Novel peptide for attenuation of hypoxia-induced pulmonary hypertension via modulation of nitric oxide release and phosphodiesterase -5 activity
► Peptide therapy attenuates hypoxia-induced pulmonary artery hypertension and vascular remodeling. ► The effect was found to be mediated by increased NO-release and inhibition of cGMP-specific PDE-5. ► Dual action of the peptide that enhance NO release and diminished PDE-5 activity resulted in sust...
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| Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2012-05, Vol.35 (1), p.78-85 |
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| creator | Hu, Hanbo Zharikov, Sergey Patel, Jawaharlal M. |
| description | ► Peptide therapy attenuates hypoxia-induced pulmonary artery hypertension and vascular remodeling. ► The effect was found to be mediated by increased NO-release and inhibition of cGMP-specific PDE-5. ► Dual action of the peptide that enhance NO release and diminished PDE-5 activity resulted in sustained elevation of cGMP. ► This novel peptide has therapeutic potential for NO/cGMP-dependent modulation of hemodynamic and structural changes in the pulmonary circulation.
Pulmonary vascular endothelial nitric oxide (NO) synthase (eNOS)-derived NO is the major stimulant of cyclic guanosine 5′-monophosphate (cGMP) production and NO/cGMP-dependent vasorelaxation in the pulmonary circulation. We recently synthesized multiple peptides and reported that an eleven amino acid (SSWRRKRKESS) peptide (P1) but not scrambled P1 stimulated the catalytic activity but not expression of eNOS and causes NO/cGMP-dependent sustained vasorelaxation in isolated pulmonary artery (PA) segments and in lung perfusion models. Since cGMP levels can also be elevated by inhibition of phosphodiesterase type 5 (PDE-5), this study was designed to test the hypothesis that P1-mediated vesorelaxation is due to its unique dual action as NO-releasing PDE-5 inhibitor in the pulmonary circulation. Treatment of porcine PA endothelial cells (PAEC) with P1 caused time-dependent increase in intracellular NO release and inhibition of the catalytic activity of cGMP-specific PDE-5 but not PDE-5 protein expression leading to increased levels of cGMP. Acute hypoxia-induced PA vasoconstriction ex vivo and continuous telemetry monitoring of hypoxia (10% oxygen)-induced elevated PA pressure in freely moving rats were significantly restored by administration of P1. Chronic hypoxia (10% oxygen for 4 weeks)-induced alterations in PA perfusion pressure, right ventricular hypertrophy, and vascular remodeling were attenuated by P1 treatment. These results demonstrate the potential therapeutic effects of P1 to prevent and/or arrest the progression of hypoxia-induced PAH via NO/cGMP-dependent modulation of hemodynamic and vascular remodeling in the pulmonary circulation. |
| doi_str_mv | 10.1016/j.peptides.2012.03.009 |
| format | Article |
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Pulmonary vascular endothelial nitric oxide (NO) synthase (eNOS)-derived NO is the major stimulant of cyclic guanosine 5′-monophosphate (cGMP) production and NO/cGMP-dependent vasorelaxation in the pulmonary circulation. We recently synthesized multiple peptides and reported that an eleven amino acid (SSWRRKRKESS) peptide (P1) but not scrambled P1 stimulated the catalytic activity but not expression of eNOS and causes NO/cGMP-dependent sustained vasorelaxation in isolated pulmonary artery (PA) segments and in lung perfusion models. Since cGMP levels can also be elevated by inhibition of phosphodiesterase type 5 (PDE-5), this study was designed to test the hypothesis that P1-mediated vesorelaxation is due to its unique dual action as NO-releasing PDE-5 inhibitor in the pulmonary circulation. Treatment of porcine PA endothelial cells (PAEC) with P1 caused time-dependent increase in intracellular NO release and inhibition of the catalytic activity of cGMP-specific PDE-5 but not PDE-5 protein expression leading to increased levels of cGMP. Acute hypoxia-induced PA vasoconstriction ex vivo and continuous telemetry monitoring of hypoxia (10% oxygen)-induced elevated PA pressure in freely moving rats were significantly restored by administration of P1. Chronic hypoxia (10% oxygen for 4 weeks)-induced alterations in PA perfusion pressure, right ventricular hypertrophy, and vascular remodeling were attenuated by P1 treatment. These results demonstrate the potential therapeutic effects of P1 to prevent and/or arrest the progression of hypoxia-induced PAH via NO/cGMP-dependent modulation of hemodynamic and vascular remodeling in the pulmonary circulation.