Angiotensin-(1–7) inhibits the angiotensin II-enhanced norepinephrine release in coarcted hypertensive rats
Since it has been suggested that angiotensin (Ang) (1–7) functions as an antihypertensive peptide, we studied its effect on the Ang II-enhanced norepinephrine (NE) release evoked by K + in hypothalami isolated from aortic coarcted hypertensive (CH) rats. The endogenous NE stores were labeled by incu...
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description | Since it has been suggested that angiotensin (Ang) (1–7) functions as an antihypertensive peptide, we studied its effect on the Ang II-enhanced norepinephrine (NE) release evoked by K
+ in hypothalami isolated from aortic coarcted hypertensive (CH) rats. The endogenous NE stores were labeled by incubation of the tissues with
3H-NE during 30 min, and after 90 min of washing, they were incubated in Krebs solution containing 25 mM KCl in the absence or presence of the peptides. Ang-(1–7) not only diminished the K
+-evoked NE release from hypothalami of CH rats, but also blocked the Ang II-enhanced NE release induced by K
+. Ang-(1–7) blocking action on the Ang II response was prevented by [
d-Ala
7]Ang-(1–7), an Ang-(1–7) specific antagonist, by PD 123319, an AT
2-receptor antagonist, and by Hoe 140, a B
2 receptor antagonist. Ang-(1–7) inhibitory effect on the Ang II facilitatory effect on K
+-stimulated NE release disappeared in the presence of
N
ω-nitro-
l-arginine methylester and was restored by
l-arginine. Our present results suggest that Ang-(1–7) may contribute to blood pressure regulation by blocking Ang II actions on NE release at the central level. This inhibitory effect is a nitric oxide-mediated mechanism involving AT
2 receptors and/or Ang-(1–7) specific receptors and local bradykinin generation. |
doi_str_mv | 10.1016/j.regpep.2003.10.026 |
format | Article |
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+ in hypothalami isolated from aortic coarcted hypertensive (CH) rats. The endogenous NE stores were labeled by incubation of the tissues with
3H-NE during 30 min, and after 90 min of washing, they were incubated in Krebs solution containing 25 mM KCl in the absence or presence of the peptides. Ang-(1–7) not only diminished the K
+-evoked NE release from hypothalami of CH rats, but also blocked the Ang II-enhanced NE release induced by K
+. Ang-(1–7) blocking action on the Ang II response was prevented by [
d-Ala
7]Ang-(1–7), an Ang-(1–7) specific antagonist, by PD 123319, an AT
2-receptor antagonist, and by Hoe 140, a B
2 receptor antagonist. Ang-(1–7) inhibitory effect on the Ang II facilitatory effect on K
+-stimulated NE release disappeared in the presence of
N
ω-nitro-
l-arginine methylester and was restored by
l-arginine. Our present results suggest that Ang-(1–7) may contribute to blood pressure regulation by blocking Ang II actions on NE release at the central level. This inhibitory effect is a nitric oxide-mediated mechanism involving AT
2 receptors and/or Ang-(1–7) specific receptors and local bradykinin generation.</description><identifier>ISSN: 0167-0115</identifier><identifier>EISSN: 1873-1686</identifier><identifier>DOI: 10.1016/j.regpep.2003.10.026</identifier><identifier>PMID: 14759556</identifier><identifier>CODEN: REPPDY</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject><![CDATA[Angiotensin antagonists ; Angiotensin I - antagonists & inhibitors ; Angiotensin I - pharmacology ; Angiotensin II - analogs & derivatives ; Angiotensin II - antagonists & inhibitors ; Angiotensin II - pharmacology ; Animals ; Antihypertensive Agents - antagonists & inhibitors ; Antihypertensive Agents - pharmacology ; Aortic Coarctation - complications ; Biological and medical sciences ; Bradykinin ; Bradykinin - analogs & derivatives ; Bradykinin - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hypertension ; Hypertension - etiology ; Hypertension - physiopathology ; Hypothalamus - drug effects ; Hypothalamus - metabolism ; Imidazoles - pharmacology ; In Vitro Techniques ; Nitric oxide ; Nitric Oxide - metabolism ; Norepinephrine - antagonists & inhibitors ; Norepinephrine - metabolism ; Peptide Fragments - antagonists & inhibitors ; Peptide Fragments - pharmacology ; Potassium - pharmacology ; Pyridines - pharmacology ; Rats ; Rats, Wistar ; Vertebrates: endocrinology]]></subject><ispartof>Regulatory peptides, 2004-04, Vol.118 (1), p.45-49</ispartof><rights>2003 Elsevier B.V.