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Biomedical subjects

K Baumann

Publications and source records attributed to K Baumann.

At least 91 records · Page 5Linked to original sources
PubMed1977

Effect of parathyroid hormone and cyclic adenosine 3',5'-monophosphate on isotonic fluid reabsorption: polarity of proximal tubular cells.

Isotomic fluid reabsorption (JV) of rat renal proximal tubules was examined by the shrinking droplet method in combination with simulatneous perfusion of blood capillaries. Sensitivity of JV measurement was improved by using each punctured tubule for control measurements: 1) Parathyroid hormoen (PTH) on the contraluminal cell side reduced JV in a dose-response behavior. The maximal inhibition was achieved at a PTH concentration of 10(-5) M, the half maximal inhibition at a concentration of 3 X 10(-9) M. PTH on the luminal cell side had a small inhibitory effect. 2) Cyclic AMP inhibited JV preferentially when applied to the luminal cell side. On the luminal cell side, both cyclic AMP and dibutyryl cyclic AMP inhibited JV in a similar dose-dependent behavior. Concentrations of both nucleotides as low as 10(-10) M had a definite inhibitory effect. Tested at a high concentration, N6-butyryl cyclic AMP was almost as effective as cyclic AMP. Deoxy cyclic AMP, 5' AMP, cyclic guanosine monophosphate (cyclic GMP), dibutyryl cyclic GMP had no effect. ATP inhibited JV to a very small extent. 3) The reduction of JV after administration of PTH and dibutyryl cyclic AMP was not additive. The similar inhibitory effect of PTH at the contraluminal cell face and of cyclic AMP at the luminal cell face suggests the following sequence of events in the mediation of the action of PTH: 1) activation of adenylate cyclase by PTH in the contraluminal cell membrane, and 2) action of the generated cyclic AMP on the luminal cell membrane. The interaction of cyclic AMP and the luminal cell membrane is initiated at the luminal cell surface.

Absorption↗
PubMed1976

[The effect of sudden changes in the stimulation rate of the heart on peak systolic pressure (author's transl)].

The changes in systolic pressure were studied in 48 patients during artificially (by electrical stimulation) induced sudden increases and consecutive decreases in heart rate. Various patterns could be separated respective to phase A (sudden switch from low (80-120 impulses/min) to higher heart rate (140-180 impulses/min)) and to phase B (sudden switch-back from high to lower (control) beating rate): AI) The systolic peak-pressure of the first contraction after the shortened stimulation interval is very low and often stays ineffective (below the aortic opening pressure). The second contraction develops already a higher pressure than the first one, during the consecutive beats the systolic pressure increases gradually until a new steady state is reached, which is usually lower than the systolic pressure during the foregoing lower beating rate. Sometimes however it can be equal or even higher. Accordingly after an elevation of heart rate arterial mean pressure can drop, stay constant or increase. AII) The systolic peak-pressure of the first contraction after the shortened stimulation interval stays relatively high and drops continuously with the succeeding contractions until a new steady state is reached according to the higher heart rate, it is however always lower than the one at a lower stimulation rate. Therefore arterial mean pressure is always decreased. AIII) Finally we observed changes in arterial systolic pressure in some patients that could not be grouped according to one or to the other pattern described above.- BI) The systolic peak of the first contraction after the switch-back from the high to the lower (control) rate is much higher than that of the last at the higher rate. The peak pressures of the consecutive contractions are then dropping continuously to the new steady-state, that can be higher, equal or lower than that at the higher stimulation rate. BII) ....

Adolescent↗
PubMed1976

On the action of nifedipine under conditions of variable stimulation patterns and [Ca2+]0 in guinea-pig atrium.