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/j.peptides.2012.03.009</identifier><identifier>PMID: 22465621</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Sequence ; amino acids ; Animals ; Blood Pressure - drug effects ; Catalytic activity ; Cell Hypoxia ; Cells, Cultured ; Cyclic GMP ; Cyclic GMP - metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism ; Elevated ; endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; endothelial nitric oxide synthase ; guanosine ; hypertension ; Hypertension, Pulmonary - drug therapy ; hypertrophy ; Hypertrophy, Right Ventricular - prevention & control ; Hypoxia ; In Vitro Techniques ; Inhibition ; Inhibitors ; Lung - drug effects ; Lung - metabolism ; lungs ; Male ; Modulation ; monitoring ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - pharmacology ; Nitric Oxide Synthase Type III - therapeutic use ; oxygen ; Peptide Fragments - pharmacology ; Peptide Fragments - therapeutic use ; Peptides ; Phosphodiesterase 5 Inhibitors - pharmacology ; Phosphodiesterase 5 Inhibitors - therapeutic use ; Phosphodiesterase-5 ; polycyclic aromatic hydrocarbons ; Protein Binding ; protein synthesis ; pulmonary artery ; Pulmonary Artery - drug effects ; Pulmonary Artery - pathology ; Pulmonary artery pressure ; Pulmonary circulation ; Pulmonary hypertension ; Rats ; Rats, Sprague-Dawley ; Remodeling ; Swine ; Synthetic peptide ; Telemetry ; therapeutics ; vasoconstriction ; vasodilation ; Vasodilator Agents - pharmacology ; Vasodilator Agents - therapeutic use</subject><ispartof>Peptides (New York, N.Y. : 1980), 2012-05, Vol.35 (1), p.78-85</ispartof><rights>2012</rights><rights>Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c561t-7d0d418aee024ae48292af15e43be434fe22550196e74f32b48140b2189e07b63</citedby><cites>FETCH-LOGICAL-c561t-7d0d418aee024ae48292af15e43be434fe22550196e74f32b48140b2189e07b63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.peptides.2012.03.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22465621$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Hanbo</creatorcontrib><creatorcontrib>Zharikov, Sergey</creatorcontrib><creatorcontrib>Patel, Jawaharlal M.</creatorcontrib><title>Novel peptide for attenuation of hypoxia-induced pulmonary hypertension via modulation of nitric oxide release and phosphodiesterase -5 activity</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>► Peptide therapy attenuates hypoxia-induced pulmonary artery hypertension and vascular remodeling. ► The effect was found to be mediated by increased NO-release and inhibition of cGMP-specific PDE-5. ► Dual action of the peptide that enhance NO release and diminished PDE-5 activity resulted in sustained elevation of cGMP. ► This novel peptide has therapeutic potential for NO/cGMP-dependent modulation of hemodynamic and structural changes in the pulmonary circulation.
Pulmonary vascular endothelial nitric oxide (NO) synthase (eNOS)-derived NO is the major stimulant of cyclic guanosine 5′-monophosphate (cGMP) production and NO/cGMP-dependent vasorelaxation in the pulmonary circulation. We recently synthesized multiple peptides and reported that an eleven amino acid (SSWRRKRKESS) peptide (P1) but not scrambled P1 stimulated the catalytic activity but not expression of eNOS and causes NO/cGMP-dependent sustained vasorelaxation in isolated pulmonary artery (PA) segments and in lung perfusion models. Since cGMP levels can also be elevated by inhibition of phosphodiesterase type 5 (PDE-5), this study was designed to test the hypothesis that P1-mediated vesorelaxation is due to its unique dual action as NO-releasing PDE-5 inhibitor in the pulmonary circulation. Treatment of porcine PA endothelial cells (PAEC) with P1 caused time-dependent increase in intracellular NO release and inhibition of the catalytic activity of cGMP-specific PDE-5 but not PDE-5 protein expression leading to increased levels of cGMP. Acute hypoxia-induced PA vasoconstriction ex vivo and continuous telemetry monitoring of hypoxia (10% oxygen)-induced elevated PA pressure in freely moving rats were significantly restored by administration of P1. Chronic hypoxia (10% oxygen for 4 weeks)-induced alterations in PA perfusion pressure, right ventricular hypertrophy, and vascular remodeling were attenuated by P1 treatment. These results demonstrate the potential therapeutic effects of P1 to prevent and/or arrest the progression of hypoxia-induced PAH via NO/cGMP-dependent modulation of hemodynamic and vascular remodeling in the pulmonary circulation.</description><subject>Amino Acid Sequence</subject><subject>amino acids</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Catalytic activity</subject><subject>Cell Hypoxia</subject><subject>Cells, Cultured</subject><subject>Cyclic GMP</subject><subject>Cyclic GMP - metabolism</subject><subject>Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism</subject><subject>Elevated</subject><subject>endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>endothelial nitric oxide synthase</subject><subject>guanosine</subject><subject>hypertension</subject><subject>Hypertension, Pulmonary - drug therapy</subject><subject>hypertrophy</subject><subject>Hypertrophy, Right Ventricular - prevention & control</subject><subject>Hypoxia</subject><subject>In Vitro Techniques</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>lungs</subject><subject>Male</subject><subject>Modulation</subject><subject>monitoring</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - pharmacology</subject><subject>Nitric Oxide Synthase Type III - therapeutic use</subject><subject>oxygen</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptide Fragments - therapeutic use</subject><subject>Peptides</subject><subject>Phosphodiesterase 5 Inhibitors - pharmacology</subject><subject>Phosphodiesterase 5 Inhibitors - therapeutic