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  • 1
    Electronic Resource
    Electronic Resource
    DOWN-REGULATION OF ANGIOTENSIN II RECEPTORS IN HYPERTROPHIED HUMAN MYOCARDIUM (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Specific [125I]-angiotensin II (AngII) binding in normal and hypertrophied human myocardial membranes was saturable and of high affinity. Low concentrations of unlabelled AngII and saralasin competed with [125I]-AngII for the binding sites in these tissues. Thus, saturable [125I]-AngII binding in human myocardium exhibited pharmacological specificity that characterized high affinity receptors for AngII.2. There was little difference in the apparent dissociation constant (Kd) values for [125I]-AngII binding between normal and hypertrophied human myocardium, whereas the maximal number of binding sites (Bmax) was significantly (51%) lower in the hypertrophied group. Further, PD123177, a selective antagonist of the AT2 receptor subtype, showed three orders of magnitude higher affinity for [125I]-AngII binding sites in both normal and hypertrophied myocardium than losartan, a selective antagonist of the AT1 receptor subtype; the Hill coefficients for these drugs were close to one.3. A significant decrease in Bmax and Kd values for (—)-[125I]-iodocyanopindolol binding between normal and hypertrophied human myocardium rarely occurred.4. The present study suggests that both normal and hypertrophied human myocardium predominantly contains the AT2 receptor subtype and that these receptors are down-regulated in hypertrophied tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02771.x
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  • 2
    Electronic Resource
    Electronic Resource
    Contribution of aranidipine metabolites with slow binding kinetics to the vasodilating activity of aranidipine (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1996), S. 119-125 
    Details
    ISSN: 1432-1912
    Keywords: Key words Aranidipine ; Metabolites ; Ca2+ channel antagonist ; 1 ; 4-Dihydropyridines ; Binding study ; Slow kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aranidipine, a novel dihydropyridine derivative, gives rise to two active metabolites, M-1(α) and M-1(β), which exhibit hypotensive activity comparable to that of nifedipine. The aim of this study was to examine the recovery phase of the vasodilating effect of M-1(α) and of M-1(β), to determine their binding characteristics and to compare the results with those for aranidipine and other dihydropyridine derivatives. During intra-arterial infusion into the femoral vascular beds of anesthetized dogs, M-1(α), M-1(β), and nifedipine, produced increases in femoral blood flow at doses three times higher than the dose of aranidipine required to produce a comparable effect. The onset and recovery of the effects of the metabolites on femoral blood flow were significantly slower than the onset and recovery of the effect of nifedipine. The inhibitory activities of M-1(α) and M-1(β) towards stimulated 45Ca uptake in isolated guinea pig aorta were less than that of aranidipine. In binding studies, using porcine heart membrane preparations, [3H]M-1(α) and [3H]M-1(β) had larger Kd values than [3H]aranidipine and [3H]nitrendipine, but the maximal binding number for each of them was almost the same. The association and dissociation rate constants for [3H]M-1(α) and [3H]M-1(β) binding, as well as those for [3H]aranidipine binding, were significantly smaller than those for [3H]nitrendipine, corresponding to the recovery of the in vivo vasodilating effects of the metabolites. The dissociation rate constants of these radiolabeled ligands were highly positively correlated with the elimination rate constants of their in vivo vasodilating effects. From these results, we conclude that M-1(α) and M-1(β), although their binding affinities and Ca2+ antagonistic actions are less potent, possess slower kinetic binding properties than many other dihydropyridines and that the slow kinetic interaction of these metabolites with the dihydropyridine receptor may contribute to the long-lasting in vivo vasodilating effect of aranidipine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004909
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  • 3
    Electronic Resource
    Electronic Resource
    Rapidly Solidified Thick Deposit of Fe-B-Cr Alloy by Plasma Spraying (2007)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 561-565 (Oct. 2007), p. 721-724 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Fe-B-Cr alloy powder in diameter of 32-53 μm made by argon atomization is low-pressureplasma sprayed to produce a rapidly solidified iron base composite deposit with finely dispersedboride particles. The constituents of the as-sprayed deposit formed on a water-cooled substrate are αphase and amorphous phase that are supersaturated with chromium and boron due to high cooling rateduring solidification of the melt. Heat treatment of deposit at 873K leads to decomposition of theamorphous phase, resulting in the formation of Fe3B. The deposit heat treated above 1073K iscomposed of α phase and (Fe,Cr)2B. The as-sprayed deposit produced on a non-cooled substrateconsists of α phase and (Fe,Cr)2B. The fine precipitates of about 0.1 μm in the as-sprayed depositcoated on a non-cooled substrate are boride. As deposit temperature increases, the coarsening of theprecipitate particles results in lowered hardness of deposits
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/17/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.561-565.721.pdf
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  • 4
    Electronic Resource
    Electronic Resource
