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Dive into the research topics where Hans-Peter Voss is active.

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Featured researches published by Hans-Peter Voss.


Journal of Pharmacological and Toxicological Methods | 1993

Use of telemetry to record electrocardiogram and heart rate in freely moving mice

K. Kramer; Saskia A.B.E. van Acker; Hans-Peter Voss; Joop A. Grimbergen; Wim J. F. van der Vijgh; Aalt Bast

This paper describes for the first time the possibility to record the electrocardiogram (ECG) and heart rate (HR) with a commercially available telemetry and data acquisition system in freely moving mice. The system comprises a telemetry transmitter implanted in the peritoneal cavity and a receiver, placed underneath the home cage, an A/D converter (MacLab) and a Macintosh LC II 4/80 computer with software (MacLab, Chart/Scope). The raw analog ECG data are digitized within the MacLab and can be converted to HR data additionally. The effects of surgery for implanting the transmitter, handling and anesthesia by either Nembutal or a mixture of Hypnorm, Dormicum, and water, on the changes in ECG and HR were examined. The telemetry system for recording the ECG and HR provides an accurate and reliable method for monitoring the direct effects of handling on HR. By using this telemetry system, we maintain that measurements in freely moving animals are more efficient, reliable, and less labor-intensive than the measurement techniques described in the literature thus far.


British Journal of Pharmacology | 1994

Characterization of the binding of the first selective radiolabeled histamine H3‐receptor antagonist, [125I]‐iodophenpropit, to rat brain

Frank P. Jansen; T.S. Wu; Hans-Peter Voss; H.W.M. Steinbusch; R.C. Vollinga; B. Rademaker; Aalt Bast; H. Timmerman

1 The binding of the first selective radiolabeled histamine H3‐receptor antagonist [125I]‐iodophenpropit to rat cerebral cortex membranes was characterized. 2 [125I]‐iodophenpropit, radiolabeled to a high specific activity of 1900 Ci mmol‐1, saturably bound to a single class of sites with a KD of 0.57 ± 0.16 nm (n = 4) and Bmax of 268 ± 119 fmol mg‐1 protein. 3 Specific binding at a concentration below 1 nm represented 50 to 60% of total binding. 4 Binding of [125I]‐iodophenpropit to rat cerebral cortex membranes was readily displaced by histamine H3‐agonists and antagonists. In contrast, the inhibitory potencies of selective histamine H1‐ and H2‐receptor ligands were very low. 5 [125]‐iodophenpropit was biphasically displaced by the histamine H3‐receptor antagonists, burimamide and dimaprit, which may indicate the existence of histamine H3‐receptor subtypes. Other histamine H3‐receptor antagonists showed a monophasic displacement. 6 Competition binding curves of H3‐agonists were biphasic and showed a rightward shift upon the addition of the nonhydrolysable GTP analogue, guanosine 5′‐o‐(3‐thio) triphosphate (GTPγS; 100 μm) which implicates the interaction of histamine H3‐receptors with G‐proteins. The affinities of the H3‐receptor antagonists iodophenpropit, thioperamide and burimamide were not altered by GTPγS. 7 Histamine competition binding curves were shifted to the right by different nucleotides (100 μm) with a rank order of potency GTPγS > Gpp(NH)p, GTP. 8 In vitro autoradiographic studies revealed a heterogeneous distribution of [125I]‐iodophenpropit binding sites in rat brain, with highest densities observed in specific cerebral cortical areas and layers, the caudate‐putamen complex, the olfactory tubercles, the hippocampal formation, the amygdala complex, the hypothalamic area and the mammillary bodies. 9 It is concluded that the histamine H3‐receptor antagonist, [125I]‐iodophenpropit, meets the criteria for a suitable radioligand for histamine H3‐receptor binding studies in rat brain.