use</subject><subject>Phosphodiesterase-5</subject><subject>polycyclic aromatic hydrocarbons</subject><subject>Protein Binding</subject><subject>protein synthesis</subject><subject>pulmonary artery</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - pathology</subject><subject>Pulmonary artery pressure</subject><subject>Pulmonary circulation</subject><subject>Pulmonary hypertension</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Remodeling</subject><subject>Swine</subject><subject>Synthetic peptide</subject><subject>Telemetry</subject><subject>therapeutics</subject><subject>vasoconstriction</subject><subject>vasodilation</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasodilator Agents - therapeutic use</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkt-O1CAUxhujccfVV1i59KYVKFC4MZqN_5KNXuheE9qe7jDpQAXa7LyFjyzNzE70aiUhJJzf-cJ3-IriiuCKYCLe7qoJpmR7iBXFhFa4rjBWT4oNkU1dciLU02KDiRKlaiS5KF7EuMMYM6bk8-KCUia4oGRT_P7mFxjRSQwNPiCTErjZJOsd8gPaHiZ_b01pXT930KNpHvfemXBYKxAyG1dysQbtfT-P50ZnU7Adys1ZOMAIJgIyLitsfcy7txAThPW25Mh0yS42HV4WzwYzRnh1Oi-L208ff15_KW--f_56_eGm7LggqWx63DMiDQCmzACTVFEzEA6sbvNmA1DK-ToAaNhQ05ZJwnBLiVSAm1bUl8W7o-40t3voO3ApmFFPwe6zN-2N1f9WnN3qO7_ouq45FTILvDkJBP9rzlb03sYOxtE48HPUpMkDpkIQ8TiKKZVKcqn-A82euOKYZ1Qc0S74GAMM58cTrNeQ6J1-CIleQ6JxrXNIcuPV39bPbQ-pyMDrIzAYr81dsFHf_sgKAq9LNauj90cC8hctFoKOnQWX82EDdEn33j72ij9KBN4P</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Hu, Hanbo</creator><creator>Zharikov, Sergey</creator><creator>Patel, Jawaharlal M.</creator><general>Elsevier Inc</general><scope>FBQ</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><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope><scope>5PM</scope></search><sort><creationdate>20120501</creationdate><title>Novel peptide for attenuation of hypoxia-induced pulmonary hypertension via modulation of nitric oxide release and phosphodiesterase -5 activity</title><author>Hu, Hanbo ; Zharikov, Sergey ; Patel, Jawaharlal M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c561t-7d0d418aee024ae48292af15e43be434fe22550196e74f32b48140b2189e07b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Amino Acid Sequence</topic><topic>amino acids</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Catalytic activity</topic><topic>Cell Hypoxia</topic><topic>Cells, Cultured</topic><topic>Cyclic GMP</topic><topic>Cyclic GMP - metabolism</topic><topic>Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism</topic><topic>Elevated</topic><topic>endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>endothelial nitric oxide synthase</topic><topic>guanosine</topic><topic>hypertension</topic><topic>Hypertension, Pulmonary - drug therapy</topic><topic>hypertrophy</topic><topic>Hypertrophy, Right Ventricular - prevention & control</topic><topic>Hypoxia</topic><topic>In Vitro Techniques</topic><topic>Inhibition</topic><topic>Inhibitors</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>lungs</topic><topic>Male</topic><topic>Modulation</topic><topic>monitoring</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - pharmacology</topic><topic>Nitric Oxide Synthase Type III - therapeutic use</topic><topic>oxygen</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptide Fragments - therapeutic use</topic><topic>Peptides</topic><topic>Phosphodiesterase 5 Inhibitors - pharmacology</topic><topic>Phosphodiesterase 5 Inhibitors - therapeutic use</topic><topic>Phosphodiesterase-5</topic><topic>polycyclic aromatic hydrocarbons</topic><topic>Protein Binding</topic><topic>protein synthesis</topic><topic>pulmonary artery</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - pathology</topic><topic>Pulmonary artery pressure</topic><topic>Pulmonary circulation</topic><topic>Pulmonary hypertension</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Remodeling</topic><topic>Swine</topic><topic>Synthetic peptide</topic><topic>Telemetry</topic><topic>therapeutics</topic><topic>vasoconstriction</topic><topic>vasodilation</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasodilator Agents - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Hanbo</creatorcontrib><creatorcontrib>Zharikov, Sergey</creatorcontrib><creatorcontrib>Patel, Jawaharlal M.</creatorcontrib><collection>AGRIS</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><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Hanbo</au><au>Zharikov, Sergey</au><au>Patel, Jawaharlal M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel peptide for attenuation of hypoxia-induced pulmonary hypertension via modulation of nitric oxide release and phosphodiesterase -5 activity</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>35</volume><issue>1</issue><spage>78</spage><epage>85</epage><pages>78-85</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><abstract>► Peptide therapy attenuates hypoxia-induced pulmonary artery hypertension and vascular remodeling. ► The effect was found to be mediated by increased NO-release and inhibition of cGMP-specific PDE-5. ► Dual action of the peptide that enhance NO release and diminished PDE-5 activity resulted in sustained elevation of cGMP. ► This novel peptide has therapeutic potential for NO/cGMP-dependent modulation of hemodynamic and structural changes in the pulmonary circulation.
