Agents and actions. Supplements最新文献

{"title":"The cardioprotective actions of iloprost in myocardial ischemia of the rabbit can be separated from its vasodilatory effects mediated by KATP(+)-channel opening.","authors":"A Vesper,&nbsp;K Schrör","doi":"10.1007/978-3-0348-7346-8_14","DOIUrl":"https://doi.org/10.1007/978-3-0348-7346-8_14","url":null,"abstract":"<p><p>The modification of cardioprotective actions of iloprost by K(+)-channel blockade was studied in ischemic rabbit hearts. Glibenclamide, a blocker of ATP-dependent K(+)-channels, prevented coronary vasodilation mediated by the prostacyclin mimetic iloprost. In contrast, the cardioprotective effects of iloprost which were determined from prevention of ischemia induced rise in left ventricular enddiastolic pressure and loss of cytosolic troponin T in hearts made globally ischemic for two hours were not affected by glibenclamide. It is concluded that the cardioprotective action of iloprost can be separated from ist coronary vasodilator effect mediated by opening KATP(+)-channels.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"45 ","pages":"93-9"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18542813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory lipocortin-derived peptides.","authors":"M Perretti,&nbsp;R J Flower","doi":"10.1007/978-3-0348-7276-8_13","DOIUrl":"https://doi.org/10.1007/978-3-0348-7276-8_13","url":null,"abstract":"<p><p>Peptide Ac2-26, drawn from the sequence of human lipocortin 1, inhibited the release of elastase activity from cytoplasmic granules of human neutrophils, and neutrophil adhesion to monolayers of endothelial cells, in a concentration-dependent manner (approximate IC50 of 100 micrograms/ml, 33 microM). The effect of peptide Ac2-26 was not restricted to a specific neutrophil activator, being effective against formyl-Met-Leu-Phe (FMLP), leukotriene B4 (LTB4) and platelet-activating factor (PAF). Peptide Ac2-26 did not alter FMLP binding to its receptor. These in vitro observations complement in vivo data obtained with this peptide and may enable a better understanding of its pharmacology and, perhaps, that of of lipocortin 1 too.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"46 ","pages":"131-8"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18615889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The use of anti-PECAM reagents in the control of inflammation.","authors":"W A Muller","doi":"10.1007/978-3-0348-7276-8_15","DOIUrl":"https://doi.org/10.1007/978-3-0348-7276-8_15","url":null,"abstract":"<p><p>Platelet/endothelial cell adhesion molecule 1 (PECAM-1/CD31) is expressed on the surfaces of neutrophils and monocytes and concentrated at the junctional surfaces of vascular endothelial cells. Monoclonal antibodies against PECAM-1 and soluble recombinant PECAM-1 selectively block the passage of these leukocytes across the endothelial monolayer without interfering with earlier adhesion events in the emigration pathway. This block is seen both in vitro and in several in vivo models of acute inflammation. Since PECAM-1 appears to be crucial for a distinct step in the emigration of leukocytes into a focus of inflammation, PECAM-1 appears to be a new and potentially important target for anti-inflammatory therapy.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"46 ","pages":"147-57"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18615891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New animal models of inflammatory disease workshop.","authors":"D S Grass,&nbsp;D E Griswold","doi":"10.1007/978-3-0348-7343-7_16","DOIUrl":"https://doi.org/10.1007/978-3-0348-7343-7_16","url":null,"abstract":"","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"47 ","pages":"165-7"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18786922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kinin-mediated activation of endothelial no formation: possible role during myocardial ischemia.","authors":"M Hecker,&nbsp;I Fleming,&nbsp;R Busse","doi":"10.1007/978-3-0348-7346-8_17","DOIUrl":"https://doi.org/10.1007/978-3-0348-7346-8_17","url":null,"abstract":"<p><p>Endothelial cells produce a variety of factors involved in the control of vascular tone, platelet activation and cell growth, one of the most important being nitric oxide (NO). Although continuously produced in response to fluid shear stress, the release of NO from these cells can be enhanced further by humoral stimuli, such as bradykinin. This is the result of a chain of complex intracellular events involving changes in Ca2+, pH and protein phosphorylation. Endothelial cells are also capable of synthesizing bradykinin from an endogenous source, the release of which is markedly enhanced under hypoxic conditions. The finding that ACE inhibitors promote the local accumulation of the peptide and increase its efficacy at the receptor level may partly explain the potent anti-ischemic and cardioprotective effects of these drugs.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"45 ","pages":"119-27"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18718602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The exercise-induced increase in plasma levels of endothelin-1 is enhanced in patients with atherosclerotic coronary artery disease. Modulation by pentaerithrityltetranitrat (PETN).","authors":"H G Predel,&nbsp;H Knigge,&nbsp;U Prinz,&nbsp;D Stalleicken,&nbsp;H J Kramer,&nbsp;R E Rost","doi":"10.1007/978-3-0348-7346-8_32","DOIUrl":"https://doi.org/10.1007/978-3-0348-7346-8_32","url":null,"abstract":"<p><strong>Background and objective: </strong>Previous studies have suggested that endothelin (ET)-1 with its marked vasoconstrictive potency may play a role in the induction of coronary artery spasms. Furthermore, it was demonstrated using in-vitro vessel preparations that the secretion of ET-1 by the vascular endothelium is enhanced in the presence of atherosclerotic alterations. The objective of the present study was to investigate a) the effects of ergometric exercise on ET-1 plasma concentrations in 10 patients with coronary artery disease (CAD) as compared to an age and sex matched control group and b) the modulatory role of the orally administered organic nitrate, pentaerithrityltetranitrat (PETN), in patients with CAD.