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-1975d29e2680d36ac102ec6bc89d40a815858f91ded6f9d5f559501cc048f8823</citedby><cites>FETCH-LOGICAL-c388t-1975d29e2680d36ac102ec6bc89d40a815858f91ded6f9d5f559501cc048f8823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.regpep.2003.10.026$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15478492$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14759556$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gironacci, Mariela Mercedes</creatorcontrib><creatorcontrib>Yujnovsky, Irene</creatorcontrib><creatorcontrib>Gorzalczany, Susana</creatorcontrib><creatorcontrib>Taira, Carlos</creatorcontrib><creatorcontrib>Peña, Clara</creatorcontrib><title>Angiotensin-(1–7) inhibits the angiotensin II-enhanced norepinephrine release in coarcted hypertensive rats</title><title>Regulatory peptides</title><addtitle>Regul Pept</addtitle><description>Since it has been suggested that angiotensin (Ang) (1–7) functions as an antihypertensive peptide, we studied its effect on the Ang II-enhanced norepinephrine (NE) release evoked by K
+ in hypothalami isolated from aortic coarcted hypertensive (CH) rats. The endogenous NE stores were labeled by incubation of the tissues with
3H-NE during 30 min, and after 90 min of washing, they were incubated in Krebs solution containing 25 mM KCl in the absence or presence of the peptides. Ang-(1–7) not only diminished the K
+-evoked NE release from hypothalami of CH rats, but also blocked the Ang II-enhanced NE release induced by K
+. Ang-(1–7) blocking action on the Ang II response was prevented by [
d-Ala
7]Ang-(1–7), an Ang-(1–7) specific antagonist, by PD 123319, an AT
2-receptor antagonist, and by Hoe 140, a B
2 receptor antagonist. Ang-(1–7) inhibitory effect on the Ang II facilitatory effect on K
+-stimulated NE release disappeared in the presence of
N
ω-nitro-
l-arginine methylester and was restored by
l-arginine. Our present results suggest that Ang-(1–7) may contribute to blood pressure regulation by blocking Ang II actions on NE release at the central level. This inhibitory effect is a nitric oxide-mediated mechanism involving AT
2 receptors and/or Ang-(1–7) specific receptors and local bradykinin generation.</description><subject>Angiotensin antagonists</subject><subject>Angiotensin I - antagonists & inhibitors</subject><subject>Angiotensin I - pharmacology</subject><subject>Angiotensin II - analogs & derivatives</subject><subject>Angiotensin II - antagonists & inhibitors</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Antihypertensive Agents - antagonists & inhibitors</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Aortic Coarctation - complications</subject><subject>Biological and medical sciences</subject><subject>Bradykinin</subject><subject>Bradykinin - analogs & derivatives</subject><subject>Bradykinin - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hypertension</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>Hypothalamus - drug effects</subject><subject>Hypothalamus - metabolism</subject><subject>Imidazoles - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Norepinephrine - antagonists & inhibitors</subject><subject>Norepinephrine - metabolism</subject><subject>Peptide Fragments - antagonists & inhibitors</subject><subject>Peptide Fragments - pharmacology</subject><subject>Potassium - pharmacology</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Vertebrates: endocrinology</subject><issn>0167-0115</issn><issn>1873-1686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFq3DAQhkVpaDZp36AEX1rSg7cay5LlSyCEtFlYyCU9C600Xmvxyo7kXcit79A3zJNE7i7sLZcZGL5_mPkI-Qp0DhTEz8084HrAYV5QytJoTgvxgcxAViwHIcVHMktYlVMAfk4uYtxQCryq2CdyDmXFa87FjGxv_dr1I_rofH4Nr3__VT8y51u3cmPMxhYzfQKyxSJH32pv0Ga-Dzg4j0MbUs0Cdqgjpmxmeh3MmJD2ZcDwP7pPgB7jZ3LW6C7il2O_JH9-3T_dPeTLx9-Lu9tlbpiUYw51xW1RYyEktUxoA7RAI1ZG1rakWgKXXDY1WLSiqS1vePqGgjG0lI2UBbsk3w97h9A_7zCOauuiwa7THvtdVJICk4zRBJYH0IQ-xoCNGoLb6vCigKpJs9qog2Y1aZ6mSXOKXR3371ZbtKfQ0WsCvh0BHY3umpCcuXjieFnJsp4OvTlwmGzsHQYVjcPJrwtoRmV79_4lb0MPns8</recordid><startdate>20040415</startdate><enddate>20040415</enddate><creator>Gironacci, Mariela Mercedes</creator><creator>Yujnovsky, Irene</creator><creator>Gorzalczany, Susana</creator><creator>Taira, Carlos</creator><creator>Peña, Clara</creator><general>Elsevier B.V</general><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>20040415</creationdate><title>Angiotensin-(1–7) inhibits the angiotensin II-enhanced norepinephrine release in coarcted hypertensive rats</title><author>Gironacci, Mariela Mercedes ; Yujnovsky, Irene ; Gorzalczany, Susana ; Taira, Carlos ; Peña, Clara</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-1975d29e2680d36ac102ec6bc89d40a815858f91ded6f9d5f559501cc048f8823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Angiotensin antagonists</topic><topic>Angiotensin