Laboratory Animals | 2000

Telemetric monitoring of blood pressure in freely moving mice: a preliminary study

K. Kramer; Hans-Peter Voss; J.A. Grimbergen; Perry A. Mills; Daniel A. Huetteman; Lynn M. Zwiers; Brian P. Brockway

This paper describes for the first time the possibility for recording the systolic pressure (SPI, diastolic pressure (DP), and the mean arterial pressure (MAP) as well as the heart rate (HR) and locomotor activity (LA) in freely moving mice, using a commercially available telemetry and data acquisition system. The system comprises a new, small radio-telemetry transmitter implanted in the peritoneal cavity, a receiver board placed underneath the home cage, a multiplexer and a computer-based data acquisition system. The signals from the receiver were consolidated by the multiplexer and were stored and analysed by the computer. The telemetered pressure signals (absolute pressure) were corrected automatically for changes in atmospheric pressure measured by an ambient pressure monitor. The effects of implantation on animal behaviour, and, after the animals had recovered, the effects of handling on the SP, DP, MAP and HR were examined. The radio-telemetry system for recording the SP, DP, MAP and HR provides an accurate and reliable method for monitoring the direct effects of handling on SP, DP, MAP and HR. In addition, by using this new blood pressure (BP) transmitter, we maintain that BP measurements in freely moving mice are more efficient, reliable, and less labour-intensive than the measurement techniques described in the literature thus far.


European Journal of Pharmacology | 1992

Atypical molecular pharmacology of a new long-acting β2-adrenoceptor agonist, TA 2005

Hans-Peter Voss; David Donnell; Aalt Bast

The molecular pharmacology of a new putative long-acting bronchodilator TA 2005 (8-hydroxy-5-[(1R)-1-hydroxy-2-[N-[(1R)-2-(p-methoxy-phenyl)- 1-methylethyl]amino]ethyl]carbostyril hydrochloride) has been compared with that of the reference compounds isoprenaline and salbutamol in both methacholine (3 x 10(-6) M) precontracted guinea pig tracheal smooth muscle relaxation and in bovine trapezium muscle binding experiments. TA 2005 appeared very potent compared with isoprenaline and salbutamol (pD2 values of 9.29 vs. 7.65 and 7.10 respectively). For isoprenaline and salbutamol a shallow displacement curve was observed and addition of the non-hydrolysable GTP analogue guanylyl-imidodiphosphate (GppNHp) gave a rightward shift (pKd,high and pKd,low values of 7.3 and 6.1 vs. 7.0 and 5.4 respectively). For TA 2005 a steep displacement curve was found with only one binding state even without GppNHp (pKd,high value of 8.2). The long duration of action of TA 2005 might be explained by tight binding of this compound to the beta 2-adrenoceptor. The extent of tight binding for TA 2005 was extremely large. The molecular basis of the tight agonist binding phenomenon for TA 2005 seems to be of different origin than for isoprenaline. It is hypothesized that a different mechanism of activation of the beta 2-adrenoceptor may be involved for TA 2005.


Biochemical and Biophysical Research Communications | 1987

The effect of ischemia and recirculation, hypoxia and recovery on anti-oxidant factors and β-adrenoceptor density: Is the damage in the erythrocytes a reflection of brain damage caused by complete cerebral ischemia and by hypoxia?

K. Kramer; Hans-Peter Voss; J.A. Grimbergen; H. Timmerman; Aalt Bast

This investigation was focussed on the gravity of tissue injury caused by complete ischemia (for five min) and hypoxia (for three weeks) in the cerebral cortex (homogenate) and the erythrocyte lysate or the erythrocyte membrane of the rat in order to investigate if the changes that occur in brain tissue are reflected in the erythrocyte. To this end, glutathione (GSH), superoxide dismutase (SOD) and catalase were measured, also alterations in beta-adrenoceptor density under these two conditions were examined. It was found that in ischemia partial parallelism in changes that occur in the central nervous system (cerebral cortex) and the erythrocyte exists. The SOD activity became higher and the beta-adrenoceptor density (measured as specific (-)-[125I] iodocyanopindolol binding) was decreased in both tissues. However after the hypoxic condition we established a decrease in the number of beta-adrenoceptors in the cerebral cortex but an increase in beta-adrenoceptor density in the erythrocyte.