</p><p><strong>Patients and methods: </strong>10 male patients with CAD confirmed by coronarography and 10 male healthy controls underwent a bicycle ergometry according to the WHO-standards upt to 125 watts. Venous blood samples for determination of ANP and ET-1 plasma concentrations were drawn in supine position directly before and 5 min after ergometric exercise. Subsequently, patients were randomized and treated for 3 days in a crossover design either with placebo or PETN (150 mg b.i.d.).</p><p><strong>Results: </strong>Basal plasma levels of ET-1 were 6.1 +/- 0.7 pg/ml (patients) and 5.5 +/- 0.6 pg/ml (controls), resp. (n.s.). After ergometric exercise ET-1 plasma concentrations rose significantly (7.3 +/- 0.9 pg/ml; p < 0.05) in the placebo-treated patient group, whereas they remained constant (5.5 +/- 0.7 pg/ml) in the PETN-treated patient group. Blood pressure and heart rate were not modified by the PETN-treatment. ET-1 plasma levels remained unaffected by ergometric exercise in controls.</p><p><strong>Discussion: </strong>In contrast to healthy controls ergometric exercise induced an increase in ET-1 plasma concentrations in patients with CAD that may be potentially harmful by promoting coronary vasospasms. The almost complete blunting of the ET-1-increase in the presence of PETN-therapy may result from local-hemodynamic effects of the organic nitrate; it may be hypothesized that the nitrate-induced rise in local NO-concentrations counteracts ET-secretion. The findings of the present study are in accordance with the beneficial clinical effects of organic nitrates in patients with CAD.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"45 ","pages":"219-25"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18719112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet-vessel wall interactions, focal adhesions, and the mechanism of action of endothelial factors.","authors":"U Walter,&nbsp;J Geiger,&nbsp;C Haffner,&nbsp;T Markert,&nbsp;C Nehls,&nbsp;R E Silber,&nbsp;P Schanzenbächer","doi":"10.1007/978-3-0348-7346-8_35","DOIUrl":"https://doi.org/10.1007/978-3-0348-7346-8_35","url":null,"abstract":"<p><p>Endothelial cells produce a variety of vasoactive substances including prostacyclin (PGI2) and endothelium-derived relaxing factor (EDRF/NO) which are potent inhibitors of platelet adhesion/aggregation and vascular smooth muscle cell contraction/proliferation. PGI2 and EDRF elevate cAMP or cGMP, respectively, in vascular cells and other targets. The intracellular effects of cAMP and cGMP in vascular smooth muscle cells and platelets are primarily mediated by the family of cAMP- and cGMP-dependent protein kinases and their substrates. Important effector systems include enzymes, channels and regulatory proteins responsible for the regulation of intracellular Ca++. Other evidence suggests that VASP, a focal adhesion protein phosphorylated in platelets and smooth muscle cells in response to PGI2 and EDRF, is important for the regulation of integrins and cell-matrix interactions.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"45 ","pages":"255-68"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18719115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of intracellular Ca2+ concentration and hypoxia on basal endothelin-1 secretion by cultured porcine aortic endothelial cells.","authors":"F Brunner,&nbsp;H Stessel,&nbsp;W F Graier","doi":"10.1007/978-3-0348-7346-8_36","DOIUrl":"https://doi.org/10.1007/978-3-0348-7346-8_36","url":null,"abstract":"<p><p>When the intracellular free Ca2+ concentration ([Ca2+]i) of porcine aortic endothelial cells incubated in normoxic or hypoxic atmosphere was varied more than tenfold, basal endothelin-1 (ET-1) secretion was maximal at control conditions ([Ca2+]i = 190 nM) and reduced at lower and higher [Ca2+]i. High [Ca2+]i reduced ET-1 synthesis only in part via activation of the NO/cGMP system. Our results provide evidence that basal ET-1 secretion is regulated by [Ca2+]i, and that Ca2+ plays a similar role in hypoxic and normoxic signal transduction.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"45 ","pages":"269-73"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18719116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isolation and functional characterization of DNA-derived aptamers that act as thrombin inhibitors in human platelets and coagulation assays.","authors":"F Bracht,&nbsp;K Schrör","doi":"10.1007/978-3-0348-7346-8_43","DOIUrl":"https://doi.org/10.1007/978-3-0348-7346-8_43","url":null,"abstract":"<p><p>Aptamer sequences were isolated from defibrotide, a single-stranded, commercial DNA preparation and studied for thrombin inhibitory activity. Three different aptamers were identified, sequenced and their biological activity was determined in platelet aggregation and coagulation assays. All aptamers were potent inhibitors of thrombin-induced platelet aggregation and thromboxane formation and prolonged the thrombin time in human plasma. There was no effect of any of these compounds when a thromboxane mimetic (U 46.1619), collagen or thrombin activating peptide (TRAP-6) were used as agonists, excluding a nonspecific binding of the compounds to the thrombin receptor. The data suggest that thrombin-inhibitory aptamers are present in the mammalian genome and may constitute an endogenous antithrombin system.</p>","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"45 ","pages":"315-22"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18721094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytokine networks in rheumatoid arthritis: implications for therapy.","authors":"G S Firestein","doi":"10.1007/978-3-0348-7343-7_3","DOIUrl":"https://doi.org/10.1007/978-3-0348-7343-7_3","url":null,"abstract":"","PeriodicalId":7491,"journal":{"name":"Agents and actions. Supplements","volume":"47 ","pages":"37-51"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18785421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}