Involvement of G-protein βγ subunits on the influence of inhibitory α2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens
The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect th...
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description | The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors. |
doi_str_mv | 10.1016/j.neuint.2006.07.002 |
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Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/j.neuint.2006.07.002</identifier><identifier>PMID: 16962210</identifier><identifier>CODEN: NEUIDS</identifier><language>eng</language><publisher>Oxford: Elsevier</publisher><subject>Adrenergic alpha-Antagonists - pharmacology ; Angiotensin II - metabolism ; Angiotensin II - pharmacology ; Animals ; Autoreceptors - drug effects ; Autoreceptors - metabolism ; Biological and medical sciences ; Electric Stimulation ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; GTP-Binding Protein beta Subunits - antagonists & inhibitors ; GTP-Binding Protein beta Subunits - metabolism ; GTP-Binding Protein gamma Subunits - antagonists & inhibitors ; GTP-Binding Protein gamma Subunits - metabolism ; Male ; Neural Inhibition - drug effects ; Neural Inhibition - physiology ; Norepinephrine - metabolism ; Norepinephrine - secretion ; Pertussis Toxin - pharmacology ; Presynaptic Terminals - drug effects ; Presynaptic Terminals - metabolism ; Presynaptic Terminals - secretion ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - metabolism ; Rats ; Rats, Wistar ; Receptor Cross-Talk - drug effects ; Receptor Cross-Talk - physiology ; Receptor, Angiotensin, Type 1 - drug effects ; Receptor, Angiotensin, Type 1 - metabolism ; Receptors, Adrenergic, alpha-2 - drug effects ; Receptors, Adrenergic, alpha-2 - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Sympathetic Fibers, Postganglionic - drug effects ; Sympathetic Fibers, Postganglionic - metabolism ; Sympathetic Fibers, Postganglionic - secretion ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology ; Tritium ; Type C Phospholipases - antagonists & inhibitors ; Type C Phospholipases - metabolism ; Vas Deferens - drug effects ; Vas Deferens - innervation ; Vas Deferens - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Neurochemistry international, 2006-12, Vol.49 (7), p.698-707</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c316t-aebe1d938fbb8b3be0f5d350d44c33e5ee6b84a7527229769caf7a078251ac133</citedby><cites>FETCH-LOGICAL-c316t-aebe1d938fbb8b3be0f5d350d44c33e5ee6b84a7527229769caf7a078251ac133</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18233007$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16962210$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TALAIA, Carlos</creatorcontrib><creatorcontrib>QUEIROZ, Gloria</creatorcontrib><creatorcontrib>PINHEIRO, Helder</creatorcontrib><creatorcontrib>MOURA, Daniel</creatorcontrib><creatorcontrib>GONCALVES, Jorge</creatorcontrib><title>Involvement of G-protein βγ subunits on the influence of inhibitory α2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors.</description><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Autoreceptors - drug effects</subject><subject>Autoreceptors - metabolism</subject><subject>Biological and medical sciences</subject><subject>Electric Stimulation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GTP-Binding Protein beta Subunits - antagonists & inhibitors</subject><subject>GTP-Binding Protein beta Subunits - metabolism</subject><subject>GTP-Binding Protein gamma Subunits - antagonists & inhibitors</subject><subject>GTP-Binding Protein gamma Subunits - metabolism</subject><subject>Male</subject><subject>Neural Inhibition - drug effects</subject><subject>Neural Inhibition - physiology</subject><subject>Norepinephrine - metabolism</subject><subject>Norepinephrine - secretion</subject><subject>Pertussis Toxin - pharmacology</subject><subject>Presynaptic Terminals - drug effects</subject><subject>Presynaptic Terminals - metabolism</subject><subject>Presynaptic Terminals - secretion</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor Cross-Talk - drug effects</subject><subject>Receptor Cross-Talk - physiology</subject><subject>Receptor, Angiotensin, Type 1 - drug effects</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Receptors, Adrenergic, alpha-2 - drug effects</subject><subject>Receptors, Adrenergic, alpha-2 - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Sympathetic Fibers, Postganglionic - drug effects</subject><subject>Sympathetic Fibers, Postganglionic - metabolism</subject><subject>Sympathetic Fibers, Postganglionic - secretion</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><subject>Tritium</subject><subject>Type C Phospholipases - antagonists & inhibitors</subject><subject>Type C Phospholipases - metabolism</subject><subject>Vas Deferens - drug effects</subject><subject>Vas Deferens - innervation</subject><subject>Vas Deferens - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkcFu1DAQQC0EokvhDxDyBW4JYzuJk2NVQalUiUs5WxNnQr3KOovtrNTPKv2P_aZ6uws9zRzePEt-jH0UUAoQzdd16WlxPpUSoClBlwDyFVuJVsui03X1mq1AdLoA0TZn7F2MawDQHdRv2ZloukZKASv2eO1387SjDfnE55FfFdswJ3Ke7__uH3lc-sW7FPnseboj7vw4LeQtHVjn71zv0hzu-f5BFrjklSxt8_h_gP63yz4fs_HiVhT_AL6Zh2XC5DKXVX4OOATyODlPPNBEGA-vPTsCJr7DyAcaKTPxPXsz4hTpw2mes1_fv91e_ihufl5dX17cFFaJJhVIPYmhU-3Y922veoKxHlQNQ1VZpagmavq2Ql1LLWWnm87iqBF0K2uBVih1zr4cvflL_iwUk9m4aGma0NO8RNO0XSs6UWewOoI2zDEGGs02uA2GeyPAHGKZtTnGModYBrTJsfLZp5N_6Tc0vByd6mTg8wnAaHEaA3rr4gvXSqVyU_UEPkmmMg</recordid><startdate>200612</startdate><enddate>200612</enddate><creator>TALAIA, Carlos</creator><creator>QUEIROZ, Gloria</creator><creator>PINHEIRO, Helder</creator><creator>MOURA, Daniel</creator><creator>GONCALVES, Jorge</creator><general>Elsevier</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>200612</creationdate><title>Involvement