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L Neyses

Publications and source records attributed to L Neyses.

64 records · Page 4Linked to original sources
PubMed1984

Angiotensin II binding to human mononuclear cells: receptor or free fluid endocytosis?

It has recently been claimed that there are angiotensin II (ANG II) receptors on human mononuclear cells and on platelets and this has been used for investigating the regulation of the renin-angiotensin system in hypertension. We here show the following. Binding kinetics of 125I-labelled ANG II and [3H]ANG II to mononuclear cells were slow (maximum at 90 min) and the same as for [3H]-inulin. As with [3H]inulin there was no binding at 4 degrees C. Release from the cells was slow and incomplete (about 30% after 15 min, 60% after 60 min). Binding was not saturable over a range from 10(-12) to 10(-6) mol of ANG II/l, about 8% of offered peptide being bound at all concentrations. Various inhibitors of free fluid endocytosis exhibited the same inhibition pattern of ANG II binding to mononuclear cells. Therefore uptake of ANG II into mononuclear cells displayed all the features of free fluid endocytosis. ANG II was degraded by carboxypeptidase A. When this degradation was prevented by D-phenylalanine, no binding occurred. In platelet preparations contaminated by 0.3-5% of mononuclear cells, 125I-labelled ANG II was degraded as well. Free fluid endocytosis of the degradation product strongly depended on the percentage of contaminating mononuclear cells. We conclude that there are no ANG II receptors on human mononuclear cells and that their presence on human platelets is doubtful.

Angiotensin II↗
PubMed1984

Human red blood cells--an ideal model system for the action of calcium agonists and antagonists.

To characterize the pharmacological properties of the slow calcium channel of human red blood cells, we studied the action of various calcium antagonists and two agonists on the 45Ca2+-influx. The Ca2+-ejecting ATPase was inhibited by vanadate. All dihydropyridine derivatives tested showed their inhibiting or stimulating effect on the channel at concentrations attainable in vivo (nitrendipine:Ki = 2.5; Bayer K 6244:Ki 5 microM; nicardipine:Ki = 15 microM, Ks = 0.5 microM; Ciba 28 392:Ki = 20, Ks = 0.3 microM; Ki = inhibition constant, Ks = stimulation constant). Of special interest was the biphasic behaviour (stimulation and inhibition) of the calcium antagonist nicardipine and the agonist Ciba 28 392. The maximum inhibition by the phenylalkylamine derivative verapamil was obtained at much higher concentrations (250 microM; Ki = 100). These data suggest that the calcium channel of human red blood cells has pharmacological properties very similar to the channel in heart and smooth muscle cells with respect to dihydropyridine action. Therefore, human red blood cells are an ideal model to study the action of calcium agonists and antagonists.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1984

Cholesterol and its oxidized derivatives modulate the calcium channel in human red blood cells.

The human red blood cell was used as a model system in order to study the effect of cholesterol and its medically important oxidized derivatives (OSC = oxidized sterol compounds) on the calcium entry channel. The calcium-ejecting adenosine triphosphatase (ATPase) was inhibited by vanadate and the influx of 45Ca2-into the cells measured. The cells were loaded with OSC at concentrations between 0.075 and 1.5 micrograms OSC/10(7) cells. Two classes of OSC could be distinguished: one stimulating Ca2+ influx dose-dependently by almost 100% at maximum concentrations, the other inhibiting it dose-dependently by up to 80%. The calcium channel blocker nitrendipine inhibited influx by 70% at 15 microM. More than 90% of the total stimulation or inhibition was accounted for by an influence on the nitrendipine-inhibitable part of influx, i.e. the calcium channel. Cholesterol (incorporated using liposomes) had a stimulatory (+288%), cholesterol depletion an inhibitory effect on calcium influx (-18%). These results demonstrate that cholesterol and its oxidized derivatives modulate the calcium channel in a highly stereospecific manner and provide new insights into the mechanism of action and the atherogenic effect of these compounds.

Calcium↗
PubMed1983

[A slide program on hypertension and obesity: a simple method of patient information].

