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Biomedical subjects

W Ziegler

Publications and source records attributed to W Ziegler.

At least 109 records · Page 6Linked to original sources
PubMed1983

Correction of altered noradrenaline reactivity in essential hypertension by indapamide.

Fourteen patients with untreated mild to moderate essential hypertension had, on average, an abnormally high cardiovascular reactivity to exogenous noradrenaline and angiotensin II, while plasma noradrenaline, renin activity, exchangeable body sodium, and blood volume were normal. Treatment with a low dose of indapamide (2.5 mg/day) for 6 weeks decreased blood pressure by 10% in these hypertensive patients but not in 13 normal control subjects. Plasma or blood volume and exchangeable sodium were not changed significantly; nevertheless, the latter, and body weight, tended to be decreased slightly. Though a mild reduction in extracellular sodium in both normal and hypertensive subjects appears possible, it may not fully explain per se the blood pressure-lowering effect of indapamide in essential hypertension. Indapamide induced a mild decrease in angiotensin II pressor responsiveness in normal or hypertensive subjects, but a possible depressor influence from this change was probably antagonized by a concomitant pronounced increase in plasma renin activity. In hypertensive patients, the abnormally high noradrenaline reactivity was corrected by indapamide without an accompanying increase in endogenous plasma noradrenaline levels. Indapamide-induced changes in blood pressure correlated with those in noradrenaline pressor dose. It was concluded, therefore, that indapamide may decrease blood pressure in essential hypertension at least in part by lowering an abnormally high cardiovascular noradrenaline reactivity without causing an equivalent increase in adrenergic nervous activity.

Adolescent↗
PubMed1982

Dibutyrylic cyclic AMP and theophylline inhibit proliferation of accessory cells in primary cultures of adrenomedullary cells.

Studies on isolated adrenal chromaffin cells in primary cultures may be seriously hampered by the presence of non-chromaffin, mainly fibroblast-like cells, which always occur in dissociates of adrenal medullary tissue and often outnumber the chromaffin cells by the end of the first week of culture, when no measures are taken to control their proliferation. The present study offers a new means to inhibit effectively the proliferation of these accessory cells by treating the cultures with dibutyrylic cyclic AMP (dbcAMP, 0.1 or 0.01 mM) and equimolar amounts of the phosphodiesterase inhibitor theophylline. With this treatment cultures of young rat adrenal chromaffin cells remain virtually free of accessory cells for two weeks of culture. Cultures of bovine adrenomedullary cells retain their initial amounts of non-chromaffin cells, which largely depends upon whether the primary cell suspensions have undergone differential plating prior to seeding. Suppression of accessory cell proliferation with dbcAMP and theophylline is partly due to maintaining differentiation of cortical cells, which otherwise dedifferentiate into rapidly dividing fibroblast-like elements. However, a more direct action of dbcAMP on accessory cells in terms of growth control is also conceivable. DbcAMP and theophylline in the doses applied do not impair the viability, ultrastructure and catecholamine-storing capacity of cultured chromaffin cells.

Adrenal Medulla↗
PubMed1981

Differential effects of cyclic AMP and cholera toxin on nerve growth factor-induced neurite outgrowth from adrenal medullary chromaffin and pheochromocytoma cells.

The extension of neurites from adrenal medullary chromaffin cells and PC 12 cells upon addition of nerve growth factor (NGF) has been proposed to be mediated by cyclic AMP. It is shown here that substances increasing intracellular cyclic AMP levels have a reverse effect on NGF-induced neurite outgrowth of these two related cell types. Hence, cyclic AMP is not generally involved in neurite outgrowth from NGF responsive cells. Furthermore, it is concluded that PC 12 cells cannot always be considered as a suitable model for adrenal medullary chromaffin cells.

Animals↗
PubMed1981

Correction of altered noradrenaline reactivity in essential hypertension by indapamide.

Fourteen patients with untreated mild to moderate essential hypertension had on average an abnormally high cardiovascular reactivity to exogenous noradrenaline and angiotension II, while plasma noradrenaline, renin activity, exchangeable body sodium, and blood volume were normal. Treatment with a low dose of indapamide (2.5 mg/day) for six weeks decreased blood pressure by 10% in these hypertensive patients but not in 13 normal control subjects. Plasma or blood volume and exchangeable sodium were not changed significantly; nevertheless, the latter, and body weight, tended to be decreased slightly. Though a mild reduction in extracellular sodium in both normal and hypertensive subjects appears possible, it may not per se fully explain indapamide's blood pressure-lowering effect in essential hypertension. Indapamide induced a mild decrease in angiotensin II pressor responsiveness in normal or hypertensive subjects, but a possible depressor influence from this change was probably antagonised by a concomitant pronounced increase in plasma renin activity. In hypertensive patients, the abnormally high noradrenaline reactivity was corrected by indapamide without an accompanying increase in endogenous plasma noradrenaline levels. Indapamide-induced changes in blood pressure correlated with those in noradrenaline pressor dose. It was concluded, therefore, that indapamide may decrease blood pressure in essential hypertension at least in part by lowering an abnormally high cardiovascular noradrenaline reactivity without causing an equivalent increase in adrenergic nervous activity.

Adolescent↗
PubMed1980

Effects of cell culture conditions, nerve growth factor, dexamethasone, and cyclic AMP on adrenal chromaffin cells in vitro.