of G-protein βγ subunits on the influence of inhibitory α2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens</title><author>TALAIA, Carlos ; QUEIROZ, Gloria ; PINHEIRO, Helder ; MOURA, Daniel ; GONCALVES, Jorge</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c316t-aebe1d938fbb8b3be0f5d350d44c33e5ee6b84a7527229769caf7a078251ac133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Autoreceptors - drug effects</topic><topic>Autoreceptors - metabolism</topic><topic>Biological and medical sciences</topic><topic>Electric Stimulation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GTP-Binding Protein beta Subunits - antagonists & inhibitors</topic><topic>GTP-Binding Protein beta Subunits - metabolism</topic><topic>GTP-Binding Protein gamma Subunits - antagonists & inhibitors</topic><topic>GTP-Binding Protein gamma Subunits - metabolism</topic><topic>Male</topic><topic>Neural Inhibition - drug effects</topic><topic>Neural Inhibition - physiology</topic><topic>Norepinephrine - metabolism</topic><topic>Norepinephrine - secretion</topic><topic>Pertussis Toxin - pharmacology</topic><topic>Presynaptic Terminals - drug effects</topic><topic>Presynaptic Terminals - metabolism</topic><topic>Presynaptic Terminals - secretion</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor Cross-Talk - drug effects</topic><topic>Receptor Cross-Talk - physiology</topic><topic>Receptor, Angiotensin, Type 1 - drug effects</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Receptors, Adrenergic, alpha-2 - drug effects</topic><topic>Receptors, Adrenergic, alpha-2 - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Sympathetic Fibers, Postganglionic - drug effects</topic><topic>Sympathetic Fibers, Postganglionic - metabolism</topic><topic>Sympathetic Fibers, Postganglionic - secretion</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Tritium</topic><topic>Type C Phospholipases - antagonists & inhibitors</topic><topic>Type C Phospholipases - metabolism</topic><topic>Vas Deferens - drug effects</topic><topic>Vas Deferens - innervation</topic><topic>Vas Deferens - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TALAIA, Carlos</creatorcontrib><creatorcontrib>QUEIROZ, Gloria</creatorcontrib><creatorcontrib>PINHEIRO, Helder</creatorcontrib><creatorcontrib>MOURA, Daniel</creatorcontrib><creatorcontrib>GONCALVES, Jorge</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>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>TALAIA, Carlos</au><au>QUEIROZ, Gloria</au><au>PINHEIRO, Helder</au><au>MOURA, Daniel</au><au>GONCALVES, Jorge</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of G-protein βγ subunits on the influence of inhibitory α2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>2006-12</date><risdate>2006</risdate><volume>49</volume><issue>7</issue><spage>698</spage><epage>707</epage><pages>698-707</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><coden>NEUIDS</coden><abstract>The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors.</abstract><cop>Oxford</cop><pub>Elsevier</pub><pmid>16962210</pmid><doi>10.1016/j.neuint.2006.07.002</doi><tpages>10</tpages></addata></record> |
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subjects | Adrenergic alpha-Antagonists - pharmacology Angiotensin II - metabolism Angiotensin II - pharmacology Animals Autoreceptors - drug effects Autoreceptors - metabolism Biological and medical sciences Electric Stimulation Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology GTP-Binding Protein beta Subunits - antagonists & inhibitors GTP-Binding Protein beta Subunits - metabolism GTP-Binding Protein gamma Subunits - antagonists & inhibitors GTP-Binding Protein gamma Subunits - metabolism Male Neural Inhibition - drug effects Neural Inhibition - physiology Norepinephrine - metabolism Norepinephrine - secretion Pertussis Toxin - pharmacology Presynaptic Terminals - drug effects Presynaptic Terminals - metabolism Presynaptic Terminals - secretion Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism Rats Rats, Wistar Receptor Cross-Talk - drug effects Receptor Cross-Talk - physiology Receptor, Angiotensin, Type 1 - drug effects Receptor, Angiotensin, Type 1 - metabolism Receptors, Adrenergic, alpha-2 - drug effects Receptors, Adrenergic, alpha-2 - metabolism Signal Transduction - drug effects Signal Transduction - physiology Sympathetic Fibers, Postganglionic - drug effects Sympathetic Fibers, Postganglionic - metabolism Sympathetic Fibers, Postganglionic - secretion Synaptic Transmission - drug effects Synaptic Transmission - physiology Tritium Type C Phospholipases - antagonists & inhibitors Type C Phospholipases - metabolism Vas Deferens - drug effects Vas Deferens - innervation Vas Deferens - metabolism Vertebrates: nervous system and sense organs |
title | Involvement of G-protein βγ subunits on the influence of inhibitory α2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens |
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