Mediators of Inflammation | 1996

Chemokines: structure, receptors and functions. A new target for inflammation and asthma therapy?

F.A.A. van Acker; Hans-Peter Voss; H. Timmerman

Five to 10% of the human population have a disorder of the respiratory tract called ‘asthma’. It has been known as a potentially dangerous disease for over 2000 years, as it was already described by Hippocrates and recognized as a disease entity by Egyptian and Hebrew physicians. At the beginning of this decade, there has been a fundamental change in asthma management. The emphasis has shifted from symptom relief with bronchodilator therapies (e.g. β2-agonists) to a much earlier introduction of anti-inflammatory treatment (e.g. corticosteroids). Asthma is now recognized to be a chronic inflammatory disease of the airways, involving various inflammatory cells and their mediators. Although asthma has been the subject of many investigations, the exact role of the different inflammatory cells has not been elucidated completely. Many suggestions have been made and several cells have been implicated in the pathogenesis of asthma, such as the eosinophils, the mast cells, the basophils and the lymphocytes. To date, however, the relative importance of these cells is not completely understood. The cell type predominantly found in the asthmatic lung is the eosinophil and the recruitment of these eosinophils can be seen as a characteristic of asthma. In recent years much attention is given to the role of the newly identified chemokines in asthma pathology. Chemokines are structurally and functionally related 8–10 kDa peptides that are the products of distinct genes clustered on human chromosomes 4 and 17 and can be found at sites of inflammation. They form a superfamily of proinflammatory mediators that promote the recruitment of various kinds of leukocytes and lymphocytes. The chemokine superfamily can be divided into three subgroups based on overall sequence homology. Although the chemokines have highly conserved amino acid sequences, each of the chemokines binds to and induces the chemotaxis of particular classes of white blood cells. Certain chemokines stimulate the recruitment of multiple cell types including monocytes, lymphocytes, basophils, and eosinophils, which are important cells in asthma. Intervention in this process, by the development of chemokine antagonists, might be the key to new therapy. In this review we present an overview of recent developments in the field of chemokines and their role in inflammations as reported in literature.


European Journal of Pharmacology | 1995

Anti-oxidant actions of oxymethazoline and xylomethazoline

Westerveld Gj; Scheeren Ra; Ingrid Dekker; Griffioen Dh; Hans-Peter Voss; Aalt Bast

Anti-oxidant actions of oxymethazoline and xylomethazoline were investigated by measuring inhibition of microsomal lipid peroxidation and hydroxyl radical scavenging activity. Oxymethazoline was shown to be a potent inhibitor of lipid peroxidation (IC50 = 4.9 microM at t = 15 min, IC50 = 8.1 microM at t = 30 min), in contrast to xylomethazoline. Both compounds were excellent hydroxyl radical scavengers. Their rate constants (ks = 1.1 x 10(12) M-1 s-1 for oxymethazoline and ks = 4.7 x 10(10) M-1 s-1 for xylomethazoline) exceeded the rate constant of a known powerful scavenger cimetidine (ks = 1.8 x 10(10) M-1 s-1). The difference in inhibiting lipid peroxidation might be explained by the fact that only oxymethazoline has a hydroxy group which can donate a hydrogen atom and terminate the chain reaction of lipid peroxidation. The mechanism of hydroxyl radical scavenging activity is still unclear. Moreover oxymethazoline seems to have a different mode of action in scavenging hydroxyl radicals than xylomethazoline and cimetidine which results in an extremely high rate constant. Because oxidants play a role in tissue damage in inflammation, it was hypothesized that especially oxymethazoline and to a lesser extent xylomethazoline may have an additional beneficial effect, due to their anti-oxidant properties, in the topical treatment of nasal inflammation.


