Nitroprusside in vitro inhibits platelet aggregation and intracellular calcium translocation. Effect of haemoglobin
The biologically final active compound of nitrovasodilators is now supposed to be nitric oxide (NO), a labile substance identical to EDRF. The effects of nitroprusside on platelet functions were studied in vitro. Platelet aggregation induced by several stimuli (ADP, collagen, arachidonic acid and PA...
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| Veröffentlicht in: | Thrombosis research 1991-01, Vol.61 (2), p.113-122 |
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| container_title | Thrombosis research |
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| creator | Pasqui, A.L. Capecchi, P.L. Ceccatelli, L. Mazza, S. Gistri, A. Laghi Pasini, F. Di Perri, T. |
| description | The biologically final active compound of nitrovasodilators is now supposed to be nitric oxide (NO), a labile substance identical to EDRF. The effects of nitroprusside on platelet functions were studied in vitro. Platelet aggregation induced by several stimuli (ADP, collagen, arachidonic acid and PAF) was inhibited by increasing concentrations of the drug (1–50 μM); interestingly, the potency of nitroprusside is higher when PAF is employed as stimulating agent in comparison with the other agonists (ED
50=2 μM for ADP, 2.5 μM for A.A., 4.5 μM for collagen and 0.3 μM for PAF-induced aggregations). The concomitant addition of haemoglobin is able to reverse the inhibitory effect of nitroprusside, according to the view that haemoglobin possesses a high affinity for NO, thus antagonizing the effect of this compound. Nitroprusside was also able to inhibit intracellular calcium translocation, as studied with the Quin 2 technique, induced by PAF and arachidonic acid. Fron these observations the hypothesis may be suggested that nitroprusside inhibits platelet functions by mimicking the endogenous NO, and that the intracellular calcium metabolism is involved in the inhibitory activity of the drug. |
| doi_str_mv | 10.1016/0049-3848(91)90238-R |
| format | Article |
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50=2 μM for ADP, 2.5 μM for A.A., 4.5 μM for collagen and 0.3 μM for PAF-induced aggregations). The concomitant addition of haemoglobin is able to reverse the inhibitory effect of nitroprusside, according to the view that haemoglobin possesses a high affinity for NO, thus antagonizing the effect of this compound. Nitroprusside was also able to inhibit intracellular calcium translocation, as studied with the Quin 2 technique, induced by PAF and arachidonic acid. Fron these observations the hypothesis may be suggested that nitroprusside inhibits platelet functions by mimicking the endogenous NO, and that the intracellular calcium metabolism is involved in the inhibitory activity of the drug.</description><identifier>ISSN: 0049-3848</identifier><identifier>EISSN: 1879-2472</identifier><identifier>DOI: 10.1016/0049-3848(91)90238-R</identifier><identifier>PMID: 1902328</identifier><identifier>CODEN: THBRAA</identifier><language>eng</language><publisher>New York, NY: Elsevier Ltd</publisher><subject>Adenosine Diphosphate - pharmacology ; Arachidonic Acid ; Arachidonic Acids - pharmacology ; Biological and medical sciences ; Blood Platelets - drug effects ; Blood Platelets - physiology ; Blood. Blood coagulation. Reticuloendothelial system ; calcium ; Calcium - blood ; Collagen - pharmacology ; Hemoglobins - pharmacology ; Humans ; In Vitro Techniques ; Intracellular Fluid - drug effects ; Intracellular Fluid - metabolism ; Medical sciences ; nitroprusside ; Nitroprusside - pharmacology ; Pharmacology. Drug treatments ; Platelet Activating Factor - pharmacology ; Platelet Aggregation - drug effects ; Platelet Aggregation Inhibitors - pharmacology ; platelets</subject><ispartof>Thrombosis research, 1991-01, Vol.61 (2), p.113-122</ispartof><rights>1991</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c326t-95204052dbcdc61f9bc6f9c88c9c3e6a9b41a4e6d093b9bf7a8010cf6d0ed9533</citedby><cites>FETCH-LOGICAL-c326t-95204052dbcdc61f9bc6f9c88c9c3e6a9b41a4e6d093b9bf7a8010cf6d0ed9533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0049-3848(91)90238-R$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4980844$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1902328$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pasqui, A.L.