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L Baumbach

Publications and source records attributed to L Baumbach.

36 records · Page 2Linked to original sources
PubMed1985

Effects of adenosine on renin release from isolated rat glomeruli and kidney slices.

Adenosine produced by the macula densa cells in response to changes in the tubular NaCl-concentration has been suggested to inhibit renin release in vivo. In order to test this suggestion we studied: incubated kidney cortical slices (KS) which contain both the macula densa and the entire afferent arteriole; superfused single microdissected glomeruli (LAG) without macula densa but with the afferent arteriole preserved; and superfused batches of selected glomeruli (SAG) containing only the juxtaglomerular cells closest to the glomerulus. For superfusion and incubation a bicarbonate Ringer solution was used. The specificity of the renin release process was validated by measuring adenylate kinase as a marker for cytoplasmatic leak. Adenosine (10 micrograms/ml) halved basal renin release from incubated KS as compared to controls (P less than 0.001, n = 8, 8). Renin release from LAG stimulated by calcium depletion was also inhibited (P less than 0.05, n = 8, 9) whereas basal release was not affected (n = 6, 12). No effect was detected neither on basal nor on calcium stimulated renin release from SAG. We conclude that adenosine inhibits renin release in vitro by a mechanism independent of a functioning nephron, and which involves only the JG-cells located in the afferent arteriole at some distance from the glomerulus.

Adenosine↗
PubMed1985

Teleocidin, a tumour promoter, stimulates synthesis of primate retroviruses in persistently infected human cells.

The naturally occurring tumour promoter teleocidin produces a pronounced but transient enhancement of the synthesis of extracellular viral particles in human cells chronically infected with simian retroviruses of type C (baboon endogenous virus, simian sarcoma virus) or type D (Mason-Pfizer monkey virus) or a human cell line-derived type D isolate (PMF virus), respectively. The retrovirus-stimulating activity of teleocidin is very similar to that previously described for the tumour-promoting phorbol ester TPA in the same cell systems.

Carcinogens↗
PubMed1984

Requirement of protein synthesis for the coupling of histone mRNA levels and DNA replication.

H1 and core histone mRNA levels have been examined in the presence of protein synthesis inhibitors with different mechanisms of action. Total HeLa cell RNAs were analyzed by Northern Blot hybridization using cloned human histone genes as probes. Inhibition of DNA replication resulted in a rapid decline in histone mRNA levels. However, in the presence of cycloheximide or puromycin, H1 and core mRNAs did not decrease in parallel with DNA synthesis, but were stabilized and accumulated. Inhibition of DNA synthesis with hydroxyurea after the inhibition of protein synthesis did not lead to a decline in histone mRNA levels. These results suggest that synthesis of a protein(s)--perhaps a histone protein(s)--is required for the coordination of DNA synthesis and histone mRNA levels.

Cloning, Molecular↗
PubMed1984

Enhancement of primate retrovirus synthesis by tumour promoters.

The tumor promoters 12-O-tetradecanoylphorbol-13-acetate (TPA) and teleocidin were found to be effective in stimulating the synthesis of primate retroviruses in chronically infected human cells. Production of baboon endogenous virus, simian sarcoma virus of woolly monkeys, Mason-Pfizer virus of rhesus monkeys and of a type D isolate from a human cell line was evaluated by assaying particle-associated reverse transcriptase activities in culture fluids of cells grown in the presence or absence of tumour promoters. Both TPA and teleocidin caused a significant but transient increase in virus production, as well as cytomorphological changes in the following infected cell types: human embryonic kidney, Tu 197 human ovarian carcinoma cells, NC 37 human lymphoblastoid line. However, infected A 204 human rhabdomyosarcoma cells were not modified by these promoters. The stimulation of virus production reached its maximum after two to four days, at which time virus production was three to forty times higher than that in controls. The optimal concentration of tumour promoters was 5-10 ng/mL. 12-O-Retinoylphorbol-13-acetate produced a similar but somewhat weaker effect. Control experiments demonstrated that enhancement was specific to those viruses that chronically infected each cell type.