Toxicology | 1997

Changes in neuroreceptor function of tracheal smooth muscle following acute ozone exposure of guinea pigs

H.J.M. van Hoof; Hans-Peter Voss; K. Kramer; A.J.F. Boere; J. A. M. A. Dormans; L. van Bree; A. Bast

We studied the effect of in vivo ozone inhalation (3 ppm, 2 h) on neuroreceptor function in guinea pig tracheal smooth muscle in vitro and the role of the epithelial layer in this process. Changes in smooth muscle tension after stimulation of the muscarinic- and beta-adrenergic receptor were recorded isometrically and stained tracheal tissue sections were histologically evaluated for changes in the epithelial and smooth muscle layer. Ozone exposure resulted in an increase in maximal contraction following stimulation of the muscarinic receptor, whereas pD2 values remained unchanged. After stimulation of the beta-adrenergic receptor no increase in maximal relaxation but only an increase in pD2 value was observed after correction for differences in precontraction level in control- and ozone-exposed situations. Mechanical removal of the epithelial layer resulted in a slight increase of the maximal contraction level after stimulation with methacholine in the control situation, whereas exposure to ozone resulted in a strong decrease of the maximal contraction level under these conditions. Histological stainings showed a slight and focal influx of neutrophilic granulocytes in the epithelial layer, submucosal layer and airway lumen after exposure to ozone. These data support the idea that ozone is able to increase the maximal degree of airway narrowing upon muscarinergic stimulation, i.e. a hyperreactivity response. The results also suggest that functionally altered epithelium plays an important role in the process of ozone-induced hyperreactivity, possibly linked with an early inflammatory response.


Journal of Agricultural and Food Chemistry | 2007

Oxidative degradation of lipids during mashing

Mariken J.T.J. Arts; Christoph Grun; Ruud L. De Jong; Hans-Peter Voss; Aalt Bast; Martin J. Mueller; Guido R.M.M. Haenen

Although hardly any polyunsaturated fatty acids (PUFAs) are present in the endproduct, the ingredients used for the production of beer contain a high concentration of PUFAs, such as linolic and linolenic acid. These compounds are readily oxidized, resulting in the formation of lipid-derived products that reduce the taste and quality of beer enormously. During mashing relatively high amounts of PUFAs are exposed to atmospheric oxygen at a relatively high temperature. This makes mashing a critical step in the brewing process with regard to the formation of lipid-derived off-taste products. F1 phytoprostane (PPF1) changes in antioxidant capacity and monohydroxy fatty acids (OH-FAs) were used as markers for the detection of oxidative damage to fatty acids during mashing. The pattern of OH-FA formation indicates that enzymatic oxidation of PUFAs is more important than nonenzymatic oxidation during the mashing process. Nevertheless, substantial nonenzymatic radical formation is evident from the increase of specific OH-FAs and PPF1s. It was found that a low oxygen tension reduces oxidative damage and gives a high antioxidant capacity of the mashing mixture. This indicates that mashing should be done under low oxygen pressure.


General Pharmacology-the Vascular System | 1992

Glutathione mobilization during cerebral ischemia and reperfusion in the rat

K. Kramer; Hans-Peter Voss; J.A. Grimbergen; Corine Smink; H. Timmerman; Aalt Bast

1. Cerebral ischemia applied for 15 min and followed by a 30 min reperfusion did not change the glutathione (GSH) levels and beta-adrenoceptor density (Bmax) in brain cortex. 2. A significant increase in erythrocyte-lysate GSH concentration (vs control) and a significant decrease of Bmax values in erythrocyte membranes (vs control) was found at the same time. 3. Pretreatment with the alpha-adrenoceptor antagonist phentolamine (5 mg/kg i.p.) prevented the erythrocyte GSH increase but not the decrease of Bmax value. Pretreatment with the beta-antagonist propranolol (2 mg/kg i.p.) did not influence the increase in erythrocyte GSH but circumvented the decrease of Bmax.

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Aalt Bast

Maastricht University

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K. Kramer

VU University Amsterdam

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A. Bast

VU University Amsterdam

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H. Timmerman

VU University Amsterdam

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L. van Bree

VU University Amsterdam

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