</creatorcontrib><creatorcontrib>Capecchi, P.L.</creatorcontrib><creatorcontrib>Ceccatelli, L.</creatorcontrib><creatorcontrib>Mazza, S.</creatorcontrib><creatorcontrib>Gistri, A.</creatorcontrib><creatorcontrib>Laghi Pasini, F.</creatorcontrib><creatorcontrib>Di Perri, T.</creatorcontrib><title>Nitroprusside in vitro inhibits platelet aggregation and intracellular calcium translocation. Effect of haemoglobin</title><title>Thrombosis research</title><addtitle>Thromb Res</addtitle><description>The biologically final active compound of nitrovasodilators is now supposed to be nitric oxide (NO), a labile substance identical to EDRF. The effects of nitroprusside on platelet functions were studied in vitro. Platelet aggregation induced by several stimuli (ADP, collagen, arachidonic acid and PAF) was inhibited by increasing concentrations of the drug (1–50 μM); interestingly, the potency of nitroprusside is higher when PAF is employed as stimulating agent in comparison with the other agonists (ED
50=2 μM for ADP, 2.5 μM for A.A., 4.5 μM for collagen and 0.3 μM for PAF-induced aggregations). The concomitant addition of haemoglobin is able to reverse the inhibitory effect of nitroprusside, according to the view that haemoglobin possesses a high affinity for NO, thus antagonizing the effect of this compound. Nitroprusside was also able to inhibit intracellular calcium translocation, as studied with the Quin 2 technique, induced by PAF and arachidonic acid. Fron these observations the hypothesis may be suggested that nitroprusside inhibits platelet functions by mimicking the endogenous NO, and that the intracellular calcium metabolism is involved in the inhibitory activity of the drug.</description><subject>Adenosine Diphosphate - pharmacology</subject><subject>Arachidonic Acid</subject><subject>Arachidonic Acids - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Platelets - drug effects</subject><subject>Blood Platelets - physiology</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>calcium</subject><subject>Calcium - blood</subject><subject>Collagen - pharmacology</subject><subject>Hemoglobins - pharmacology</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Intracellular Fluid - drug effects</subject><subject>Intracellular Fluid - metabolism</subject><subject>Medical sciences</subject><subject>nitroprusside</subject><subject>Nitroprusside - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Platelet Activating Factor - pharmacology</subject><subject>Platelet Aggregation - drug effects</subject><subject>Platelet Aggregation Inhibitors - pharmacology</subject><subject>platelets</subject><issn>0049-3848</issn><issn>1879-2472</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFqFTEUhoMo9Vp9A4UspOhiajKTO5NsBCnVCkWh6DpkTk5uI5nJNckU-vbN9F7qzlXCf77zc_gIecvZOWe8_8SYUE0nhfyg-EfF2k42N8_IhstBNa0Y2udk84S8JK9y_sMYH7janpATvvKt3JD8w5cU92nJ2VukfqZ3a1A_t370JdN9MAUDFmp2u4Q7U3ycqZltJUoygCEswSQKJoBfJlqzOYcIj9w5vXQOodDo6K3BKe5CHP38mrxwJmR8c3xPye-vl78urprrn9--X3y5bqBr-9KobcsE27Z2BAs9d2qE3imQEhR02Bs1Cm4E9papblSjG4xknIGrAVq17bpTcnbo3af4d8Fc9OTzerGZMS5Zy1o-9GIFxQGEFHNO6PQ--cmke82ZXl3rVaReRWrF9aNrfVPX3h37l3FC-2_pILfO3x_nJlc_rqoBn58woSSTQlTs8wHD6uLOY9IZPM6A1qcqT9vo_3_HAywXnew</recordid><startdate>19910115</startdate><enddate>19910115</enddate><creator>Pasqui, A.L.</creator><creator>Capecchi, P.L.</creator><creator>Ceccatelli, L.</creator><creator>Mazza, S.</creator><creator>Gistri, A.</creator><creator>Laghi Pasini, F.</creator><creator>Di Perri, T.