    Evaluation with Surface Analysis Equipment, of Casting Defects in Cast Iron Articles (review) (2007)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 539-543 (Mar. 2007), p. 1110-1115 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Authors have reported theses concerning the cast defect for publication in journal of Japanese FoundryEngineering Society and AFS Transactions. This is a review of these reports. There are various factors inthe casting defect that occurs in the article of casting metal, and specific of the generation factor is difficult.Moreover, it is necessary to decrease the casting defect to reduce the cost of goods manufactured andenergy of production. It is effective to the evaluation and the classification method of the casting defect toemploy Scanning Electron Microscopy with Energy Dispersion Spectrometer (SEM-EDS) and ElectronProbe Micro-Analysis (EPMA). Casting defects chose the one that the incidence was high and specific ofthe generation factor is difficult, and the pinhole defect and inclusion defects were classified according tothe generation factor, and penetration defect showed the relation of physical factor, chemical factor, andthose interactions, and examined whether specific of the factor was possible by the surface analysisequipment about other defects (Blow hole, Shrinkage, Orange peel, Cold shut, Cracks and Veining)
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/15/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.539-543.1110.pdf
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  • 5
    Electronic Resource
    Electronic Resource
    Receptor Occupancy in Myocardium, Adrenal Cortex, and Brain by TH-142177, a Novel AT1 Receptor Antagonist in Rats, in Relation to Its Plasma Concentration and Hypotensive Effect (1998)
    Springer
    Pharmaceutical research 15 (1998), S. 911-917 
    Details
    ISSN: 1573-904X
    Keywords: angiotensin II receptor antagonist ; TH-142177 ; rat tissues ; ex vivo receptor occupancy ; pharmacokinetics ; pharmacodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. To study the relationship between angiotensin II (All) receptor occupancy ex vivo in tissues plasma concentration and hypotensive effect of a novel All receptor antagonist, TH-142177 and losartan in rats. Methods. At 2, 8 and 24 hr after oral administration of TH-142177 and losartan in rats, All receptors in myocardium, adrenal cortex and cerebral cortex were determined by radioligand binding assay using [125I]Sar1,Ile8-AII. Plasma concentrations of both drugs and metabolite in rats were also measured using validated HPLC assays. Further, systolic blood pressure (SBP) in conscious renal hypertensive rats treated orally with TH-142177 and losartan were measured by using a tail cuff plethysmographic method. Results. Oral administration of TH-142177 (1.8 and 5.5 μmol/kg) and losartan (6.5 and 21.7 μmol/kg) in rats brought about dose-dependent decreases in [125I]Sar1,Ile8-AII binding sites (Bmax) in myocardium and adrenal cortex. The extent of receptor occupancy by both drugs in adrenal cortex was maximal at 2 hr later but that in myocardium at 8 hr later. Further, the receptor occupancy was more sustained in myocardium than adrenal cortex. The ex vivo binding affinity of TH-142177 for All receptors in these tissues was roughly three times higher than that of losartan. Also, cerebral cortical [125I]Sar1,Ile8-AII binding was significantly reduced by oral administration of losartan but not by TH-142177. The time course of All receptor occupancy by both drugs in adrenal cortex appeared to be in parallel with that of their plasma concentrations, while the time course in myocardium correlated with that of their hypotensive effects rather than plasma concentrations. Conclusions. TH-142177 produced a relatively selective and sustained occupancy ex vivo of All receptors in myocardium and adrenal cortex of rats with approximately three times greater potency than losartan. Its time course of myocardial receptor occupancy was in parallel with that of hypotensive effect rather than plasma concentration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1011932800729
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  • 6
    Electronic Resource
    Electronic Resource
    MET-88 a γ-butyrobetaine hydroxylase inhibitor, improves cardiac SR Ca2+ uptake activity in rats with congestive heart failure following myocardial infarction (2000)
    Springer
    Molecular and cellular biochemistry 209 (2000), S. 39-46 
    Details
    ISSN: 1573-4919
    Keywords: sarcoplasmic reticulum ; SR Ca2+-ATPase ; [Ca2+]i transients ; cell shortening ; γ-butyrobetaine hydroxylase inhibitor ; heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We previously reported that MET-88, 3-(2,2,2-trimethylhydrazinium) propionate, improved left ventricular diastolic dysfunction induced by congestive heart failure (CHF) in rats. The present study was designed to investigate the mechanism by which MET-88 improved the cardiac relaxation impaired in CHF rats. The left coronary artery of the animals was ligated, and the rats were then orally administered vehicle (control), MET-88 at 50 or 100 mg/kg or captopril at 20 mg/kg for 20 days. Myocytes were isolated from the non-infarcted region in the left ventricle, and cell shortening and [Ca2+]i transients were measured with a video-edge detector and by fluorescence analysis, respectively. In CHF control rats, the diastolic phase of cell shortening was prolonged compared with that of the sham-operated (sham) rats. This prolongation was prevented by treatment with MET-88 at 100 mg/kg or captopril at 20 mg/kg. CHF control rats also showed an increase in the decay time of [Ca2+]i transients compared with sham rats. MET-88 at 100 mg/kg and captopril at 20 mg/kg attenuated the increase in decay time of [Ca2+]i transients. Ca2+ uptake activity of the sarcoplasmic reticulum (SR) isolated from the non-infarcted region in the left ventricle was measured, and Lineweaver-Burk plot analysis of the activity was performed. CHF control rats revealed a decrease in the Vmax for SR Ca2+ uptake activity without alteration in Kd. MET-88 at 100 mg/kg significantly prevented the decrease in Vmax, but had no effect on Kd. Also, treatment with MET-88 at 100 mg/kg improved myocardial high-energy phosphate levels impaired in CHF rats. These results suggest that one of the mechanisms by which MET-88 improved cardiac relaxation in CHF rats is based on the amelioration of [Ca2+]i transients through increase of SR Ca2+ uptake activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007093926315
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