Adrenal chromaffin cells from young rats, newborn guinea pigs, and adult cattle were grown under various cell culture conditions. Nerve growth factor (NGF) elicited the outgrowth of neurite-like processes from rat, but not from bovine and guinea pig, chromaffin cells. Dexamethasone, dibutyryl cAMP, theophylline, and cholera toxin, which are known to augment intracellular cAMP, specifically inhibited neurite outgrowth. We propose that glucocorticoid hormones and mechanisms which act through an increase of cAMP are prerequisites for the acquisition and maintenance of differentiation and expression of an endocrine instead of a neuronal phenotype of adrenal chromaffin cells.

Adrenal Medulla↗
PubMed1978

Studies on bovine brain membrane-bound neuraminidase (sialidase).

1) Lipophilic ganglioside GD1a (IV3NeuAc, II3NeuAc-GgOse4-Cer) is taken up by the cell membranes and hydrolyzed faster by membrane-bound neuraminidase than are water soluble substrates of the enzyme. 2) The enzymic breakdown of ganglioside GD1a is enhanced by general anesthetics whereas the degradation of the hydrophilic substrate sialyllactitol is reduced by these same agents. 3) General anesthetics lower the microviscosity of membranes as indicated by studies of fluorescence depolarisation with the indicator 1,6-diphenylhexatrien. Decreased microviscosity can result in a higher lateral diffusion of ganglioside GD1a, increasing its interaction with membrane-bound neuraminidase. 4) In vitro studies indicate that the activity of membrane-bound neuraminidase on gangliosides of brain membranes is regulated by the viscosity of these membranes and their monosialoganglioside content.

Animals↗
PubMed1977

Studies of the ligand binding to cholera toxin, II. The hydrophilic moiety of sialoglycolipids.

The binding between cholera toxin or its B-protein subunit and various ganglioside-related oligosaccharides was studied by equilibrium displacement dialysis. At low concentrations of ligand, the binding of monosialo-gangliotetraitol exceeded that of the parent ganglioside II3NeuAcGgOse4-Cer, the possible cell surface receptor for the toxin. The terminal galactose residue and an intact carboxyl group of the sialic acid moiety of monosialo-gangliotetraose were found to be necessary for strong binding to the toxin.

Chemical Phenomena↗
PubMed1976

Effects of angiotensin II and noradrenaline on intrarenal haemodynamics in the rat.

The haemodynamic effects of angiotensin II and noradrenaline were studied in the rat kidney. These pressors were given by intravenous infusion in stepwise increasing doses. Intrarenal haemodynamics were analyzed by the 133xenon washout technique, 85krypton autoradiography and silastic casting of the renal vascular tree. Angiotensin II induced significant changes in intrarenal haemodynamics before any changes in systemic blood pressure were detected. The decrease in mean renal blood flow (2.91 ml.min-1.g-1 in controls, 1.76 ml.min-1.g-1 in rats given 50 mug of angiotensin II.kg-1.h-1) reflects a reduction in component I blood flow rate (from 3.9 to 2.9 ml.min-1.g-1) as well as a decrease in the fraction of total renal blood flow supplied to component I of the washout curve (from 84% to 62%). With noradrenaline an increase in total renal resistance occurred simultaneously with the elevation of mean arterial blood pressure. The resulting reduction in mean renal blood flow (from 2.76 ml.min-1.g-1 in controls to 1.55 ml.min-1.g-1 in rats given 1000 mug of noradrenaline kg-1.h-1) reflects a decrease in component I blood flow rate with lower infusion rates and a drop in component I flow fraction (from 82% to 52%) whith higher doses. In contrast to canine kidneys, no evidence for a patchy cortical vasoconstriction was found in the rat. Using autoradiography it was possible to attribute component I to the renal cortex and subcortical area of the kidney.

Angiotensin II↗
PubMed1976

[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)].

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.

Adrenergic beta-Antagonists↗
PubMed1976

Studies of the ligand binding to cholera toxin, I. The lipophilic moiety of sialoglycolipids.

The fixation of cholera toxin by ganglioside GGtet1 is dependent on the nature of the carbohydrate as well as the lipid moiety of the glycolipid. The role of the lipid in binding to the toxin investigated with synthetic ganglioside analogues (gangliosidoides). The interaction between glycolipid and toxin was followed by precipitate formation, by inhibition of toxicity and in polyacrylamide gel electrophoresis. For specific precipitation, an aliphatic hydrocarbon chain at least 14 C-atoms in length is required. Some of the gangliosidoides form high molecular weight complexes with cholera toxin at lower molar ratios of ligand to protein than the natural compound. None of the synthetic gangliosidoides equalled natural ganglioside in its ability to inhibit the effects of the toxin in vivo, but some did show considerable inhibitory activity ih monosialo-gangliotetraose or corresponding sialo-glycolipids prevents the easy degradation of the B-protein of cholera toxin into protein subunits by sodium dodecylsulfate.

Bacterial Toxins↗
PubMed1975

[Quantitative determination of tissue tolerance to corrosion products in organ culture].

The tissue tolerance for metal was investigated using an organ culture of embryonic rat femora. We found reproducible results using a standardized experimental method. A good correlation between the applied concentrations and resulting growth inhibition occurred and dose-response curves were established. The experimental model is applicable for testing tissue tolerance for the soluble products.

Animals↗