHR and WKY rats fed high amounts of refined CHO, the BP increases were greater in the former. The strain differences were explained by the known dissimilar response of their blood vessels to catecholamines. The results suggest that BP elevation after high CHO ingestion is mediated via increased catecholamine production and/or release, thus implying a neurogenic mechanism.

Age Factors↗
PubMed1986

Refined carbohydrates affect blood pressure and retinal vasculature in spontaneously hypertensive and Wistar-Kyoto rats.

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats received diets differing in amount and source of carbohydrates (CHO). When the CHO was in excess and the source was refined sugar or starch rather than natural ingredients, blood pressure (BP) rose, more so in SHR. This BP increase was observed whether sucrose, glucose, fructose or starch was the principal CHO. Increased urinary excretion of norepinephrine, dopamine and epinephrine also occurred. After only 2-3 months retinal capillary basement membrane damage was demonstrated in SHR and WKY rats ingesting large amounts of sucrose. No similar changes occurred on a high-starch diet. The damage consisted of thickening of capillary basement membranes, loss of homogeneity, and debris inclusions. These results suggest: that high dietary ingestion of CHO in the form of refined CHO augments BP in SHR and WKY rats via increased catecholamine production and/or release, and that the temporally foreshortened experimental period offered by the SHR/WKY model may be valuable in the study of diet-induced retinopathies.

Animals↗
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↗
PubMed1983

The regulation of renal ammoniagenesis in the rat by extracellular factors. III. Effects of various fuels on in vitro ammoniagenesis.

The addition of many oxidizable substrates to the medium of incubating rat renal slices decreases ammoniagenesis from glutamine and glutamate. Interestingly, lactate and beta-hydroxybutyrate depress ammoniagenesis less in renal slices from acidotic rats compared with normal-control rats. In this study, the effects of an expanded panel of substrates on ammoniagenesis in kidney slices from control and acidotic rats were followed to discern patterns of inhibition. In addition to lactate and beta-hydroxybutyrate, acetate, pyruvate, and perhaps acetoacetate caused relatively less depression of ammoniagenesis in acidotic slices. Citrate, succinate, fumarate, octanoate, and alpha-ketoglutarate decreased ammoniagenesis to the same extent or more in acidotic slices compared with that in normal-control slices. Glycerol had little effect on ammoniagenesis under either condition. From the substrates tested, it can be generalized that those outside the TCA cycle (with exception of octanoate) depress ammoniagenesis less during acidosis, while those in the TCA cycle depress ammoniagenesis equally or even more during acidosis. We hypothesize from the pattern of our results that changes in renal intermediary metabolism at or before citrate formation occur during acidosis and are important regulatory mechanisms for ammoniagenesis.

3-Hydroxybutyric Acid↗
PubMed1983

Polyamine metabolism in compensatory renal growth.

The aliphatic polyamines, putrescine, spermidine, and spermine, appear to play an important role in many forms of rapid growth including embryonic, regenerative, hormone-induced, and neoplastic. While the exact biochemical function of polyamines is unclear, current evidence suggests they are probably involved in the biosynthesis and accumulation of nucleic acids and proteins. Increased levels of polyamines and their biosynthetic enzymes are associated with augmented kidney growth stimulated by renal mass extirpation, as well as by various hormones, toxins, and carcinogens. These observations are reviewed and additional data is provided pertaining to alterations in polyamine metabolism during compensatory renal growth following unilateral nephrectomy (uni). To further explore the effect of growth stimuli on renal polyamine synthesis, an in vitro system was employed which previously provided evidence for a circulating renal growth factor after unilateral nephrectomy. These in vitro observations underscore the rapid inducibility of ornithine decarboxylase, the rate limiting enzyme for polyamine biosynthesis; illustrate the association of polyamine and nucleic acid synthesis during enhanced kidney growth; and support the existence of a circulating renal growth regulator which apparently contributes to compensatory responses following loss of functional renal parenchyma.

Animals↗
PubMed1983

Serum renotropic activity and renal growth in spontaneously hypertensive rats.

Studies performed in the 1950's suggested that a circulating factor controlling renal growth (renotropin) could contribute to hypertension. However, no assay was available to prove its existence. Recently, different assays have been able to demonstrate the presence of a circulating renotropic factor following unilateral nephrectomy in rats. Therefore, we investigated certain aspects of renal growth in SHR, especially serum renotropic activity, and compared these with the same parameters in three strains of normotensive rats (SD, NWR, and WKY). Renal slice and renal DNA synthesis in response to unilateral nephrectomy were not unusual in SHR compared to other strains previously studied. Sera and renal extracts from young SHR following unilateral nephrectomy compared to sera and renal extracts from sham-operated SHR stimulated 3H-thymidine incorporation into the DNA of renal fragments. This pattern was similar to findings when sera and renal extracts from unilaterally nephrectomized SD were investigated, but the sera and extracts from SHR may have shown greater overall stimulation. Interestingly, a relative increase in renotropic activity was found in the serum of untouched SHR (11.1% +/- 1.7 (SEM), P less than 0.001) but not untouched NWR, SD, and WKY. The greatest renotropic activity in SHR was found at 6 to 16 weeks of age (13.5% +/- 2.1 (SEM), P less than 0.001). The previously reported activator found in renal tissue after unilateral nephrectomy was not found to be increased in untouched SHR. No studies were performed on SHR greater than 25 weeks of age. As a first approximation, our investigations are consistent with a previously hypothesis that renotropin may play some role in hypertension.