The effect of nifedipine is studied in perfused isolated guinea-pig left atrium at a temperature of 37 degrees C and a stimulation rate between 60 and 240/min. Rhythmical stimulation at 240/min was interrupted by interposed stimulus intervals (test intervals) in a range of 0.1-4 s. The pressure amplitudes developed during subsequent test contractions rise up to a maximum with increasing test intervals. This time course is described as restitution in contractile response. Results. Restitution is somewhat faster in earlier than in later stages of perfusion. A rise in [Ca2+]0 accelerates restitution without changing maximal pressure development. Lowering [Ca2+]0 depresses pressure amplitudes over the whole range of test intervals. Nifedipine slows down restitution but has (in concentrations up to 10(-6) M) no effect on the maximum achieved after long test intervals following stimulation at 240/min. The negative inotropic effect of nifedipine on rhythmical pressure development rises with increasing stimulation frequency in the range from 60-240/min. An elevation in [Ca2+]0 does not reestablish control pressure-frequency relationship. Conclusions. In respect to the restitution process and also to the pressure-frequency relationship the effect of nifedipine can neither be simulated by a reduction in [Ca2+]0 nor abolished by an elevation in [Ca2+]0.

Animals↗
PubMed1976

Effect of cyclic nucleotides on the isotonic fluid reabsorption in the proximal convoluted tubule of rat kidney.

In order to reveal the sidedness of the cyclic AMP action on renal tubules the effect of cyclic nucleotides on isotonic fluid reabsorption was examined in proximal convoluted rat kidney tubules by using advanced micropuncture techniques. Cyclic AMP inhibited isotonic fluid reabsorption preferentially when applied on the luminal cell side. This finding coincides with a predominant distribution of a membrane bound cyclic AMP dependent protein kinase in a luminal cell membrane fraction. On the luminal cell side cyclic AMP and dibutyryl cyclic AMP inhibited isotonic fluid reabsorption in a similar dose dependent behaviour. Concentrations of both nucleotides as low as 10-10M had a definite inhibitory effect. Tested at a high concentration N6-butyryl cyclic AMP was almost as effective as cyclic AMP. Deoxy cyclic AMP, 5' AMP, cyclic GMP and dibutyryl cyclic GMP had no effect. ATP inhibited isotonic fluid reabsorption to a very small extent. The data indicate that the observed inhibition of isotonic fluid reabsorption is specific for cyclic AMP and that the interaction of cyclic AMP and the luminal cell membrane is initiated at the luminal cell surface.

Animals↗
PubMed1976

Plasma renin activity (PRA) and plasma aldosterone (PA) in hypertensive kidney allograft recipients.

Basal and stimulated plasma renin activity (PRA) and plasma aldosterone (PA) were measured in 13 hypertensive and 16 normotensive patients with kidney allografts one to nine years after transplantation. In both groups no significant differences were observed between mean basal and stimulated PRA and PA values. Therefore, we conclude that abnormal renin secretion might not be the main factor causing hypertension in renal allograft recipients. Other mechanisms seem to be involved in the pathogenesis of hypertension in these patients.

Aldosterone↗
PubMed1975

Renal proximal tubular buffer-(glycodiazine) transport. Inhomogeneity of local transport rate, dependence on sodium, effect of inhibitors and chronic adaptation.

Using the stop flow microperfusion technique with simultaneous capillary perfusion the secretory rate of H+ ions in the proximal tubule was evaluated by measuring the level flow reabsorption as well as the static head concentration difference of 3H labeled glycodiazine. At ambient glycodiazine concentration of 21 mmol/l the level flow reabsorption is in the same range as that of bicarbonate. In the early proximal loops the reabsorption is 20% greater than in the late proximal loops. The carbonic anhydrase inhibitors acetazolamide and 3,4-methylene-dioxyphenyl-sulfonamide (both 10(-4) M) as well as furosemide (10 (-3) M) inhibit the glycodiazine reabsorption 43%, 27% and 22% respectively. Thiocyanate (2-10(-2) M), however, exerted only an insignificant inhibition (12%). When Na+ in the ambient perfusion solutions was replaced by Li+ or choline+ the glycodiazine transport was strongly reduced. Ouabain (5-10(-2) M) inhibited too, but amiloride (10(-3) M) had no effect on glycodiazine transport. The glycodiazine transport was 28% reduced in metabolic alkalosis and to a smaller although significant extent (17%) in metabolic acidosis; it was unchanged in chronic hypercapnia. In chronic K+ depletion the glycodiazine reabsorption was accelerated by 12% only in the early proximal loops. Chronic parathyroidectomy as well as acute substitution with parathyroid hormone had no effect on the glycodiazine absorption. The main conclusions are: Proximal H+ transport proceeds with suitable buffers. Although independent of HCO3- and carbonic anhydrase, it could be partially inhibited by CA inhibitors. H+ transport is supposed to proceed as countertransport with Na+ ions. In chronic alkalosis the H+ transport is reduced.