Carcinogens↗
PubMed1983

An oscillating intratubular pressure response to alterations in Henle loop flow in the rat kidney.

We describe in gas anesthetized rats an oscillating intratubular pressure response, probably of vascular origin, sensitive to small physiological changes in fluid delivery to the distal tubule. The oscillation apparently indicates that an adjustment of vascular resistance is in operation, but at present it reveals neither the effector site (afferent and/or efferent arteriole) nor the effector mechanism (vasoconstriction and/or dilatation). The renin-angiotensin system seems to be involved in this phenomenon.

Animals↗
PubMed1982

Histone proteins in HeLa S3 cells are synthesized in a cell cycle stage specific manner.

The synthesis of histone proteins in G1 and S phase HeLa S3 cells was examined by two-dimensional electrophoretic fractionation of nuclear and total cellular proteins. Newly synthesized histones were detected only in S phase cells. Histone messenger RNA sequences, as detected by hybridization with cloned human histone genes, were present in the cytoplasm of S phase but not G1 cells.

Cell Cycle↗
PubMed1982

Tumor promoter-stimulated synthesis of Mason-:Pfizer monkey virus.

The tumor promoter 12-0-tetradecanoyl-phorbol-14-acetate (TPA) increases by severalfold the synthesis of Mason-Pfizer monkey virus (MPMV), a type D retrovirus, when the virus is growing in human embryo kidney (HEK) cells. The effect is transient and paralleled by a striking morphological alteration of the cells. The optimal TPA concentration for stimulation is 5 ng. ml-1. Contrary to infected HEK cells, TPA induces at similar concentrations neither stimulation of MPMV synthesis nor altered morphology in persistently MPMV-infected cells of the continuous human tumor cell line A 204.

Animals↗
PubMed1982

Isolated glomeruli in vitro: an approach to the macula-densa-mediated renin release.

The introduction of an assay for adenylate kinase into the study of renin release from isolated glomeruli is a useful tool in determining the specificity of the release process. Interestingly, even the absolute values of AK activity yield information that might be of value in understanding the effects on net renin output in media of grossly unphysiological composition. In qualitative terms, though, the AK measurements provide evidence against an unspecific loss of cytoplasmatic proteins as the cause of increased release of renin after removal of calcium or sodium bicarbonate. This renin release must have come from a compartment other than the cytoplasma of the juxtaglomerular cells. The in vivo position of the juxtaglomerular cells remaining in the present preparation, situated at the polkissen only few microns from the only hypoosmotic area in the body, suggests that the extreme osmosensitivity of renin release from isolated glomeruli represents a physiologic phenomenon. Because urea and sodium chloride are the predominant solutes in the tubular fluid at the macula densa, available data from isolated glomeruli are consistent with a macula densa feedback mechanism if it is accepted that a decrease in tubular sodium chloride concentration (and osmolality) increases the release of renin.

Adenylate Kinase↗
PubMed1982

[Germination of Clostridium oncolyticum in spheroid cell cultures as an in vitro tumor model].

An aggregation technique is used for construction of multicellular spheroids from trypsinized cell cultures of several normal and cancerous cell lines. This technique is applicable also in the presence of 1 X 10(9)/ml spores of Clostridium oncolyticum, and spores and vegetative bacterial cells can be counted by a soft agar colonization technique after trypsinization of spheroids. 24 hours after aerobic cultivation of spore-containing spheroids, germination and multiplication of Clostridium is detected by microscopy, electron-microscopy, and by bacterial cultivation technique. In this response there was no considerable difference between spheroids from tumour or from fresh cell lines. By electron microscopy many spores and vegetatively multiplying Clostridia became visible in the central necrotic part of spheroids. In the peripheral aerobic rim of spheroids, however, also few vegetative Clostridia were detectable.

Cell Aggregation↗
PubMed1981

Renin release from isolated rat glomeruli: seasonal variations and effects of D600 on the response to calcium deprivation.