</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19910115</creationdate><title>Nitroprusside in vitro inhibits platelet aggregation and intracellular calcium translocation. Effect of haemoglobin</title><author>Pasqui, A.L. ; Capecchi, P.L. ; Ceccatelli, L. ; Mazza, S. ; Gistri, A. ; Laghi Pasini, F. ; Di Perri, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-95204052dbcdc61f9bc6f9c88c9c3e6a9b41a4e6d093b9bf7a8010cf6d0ed9533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Adenosine Diphosphate - pharmacology</topic><topic>Arachidonic Acid</topic><topic>Arachidonic Acids - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood Platelets - drug effects</topic><topic>Blood Platelets - physiology</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>calcium</topic><topic>Calcium - blood</topic><topic>Collagen - pharmacology</topic><topic>Hemoglobins - pharmacology</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Intracellular Fluid - drug effects</topic><topic>Intracellular Fluid - metabolism</topic><topic>Medical sciences</topic><topic>nitroprusside</topic><topic>Nitroprusside - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Platelet Activating Factor - pharmacology</topic><topic>Platelet Aggregation - drug effects</topic><topic>Platelet Aggregation Inhibitors - pharmacology</topic><topic>platelets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pasqui, A.L.</creatorcontrib><creatorcontrib>Capecchi, P.L.</creatorcontrib><creatorcontrib>Ceccatelli, L.</creatorcontrib><creatorcontrib>Mazza, S.</creatorcontrib><creatorcontrib>Gistri, A.</creatorcontrib><creatorcontrib>Laghi Pasini, F.</creatorcontrib><creatorcontrib>Di Perri, T.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Thrombosis research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pasqui, A.L.</au><au>Capecchi, P.L.</au><au>Ceccatelli, L.</au><au>Mazza, S.</au><au>Gistri, A.</au><au>Laghi Pasini, F.</au><au>Di Perri, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitroprusside in vitro inhibits platelet aggregation and intracellular calcium translocation. Effect of haemoglobin</atitle><jtitle>Thrombosis research</jtitle><addtitle>Thromb Res</addtitle><date>1991-01-15</date><risdate>1991</risdate><volume>61</volume><issue>2</issue><spage>113</spage><epage>122</epage><pages>113-122</pages><issn>0049-3848</issn><eissn>1879-2472</eissn><coden>THBRAA</coden><abstract>The biologically final active compound of nitrovasodilators is now supposed to be nitric oxide (NO), a labile substance identical to EDRF. The effects of nitroprusside on platelet functions were studied in vitro. Platelet aggregation induced by several stimuli (ADP, collagen, arachidonic acid and PAF) was inhibited by increasing concentrations of the drug (1–50 μM); interestingly, the potency of nitroprusside is higher when PAF is employed as stimulating agent in comparison with the other agonists (ED
50=2 μM for ADP, 2.5 μM for A.A., 4.5 μM for collagen and 0.3 μM for PAF-induced aggregations). The concomitant addition of haemoglobin is able to reverse the inhibitory effect of nitroprusside, according to the view that haemoglobin possesses a high affinity for NO, thus antagonizing the effect of this compound. Nitroprusside was also able to inhibit intracellular calcium translocation, as studied with the Quin 2 technique, induced by PAF and arachidonic acid. Fron these observations the hypothesis may be suggested that nitroprusside inhibits platelet functions by mimicking the endogenous NO, and that the intracellular calcium metabolism is involved in the inhibitory activity of the drug.</abstract><cop>New York, NY</cop><pub>Elsevier Ltd</pub><pmid>1902328</pmid><doi>10.1016/0049-3848(91)90238-R</doi><tpages>10</tpages></addata></record> |
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| ispartof | Thrombosis research, 1991-01, Vol.61 (2), p.113-122 |
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| subjects | Adenosine Diphosphate - pharmacology Arachidonic Acid Arachidonic Acids - pharmacology Biological and medical sciences Blood Platelets - drug effects Blood Platelets - physiology Blood. Blood coagulation. Reticuloendothelial system calcium Calcium - blood Collagen - pharmacology Hemoglobins - pharmacology Humans In Vitro Techniques Intracellular Fluid - drug effects Intracellular Fluid - metabolism Medical sciences nitroprusside Nitroprusside - pharmacology Pharmacology. Drug treatments Platelet Activating Factor - pharmacology Platelet Aggregation - drug effects Platelet Aggregation Inhibitors - pharmacology platelets |
| title | Nitroprusside in vitro inhibits platelet aggregation and intracellular calcium translocation. Effect of haemoglobin |
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