Animals↗
PubMed1983

Partial characterization of a renotropic factor.

In 70 experiments, the existence of a circulating renal growth factor was confirmed by 9.3% stimulation of 3H-thymidine into the DNA of renal fragments incubating for 90 min in the presence of sera from 20-hour unilaterally nephrectomized rats compared to sera from 20-hour sham-operated rats (p less than 0.001). Dialysis (7.4%, p less than 0.01) or removal of albumin (11.8%, p less than 0.001) from sera of both sham-operated and unilaterally nephrectomized rats did not appreciably change the magnitude of the statistically significant stimulation. When albumin-free sera were placed in boiling water for 1-3 min to coagulate protein, the stimulation was still significantly different from control (5%, p less than 0.05). Addition of sera from unilaterally nephrectomized rats (20 h) to isolated nuclei, even isolated nuclei removed from growing kidneys (72 h after unilateral nephroctomy), failed to enhance DNA synthesis significantly.

Animals↗
PubMed1983

Effects of 2-oxoglutarate concentrations on canine slice ammoniagenesis.

The concentration of renal 2-oxoglutarate has been proposed as an important regulator of ammoniagenesis in dog kidneys. In the present study, canine kidney slices produced less ammonia from glutamine and glutamate when 2-oxoglutarate was present in the incubation medium. However, the addition of arsenite, a metabolic blocker known to block 2-oxoglutarate metabolism and lead to its accumulation, overcame 2-oxoglutarate inhibition of ammoniagenesis when glutamine and glutamate were the ammonia precursors. Therefore, metabolism of 2-oxoglutarate, rather than its concentration, governed ammonia production from glutamine and glutamate in incubating dog renal tissue. In contrast to the results with 2-oxoglutarate, inhibition of glutamine ammoniagenesis by glutamate was not overcome by arsenite. The results suggest that renal ammonia adaptation in acidotic dogs cannot be ascribed to a theory based upon 2-oxoglutarate concentrations controlling the direction of the glutamate dehydrogenase pathway (GDH), decreasing glutamine transport, or directly inhibiting GDH enzyme activity.

Ammonia↗
PubMed1982

Effects of in vitro potassium on ammoniagenesis in rat and canine kidney tissue.

Decreased ammonium (NH4+) excretion is associated with hyperkalemia. To determine if potassium could directly influence renal ammonia production, we investigated ammoniagenesis by rat and canine renal cortical tissues in vitro at different potassium concentrations. Renal tissue from normal and acidotic rats and normal dogs incubated in glutamine, lactate, and 7 to 10 mEq/liters of potassium or 25 mEq/liters of potassium produced significantly less ammonia than slices incubating in glutamine, lactate, and 4 to 5 mEq of potassium. Glutamate accumulation, which follows glutamine deamidation, did not decrease and even increased at 25 mEq/liters of potassium. With glutamine as the sole substrate, decreased ammoniagenesis was seen only at higher potassium concentrations (greater than 16 mEq/liters) than when lactate was also present. The depression to glutamine ammoniagenesis by high concentrations of potassium was partially obliterated in an anaerobic environment. When glutamate replaced glutamine as the precursor, renal ammonia produced by slices in 7 and 25 mEq/liters was again significantly lower than by slices incubating in 4 mEq/liters. We blocked glutamine synthesis by rat kidney slices with dl-methionine dl-sulfoximine when glutamate was the renal ammonia precursor. This essentially allows glutamate deamination to produce ammonia. Potassium depressed glutamate deamination significantly at 7 mEq/liters (decreases 13%) and at 25 mEq/liters of potassium (decreases 35%) as compared to 4 mEq/liters. The above findings are consistent with a major depressive effect of in vitro potassium on glutamate deamination in rat and canine kidneys. Other evidence, especially from rat tissue studies, suggests that potassium also may affect glutamine deamination directly. Rat kidney slices incubating in the high potassium medium of 7 mEq/liter or greater also consumed less oxygen in the presence of glutamine (P less than 0.01), oxidatively decarboxylated less glutamine (P less than 0.02) and produced less glucose from glutamine (P less than 0.01).

Acidosis↗
PubMed1982

The mechanism of acetate stimulation of PAH transport in rat kidney fragments.

Accumulation of p-aminohippurate (PAH) by rat kidney fragments incubating in vitro is enhanced as medium pH rises from 7.4 toward 7.8. Since medium pH increases from 7.4 to 7.8 over a 90-min period in the presence of acetate, we were unsure whether acetate had any direct stimulatory effect on transport. Rat renal fragments incubating in acetate showed no enhanced PAH accumulation at 30 and 60 min when medium pH was less than 7.6 but did increase approximately 25% after 90 min when pH approached 7.8. By a number of different procedures, we consistently found that when medium pH was not allowed to rise, acetate did not stimulate PAH accumulation. We conclude that at an initial pH of 7.4, acetate stimulation of PAH uptake by rat kidney fragments during the course of a 90-min incubation can be explained almost entirely by a rise in pH to a more optimal range for transport. In contrast, stimulation of PAH accumulation by lactate and pyruvate cannot be explained solely by changes in medium pH.

Acetates↗