Willi Diederen
Boehringer Ingelheim
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Willi Diederen.
Journal of Cardiovascular Pharmacology | 1989
Jacques C.A. Van Meel; Annerose Mauz; Wolfgang Wienen; Willi Diederen
Summary: We investigated the effect of the new cardiotonic drug pimobendan on survival of hereditary cardiomyopathic hamsters. Untreated cardiomyopathic hamsters served as controls. A 50% mortality was observed after 280 days for the control group and after 318 days for the pimobendan-treated animals. After 340 days, survival was 0% for the untreated cardiomyopathic hamsters and 27% in the pimobendan-treated group. We conclude that pimobendan slows the progression of heart failure in cardiomyopathic hamsters.
Archive | 1998
Michel Pairet; J. Van Ryn; Annerose Mauz; Hans Schierok; Willi Diederen; D. Türck; Guenther Dr Engelhardt
Since the discovery of a second isoenzyme of cyclooxygenase (COX), COX-21,2, it has been hypothesized that the anti-inflammatory effects of non-steroid anti-inflammatory drugs (NSAIDs) are achieved through a mechanism different from that underlying the often seen side-effects of these compounds, including disruption of cytoprotection of the stomach, toxic effects on the kidney and inhibition of platelet aggregation3. COX-1 is the constitutive isozyme found under physiological conditions in most tissues, a so-called ‘housekeeping’ enzyme, while COX-2 expression is induced, particularly during inflammatory processes4. It has been proposed that COX-2 inhibition is the relevant target for the anti-inflammatory effects of NSAIDs, whereas inhibition of COX-1 is responsible for their gastric and renal side-effects3,4. Most available NSAIDs block both COX-1 and COX-2 to a similar degree; however, newer compounds with selective inhibition of COX-2 should retain the anti-inflammatory activity of NSAIDs but have minimal gastro-intestinal side-effects.
European Journal of Pharmacology | 1993
Jacques C.A. Van Meel; Willi Diederen; Robert M. Haigh; Wolfgang Wienen; Michel Pairet; Marco Turconi; Henri Doods
The 5-HT4 receptor antagonist action of DAU 6285 was investigated in vivo in anesthetized pigs. DAU 6285 (0.3-3 mg/kg i.v.) dose dependently antagonized 5-hydroxytryptamine (5-HT)-induced tachycardiac responses. In contrast, the 5-HT3 receptor antagonist, ondansetron (0.3-3 mg/kg i.v.) did not influence the tachycardia induced by 5-HT. These results indicate that DAU 6285 is a potent antagonist of 5-HT4 receptor-mediated responses in vivo.
Drug Development Research | 1997
Michel Pairet; Willi Diederen; Brian Guth; Kozo Kanai; Annerose Mauz; Michael P. Pieper; Joanne van Ryn; Hans Schierok; Alexander Walland; Ray Winquist
The objectives of general pharmacology (GP) studies from the point of view of pharmacologists working in the pharmaceutical industry are presented and compared with the requirements of regulatory authorities, using the Japanese Guidelines as an example. Based on these requirements, as well as the internal requirements of other departments involved in drug research and development, a strategy for a basic program of GP studies is suggested. This strategy involves the consideration of practical aspects, animal species, route of administration, and recommended doses.
Naunyn-schmiedebergs Archives of Pharmacology | 1995
Jacques C.A. Van Meel; Norbert Redemann; Willi Diederen; Robert Haigh
Recent data show that UD-CG 212 in nanomolar concentrations increases myofibrillar Ca++ responsiveness of chemically skinned cardiac preparations in the presence of elevated inorganic phosphate. We studied the effects of UD-CG 212 on cell shortening of intact myocytes and in addition measured the intracellular calcium transients with the aid of INDO-1 fluorescence in the presence of 5 mM inorganic phosphate.The validity of our experimental system was first tested with the calcium channel opener Bay k 8644. Bay k 8644 at 10−8 M did not significantly influence myocyte shortening ( + 13.9 ± 4.6%, n = 9) but at 10−7 M and 10−6 M significantly increased contraction by 40.1 +- 13.6%and52.5 ± 17.0% respectively. Bay k 8644 at 10−8 M increased the INDO-1 fluorescence ratio by 17.3 ± 4.7% (P < 0.01; n = 9), and at 10−7 M by 21.5 + 4.3% (P < 0.01; n = 9), whereas 10−6 M Bay k 8644 had no significant effect on peak INDO-1 ratio. However, 10−7and 10−6 M Bay k 8644 accelerated and broadened the calcium transients.Cell shortening of guinea pig ventricular myocytes electrically stimulated at 1 Hz was significantly increased by UD-CG 212 (10−9-10−7 M) and isoprena line(3 × 10−8 M). An increase of 37.0 ± 14.0% (P < 0.05; n = 9) was observed at 10−9 M UD-CG 212, 90.5±18.2% (P<0.05; n=9) at 10−8 M UD-CG 212, 164.0 ± 34.9% (P < 0.05; n = 9) at 10−7 M UD-CG 212, and 258.2 ± 67.4% (P < 0.05; n = 9) at 3 × 10-8 M isoprenaline. Peak INDO-1 fluorescence ratios were not significantly (P > 0.05) influenced after addition of 10−9 M and 10−8 M UD-CG 212, but significantly increased by 19.4 ± 4.9%(P < 0.05; n = 9) at 10−7 MUD-CG 212 and by 81.1 ± 11.1% (P < 0.05; n = 9) at 3 x 10−8 M isoprenaline.In conclusion, UD-CG 212 (10−9 - 10−7 M) Concentration-dependently increased myocyte shortening in the presence of 5 mM inorganic phosphate. Low concentrations of 10−9 and 10−8 M UD-CG 212 increased myocyte contractility without altering the peak INDO-1 fluorescence ratio whereas 10−7 M UD-CG 212 and 3 × 10−8 M isoprenaline increased cell shortening as well as peak INDO-1 fluorescence ratio. These data suggest that low concentrations of UD-CG 212 increase myocyte contractility by enhancing myofibrillar calcium responsiveness whereas higher concentrations elevate intracellular calcium probably via increased intracellular CAMP brought about by phosphodiesterase inhibition.
Archive | 1975
Eberhard Kutter; Volkhard Austel; Willi Diederen
Archive | 1973
Eberhard Dipl Chem Dr Kutter; Volkhard Austel; Willi Diederen
Archive | 1986
Berthold Narr; Norbert Dipl Chem Dr Hauel; Klaus Dipl Chem Dr Noll; Joachim Heider; Manfred Psiorz; Andreas Bomhard; Jacobus Van Dr Meel; Willi Diederen
Archive | 1975
Volkhard Austel; Eberhard Kutter; Joachim Heider; Wolfgang Eberlein; Rudolf Kadatz; Willi Diederen
Archive | 1987
Berthold Narr; Norbert Hauel; Klaus Noll; Joachim Heider; Manfred Psiorz; Andreas Bomhard; Jacques C.A. Van Meel; Willi Diederen