Acid-Base Equilibrium↗
PubMed1975

[Stress sensitivity and adaptation].

On the basis of theoretical, clinical and experimental analyses the influence of different stress categories, especially of psycho-emotional and socio-emotional stress, upon cerebro-visceral regulation processes is investigated. Central-nervous information processing in various brain areas (neocortex, limbic system, hypothalamus, formatio reticularis mesencephali etc.) and learning processes are equally affected by stress factors as are haemodynamic and biochemical parameters. Changes of the carbohydrate and lipid metabolism, of plasma renin activity, catechol amine release and the counter-regulatory insulin enhancement are especially pronounced in "stress-sensitive risk persons", e.g. in the hypertensive as a maladaptive dysregulation-as opposed to the adaptive regulation capacity of healthy individuals. The investigated functional patterns of different systems of the organism allow the distinction of hyper- and hyporeactive forms of maladaptation. The pathogenetic efficiency of stress is determined not only by the quantity, quality, duration of exposure and basic processes of the central nervous system, but also by man's personality structure and his sensitivity to stress (genetic predisposition and/or acquired maladaptation). More insight into the neuro-biological processes underlying the motivational and psycho-emotional performance of the brain and its connection withe humoral-hormonal and cardiovascular systems is necessary to treat and to control cerebrovisceral dysregulations such as arterial essential hypertension. It will be a task of psychotherapy to help improve man's adaptive capacity and to desensibilize stress-sensitive risk persons.

Adaptation, Physiological↗
PubMed1975

Renal phosphate transport: inhomogeneity of local proximal transport rates and sodium dependence.

The standing droplet method has been used in combination with the peritibular perfusion of blood capillaries to determine the build up of transtubular concentration differences of phosphate (Piota) in the renal proximal convoluted tubule of parathyroidectomized rats. Electron probe analysis was used to estimate Piota. At zero time both the intraluminal and the contraluminal Piota concentration was 2 mM. The time dependent decrease of the intraluminal Piota concentration was approximately 4 times faster in the early than in the late proximal convoluted tubule. After 45 sec an intraluminal steady state concentration of 0.20 mM Piota was achieved in the early part. In the late part the intraluminal Piota concentration approached a steady statevalue of 0.54 mM at 123 sec. When sodium free solutions were used the intaluminal Piota concentration increased to 2.22 mM in the earlier and to 2.76 mM in the late part. The data indicate that in the proximal convoluted tubule 1. the rate of phosphate reabsorption is greater in the early part than in the later part, and 2. phospate reabsorption might occur as co-transport with Na+ ions.

Animals↗
PubMed1974

Analysis of the pinocytic process in rat kidney. I. Isolation of pinocytic vesicles from rat kidney cortex.

Pinocytosis was induced in rat kidney by exposure to horseradish peroxidase (HRP). Pinocytic vesicle preparations were enriched after homogenization of kidney cortex by differential centrifugation and free-flow electrophoresis with HRP as an exogenous marker. Vesicles were identified by enzymatic analysis and by electron microscopy, including specific staining procedures. Typical brush-border enzymes such as alkaline phosphatase, aminopeptidase, 5'-nucleotidase, lysosomal acid phosphatase, and mitochondrial succinic dehydrogenase were reduced in the vesicular fraction, compared to the kidney cortex homogenate. Glucose-6-phosphatase and Na(+)-K(+)-ATPase were only slightly increased in the fraction. These results indicate that preparations of pinocytic vesicles from rat kidney cortex can be enriched. They have biochemical characteristics that differ from those of the cell organelles and membranes previously purified from renal tissue.

Acid Phosphatase↗