I - antagonists & inhibitors</topic><topic>Angiotensin I - pharmacology</topic><topic>Angiotensin II - analogs & derivatives</topic><topic>Angiotensin II - antagonists & inhibitors</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Antihypertensive Agents - antagonists & inhibitors</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Aortic Coarctation - complications</topic><topic>Biological and medical sciences</topic><topic>Bradykinin</topic><topic>Bradykinin - analogs & derivatives</topic><topic>Bradykinin - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hypertension</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>Hypothalamus - drug effects</topic><topic>Hypothalamus - metabolism</topic><topic>Imidazoles - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Norepinephrine - antagonists & inhibitors</topic><topic>Norepinephrine - metabolism</topic><topic>Peptide Fragments - antagonists & inhibitors</topic><topic>Peptide Fragments - pharmacology</topic><topic>Potassium - pharmacology</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gironacci, Mariela Mercedes</creatorcontrib><creatorcontrib>Yujnovsky, Irene</creatorcontrib><creatorcontrib>Gorzalczany, Susana</creatorcontrib><creatorcontrib>Taira, Carlos</creatorcontrib><creatorcontrib>Peña, Clara</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>Regulatory peptides</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gironacci, Mariela Mercedes</au><au>Yujnovsky, Irene</au><au>Gorzalczany, Susana</au><au>Taira, Carlos</au><au>Peña, Clara</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin-(1–7) inhibits the angiotensin II-enhanced norepinephrine release in coarcted hypertensive rats</atitle><jtitle>Regulatory peptides</jtitle><addtitle>Regul Pept</addtitle><date>2004-04-15</date><risdate>2004</risdate><volume>118</volume><issue>1</issue><spage>45</spage><epage>49</epage><pages>45-49</pages><issn>0167-0115</issn><eissn>1873-1686</eissn><coden>REPPDY</coden><abstract>Since it has been suggested that angiotensin (Ang) (1–7) functions as an antihypertensive peptide, we studied its effect on the Ang II-enhanced norepinephrine (NE) release evoked by K
+ in hypothalami isolated from aortic coarcted hypertensive (CH) rats. The endogenous NE stores were labeled by incubation of the tissues with
3H-NE during 30 min, and after 90 min of washing, they were incubated in Krebs solution containing 25 mM KCl in the absence or presence of the peptides. Ang-(1–7) not only diminished the K
+-evoked NE release from hypothalami of CH rats, but also blocked the Ang II-enhanced NE release induced by K
+. Ang-(1–7) blocking action on the Ang II response was prevented by [
d-Ala
7]Ang-(1–7), an Ang-(1–7) specific antagonist, by PD 123319, an AT
2-receptor antagonist, and by Hoe 140, a B
2 receptor antagonist. Ang-(1–7) inhibitory effect on the Ang II facilitatory effect on K
+-stimulated NE release disappeared in the presence of
N
ω-nitro-
l-arginine methylester and was restored by
l-arginine. Our present results suggest that Ang-(1–7) may contribute to blood pressure regulation by blocking Ang II actions on NE release at the central level. This inhibitory effect is a nitric oxide-mediated mechanism involving AT
2 receptors and/or Ang-(1–7) specific receptors and local bradykinin generation.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>14759556</pmid><doi>10.1016/j.regpep.2003.10.026</doi><tpages>5</tpages></addata></record> |
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subjects | Angiotensin antagonists Angiotensin I - antagonists & inhibitors Angiotensin I - pharmacology Angiotensin II - analogs & derivatives Angiotensin II - antagonists & inhibitors Angiotensin II - pharmacology Animals Antihypertensive Agents - antagonists & inhibitors Antihypertensive Agents - pharmacology Aortic Coarctation - complications Biological and medical sciences Bradykinin Bradykinin - analogs & derivatives Bradykinin - pharmacology Fundamental and applied biological sciences. Psychology Hypertension Hypertension - etiology Hypertension - physiopathology Hypothalamus - drug effects Hypothalamus - metabolism Imidazoles - pharmacology In Vitro Techniques Nitric oxide Nitric Oxide - metabolism Norepinephrine - antagonists & inhibitors Norepinephrine - metabolism Peptide Fragments - antagonists & inhibitors Peptide Fragments - pharmacology Potassium - pharmacology Pyridines - pharmacology Rats Rats, Wistar Vertebrates: endocrinology |
title | Angiotensin-(1–7) inhibits the angiotensin II-enhanced norepinephrine release in coarcted hypertensive rats |
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