1. The effects of calcium deprivation and D600 on the rate of renin release and seasonal variations in the response were studied on juxtaglomerular cells from a preparation of isolated rat glomeruli superfused in vitro. 2. Reduction of superfusate calcium concentration caused an increase in renin release, which was significantly higher during the summer (May-August) than during the rest of the year. 3. Addition of D600 (2 X 10(-4) M) to a calcium-free medium in the low responsive period caused a markedly increased renin release. In the high responsive period renin release increased more rapidly and to a higher level initially than observed in the control lines without D600. 4. It is suggested that the effect of calcium on renin release predominantly is mediated by changes in calcium bound to the plasma membrane of the juxtaglomerular cell. The sensitivity of this cell to changes in the extracellular calcium concentration seems to be regulated and varies with season, possibly due to regulation of the amount of calcium bound to the membrane.

Animals↗
PubMed1981

[Phorbol ester-induced expression of primate retroviruses (author's transl)].

Addition of the tumor promoter 12-0-Tetradecanoyl-phorbol-13-acetate (TPA) to the growth medium of certain human cell cultures persistently infected with simian retroviruses of type C (BaEV, SSV) or type D (MPMV) or a human cell line-derived type D isolate (PMFV), respectively, resulted in a considerable but transient stimulation of virus production. Enhanced virus expression was paralleled by striking morphological alterations of the cells. Among four infected cell types tested so far, ony one (A 204) failed to respond to TPA with significant virus stimulation or altered morphology.

Cell Line↗
PubMed1981

Cocultivation of Clostridium oncolyticum with normal and tumour cell lines.

During incubation of monolayer cell cultures with clostridia spores in the presence of 1.5 per cent of oxygen vegetative bacterial rods become visible and cell necrosis occurs preferentially in tumour cell lines. After such cocultivation tumour cells show a higher amount of clostridia not elutable by washing than finite cells. Electron microscopy of associated clostridia shows vegetative rods in contact to and inside of tumour cells.

Anaerobiosis↗
PubMed1980

Renin release from isolated rat glomeruli: effects of colchicine, vinca alkaloids, dimethylsulphoxide, and cytochalasins.

1. Preparations of isolated glomeruli were superfused and the effects of colchicine, the vinca alkaloids, and the cytochalasins A, B, D, and E investigated on basal renin release and the response of the glomeruli to osmotic stress. 2. Colchicine (10(-3) M) had no effect, whereas vinblastine and vincristine (10(-5) M) caused a progressive increase in basal renin release from isolated glomeruli. 3. After 60 min exposure to either colchicine or the vinca alkaloids, the first renin release response to a hypoosmotic challenge (reduction in sucrose or sodium chloride concentration) was depressed while that of the second (after 120 min exposure) was enhanced. 4. Addition of 0.5% dimethylsulphoxide (DMSO) and each of the cytochalasins A, B, D, and E (5 micrograms/ml.) had no significant effect on basal renin release. 5. DMSO (0.5%) depressed the release response to the first 20 m-osmole/kg reduction in medium osmolality obtained by lowering the sucrose concentration. This effect had vanished at the time of the second 20 m-osmole stimulus (120 min). 6. The normal response to the first 30 m-osmole/kg reduction in NaCl concentration (and medium osmolality) was abolished by 0.5% DMSO. Rather, a depressed release compared to unstimulated control experiments was observed. The response to the second stimulus in the presence of DMSO was about half that of control experiments. 7. Following the first hypoosmotic stimulus (by lowering the concentrations of sucrose of NaCl) the cytochalasins A, B, D and E (5 micrograms/ml.) caused an increased release of renin which persisted throughout the length of the experiment. The cytochalasins used were equally potent in this respect. 8. The results are in agreement with previous findings, suggesting that renin release from the juxtaglomerular cells adhering to isolated glomeruli is mediated through a mechanism different from exocytosis.

Animals↗
PubMed1980

Demonstration of C-type viruses in N-methyl-N-nitroso urea (MNU)-induced leukemia of mice by reverse transcriptase activity and XC assay.

A significantly higher MuLV expression was demonstrated in cells of MNU-induced leukemia of mice compared to corresponding cells of untreated control animals by reverse transcriptase activity and XC cell assay. These positive findings were verified by determination of indirect immunofluorescence test to look for intracytoplasmic MuLV p30. The problem is discussed whether these viruses play a role in chemical leukemogenesis.