Pulmonary vascular endothelial nitric oxide (NO) synthase (eNOS)-derived NO is the major stimulant of cyclic guanosine 5′-monophosphate (cGMP) production and NO/cGMP-dependent vasorelaxation in the pulmonary circulation. We recently synthesized multiple peptides and reported that an eleven amino acid (SSWRRKRKESS) peptide (P1) but not scrambled P1 stimulated the catalytic activity but not expression of eNOS and causes NO/cGMP-dependent sustained vasorelaxation in isolated pulmonary artery (PA) segments and in lung perfusion models. Since cGMP levels can also be elevated by inhibition of phosphodiesterase type 5 (PDE-5), this study was designed to test the hypothesis that P1-mediated vesorelaxation is due to its unique dual action as NO-releasing PDE-5 inhibitor in the pulmonary circulation. Treatment of porcine PA endothelial cells (PAEC) with P1 caused time-dependent increase in intracellular NO release and inhibition of the catalytic activity of cGMP-specific PDE-5 but not PDE-5 protein expression leading to increased levels of cGMP. Acute hypoxia-induced PA vasoconstriction ex vivo and continuous telemetry monitoring of hypoxia (10% oxygen)-induced elevated PA pressure in freely moving rats were significantly restored by administration of P1. Chronic hypoxia (10% oxygen for 4 weeks)-induced alterations in PA perfusion pressure, right ventricular hypertrophy, and vascular remodeling were attenuated by P1 treatment. These results demonstrate the potential therapeutic effects of P1 to prevent and/or arrest the progression of hypoxia-induced PAH via NO/cGMP-dependent modulation of hemodynamic and vascular remodeling in the pulmonary circulation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22465621</pmid><doi>10.1016/j.peptides.2012.03.009</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Peptides (New York, N.Y. : 1980), 2012-05, Vol.35 (1), p.78-85 |
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| subjects | Amino Acid Sequence amino acids Animals Blood Pressure - drug effects Catalytic activity Cell Hypoxia Cells, Cultured Cyclic GMP Cyclic GMP - metabolism Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism Elevated endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism endothelial nitric oxide synthase guanosine hypertension Hypertension, Pulmonary - drug therapy hypertrophy Hypertrophy, Right Ventricular - prevention & control Hypoxia In Vitro Techniques Inhibition Inhibitors Lung - drug effects Lung - metabolism lungs Male Modulation monitoring Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - pharmacology Nitric Oxide Synthase Type III - therapeutic use oxygen Peptide Fragments - pharmacology Peptide Fragments - therapeutic use Peptides Phosphodiesterase 5 Inhibitors - pharmacology Phosphodiesterase 5 Inhibitors - therapeutic use Phosphodiesterase-5 polycyclic aromatic hydrocarbons Protein Binding protein synthesis pulmonary artery Pulmonary Artery - drug effects Pulmonary Artery - pathology Pulmonary artery pressure Pulmonary circulation Pulmonary hypertension Rats Rats, Sprague-Dawley Remodeling Swine Synthetic peptide Telemetry therapeutics vasoconstriction vasodilation Vasodilator Agents - pharmacology Vasodilator Agents - therapeutic use |
| title | Novel peptide for attenuation of hypoxia-induced pulmonary hypertension via modulation of nitric oxide release and phosphodiesterase -5 activity |
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