It is well established that information on their disease is one of the prerequisites for improvement of patients' compliance with therapy. The authors have therefore developed a simple slide program presenting information on hypertension and obesity. Consisting of 52 slides, it was shown in the central waiting room of the medical outpatient department at the University Hospital, Zurich. In order to assess learning, 841 patients were asked to fill in a questionnaire. 485 had seen the program and 356 served as controls with the program switched off. Four main results emerged: 1. The percentage of subjects scoring greater than or equal to 4 correct answers (of a maximum of 5) rose significantly from 22.6% to 64.2%. 2. The number of incorrect answers (maximum 3) remained unchanged. 3. Learning decreased with age. 4. Occupation did not have a significant effect on learning. The results clearly show that the program represents an effective method of teaching patients and may therefore serve to improve compliance with therapy.

Adult↗
PubMed1983

Altered calcium and sodium metabolism in red blood cells of hypertensive man: assessment by ion-selective electrodes.

Free intracellular calcium [Ca2+]i, sodium [Na+]i and potassium [K+]i were assessed in freeze-thawed human red blood cells (RBC) by ion-selective electrodes. After metabolic depletion by 30 mM 2-desoxy-glucose, [Ca2+]i increased faster and to significantly higher values in RBC from 16 patients with mild to moderate essential hypertension (mean diastolic blood pressure 111 +/- 10 mmHg) than in the RBC of 24 normotensives. The rate of [Ca2+]i increase was 7.0 +/- 3.6 versus 3.7 +/- 4.0 mumol/h/l cells (P less than 0.01) for the first 24 h and 8.1 +/- 4.8 versus 6.4 +/- 3.5 mumol/h/l cells for the following 24 h. [Na+]i before and after 24 h incubation was significantly higher in hypertensives, whereas basal [Ca2+]i and [K+]i before and after incubation were the same in both groups. After Ca loading by ionophore A 23187, the maximum rate of [Ca2+]i extrusion was not significantly lower in intact RBC from hypertensives than in those from normotensives (59.5 +/- 7.8 versus 87.9 +/- 18.1 mumol/min/l cells). These results indicate disturbances in RBC Ca metabolism similar to those observed earlier for Na and K. If generalized, the defect could lead to raised [Ca2+]i in smooth muscle and sympathetic nerve tissue, thus causing increased vascular tone and probably catecholamine release with subsequent arterial hypertension.

Adenosine Triphosphate↗
PubMed1982

Isolation and characterization of the C3b-binding entity of C3b-receptor from human erythrocytes.

Applying 2 M KBr, membranes of Ehu were solubilized. By C3-affinity chromatography an activity could be isolated that inhibited the immune adherence reaction and C3b-dependent rosette formation. Since this material did not agglutinate EAC14oxy23b we termed it monovalent C3b receptor (mC3bR). PAGE and SDS-PAGE and staining with Coomassie brilliant blue and PAS reagent revealed a single glycoprotein band with a mol. wt. of 55,000-60,000 daltons and an electrophoretic mobility comparable to ovalbumin. This mC3bR proved to be antigenetically related to gp 205 [17]. The potential of mC3bR to react with C3b-carrying particles was not destroyed by heat and trypsin treatment but by neuraminidase or periodic acid treatment suggesting that mC3bR reacted by its carbohydrate moiety with C3b. As by mC3bR, immune adherence could be inhibited by D-glucose and D-galactose but not by their optical antipodes, L-glucose and L-galactose.

Animals↗
PubMedDate not supplied

Estrogen effects in the heart.

Gender specific differences in cardiovascular disease are largely mediated by sex hormones. The use of estrogens significantly reduces the overall incidence of heart disease in postmenopausal women. Beneficial effects of estrogens on plasma lipoprotein levels are clearly established. However, these do not explain the magnitude of risk reduction seen in clinical studies. Thus additional and currently unknown functions of estrogens must be operative. Elucidation of the exact estrogen action in the heart will have important implications in the treatment of cardiovascular disease. It will probably enhance the therapeutic repertoire in treating heart disease, the most common cause of death in industrialized countries. We will review the current understanding of the function of estrogens in the heart and discuss potential strategies on how to apply these data to clinical practice.

Animals↗