Animals↗
PubMed1977

Studies on the mechanism of renin release from isolated superfused rat glomeruli: effects of calcium, calcium ionophore and lanthanum.

1. The effects of external medium calcium concentration, the ionophore A(23187) and lanthanum on the rate of renin release in vitro were studied with particular emphasis on results obtained from isolated superfused glomeruli of rat kidneys.2. The response to reduction in superfusate calcium concentration from 2 mM was a graded and reversible increase in the rate of renin release. An increase in release was detectable at 0.2 mM calcium; a threefold increase was found 36 min after a change from 2 mM calcium to calcium-free superfusate. A similar relative increase in release resulted from reductions from 0.1 mM to zero calcium, but the absolute amounts of renin released were greater in this latter series. Renin release from kidney cortical slices similarly increased in response to calcium-free incubation medium.3. The effects of A(23187) on renin release were modest. Changing from 2 mM calcium during control periods to calcium-free Ringer with A(23187) added caused an attenuated and more delayed increase in release than the change to calcium-free Ringer without ionophore. This difference in response was abolished when glomeruli were superfused with 0.1 mM calcium during the preceding 1 hr control period. There was no significant difference in renin release from glomeruli exposed to calcium-free EGTA-Ringer with and without A(23187) in the 2 mM calcium series; in the 0.1 mM calcium series the increase in release following a shift to calcium-free EGTA-containing superfusate with A(23187) added was significantly greater than in the absence of the ionophore.4. Addition of lanthanum (1 or 0.05 mM) to calcium-containing as well as calcium-free superfusate resulted in a significant depression of renin release. Subsequent removal of the lanthanum did not restore the rate of release unless EGTA was added; in the latter case a massive increase in renin release occurred resulting in a marked depletion of the remaining renin content of the glomeruli.5. It is concluded that calcium influences renin release by a direct action on the juxtaglomerular cells. The data support the previous suggestion that basal renin release is a function of active, calcium-dependent cell volume regulation - swelling causing an increase in the release; and further suggest that membrane-bound calcium has a direct effect on the cell membrane permeability to renin.6. The results exclude that calcium-stimulated exocytosis is responsible for basal renin release from the juxtaglomerular cells adhering to isolated glomeruli.

Animals↗
PubMed1976

Studies on renin release from isolated superfused glomeruli: effects of temperature, urea, ouabain and ethacrynic acid.

1. The effects of different energy substrates, of low temperature, of urea, and of ouabain and ethacrynic acid were studied on the rate of renin release from viable juxtaglomerular cells during superfusion of isolated rat glomeruli. 2. Neither lactate nor glutamate altered renin release rate from that observed using glucose as the sole energy substrate. Succinate 10 mM elevated release transiently but did not influence the release caused by reductions in osmolality through lowering sucrose concentration. 3. Peak renin release was more prolonged and returned more slowly to control following reductions in osmolality in phosphate-Ringer than in bicarbonate-Ringer. 4. At 37 degrees C, the peak of renin released induced by hypo-osmolality was smaller and delayed, and returned earlier to control than at 30 degrees C. Reduction in temperature from 30 to 4 degrees C resulted in a 32-fold increase in basal release rate. At 4 degrees C a 20 m-osmole/kg reduction in tonicity caused an additional 2-5-fold increase in release rate. 6. Increasing superfusate osmolality with urea did not affect basal renin release but 100 mM urea suppressed the releasing effect of a 15 mM reduction in NaCl concentration. 7. Ouabain (10(-4) M) caused a small (33 +/- 9%, P less than 0-025) transient increase in renin release. Ethacrynic acid (10(-3) M) provoked a progressive increase in release reaching 100 +/- 15% above control within 50 min. In the presence of both inhibitors the release provoked by hyposmolality was prolonged. 8. It is concluded that renin release in vitro is a function of actively regulated cell volume and it is proposed that a similar mechanism could underline both barorecptor and macula densa controls of renin secretion in vivo.

Animals↗