Regional haemodynamic effects of endothelin‐1 and endothelin‐3 in conscious Long Evans and Brattleboro rats

1 The regional haemodynamic effects of bolus doses (4 and 40 pmol) and infusions (12 and 120 pmol h−1) of endothelin‐1 and endothelin‐3 were assessed in conscious, Long Evans and Brattleboro (i.e. vasopressin‐deficient) rats, chronically‐instrumented with pulsed Doppler flow probes. 2 In both strain...

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Veröffentlicht in:British journal of pharmacology 1990-01, Vol.99 (1), p.107-112
Hauptverfasser: Gardiner, S.M., Compton, A.M., Bennett, T.
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description 1 The regional haemodynamic effects of bolus doses (4 and 40 pmol) and infusions (12 and 120 pmol h−1) of endothelin‐1 and endothelin‐3 were assessed in conscious, Long Evans and Brattleboro (i.e. vasopressin‐deficient) rats, chronically‐instrumented with pulsed Doppler flow probes. 2 In both strains of rat the lower bolus dose of endothelin‐1 caused only a slight pressor effect, but there were marked renal and mesenteric vasoconstrictions and hindquarters vasodilatation. 3 The lower bolus dose of endothelin‐3 did not affect blood pressure significantly, although the changes in regional haemodynamics were qualitatively similar to those seen following endothelin‐1 in Long Evans and Brattleboro rats. 4 The higher dose of endothelin‐1 caused an initial hypotension accompanied by substantial hindquarters vasodilatations in Long Evans and Brattleboro rats. Subsequently, in both strains, there was a rise in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstrictions. 5 The higher bolus dose of endothelin‐3 caused initial hypotension and hindquarters vasodilatation similar to those seen with endothelin‐1. However, the subsequent pressor effect was less with endothelin‐3, as was the renal vasoconstriction, and it did not cause any increase in hindquarters vascular resistance. 6 Infusion of endothelin‐1 at the lower rate (12 pmol h−1) caused renal and mesenteric vasoconstrictions in both strains of rat, whereas endothelin‐3 at this rate caused only mesenteric vasoconstriction. 7 Infusion of endothelin‐1 at the higher rate (120 pmol h−1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. Endothelin‐3 had a smaller pressor effect and a lesser constrictor action on the renal and mesenteric vascular beds; it did not constrict the hindquarters vascular bed. 8 These results show, that in conscious Long Evans and Brattleboro rats, the initial depressor effects of the higher bolus doses of endothelin‐1 and −3 were similar, and, hence, not influenced by the absence of endogenous vasopressin. Endothelin‐1 and −3 appear equipotent in their initial hyperaemic vasodilator effects in the hindquarters vasculature in both strains, making it unlikely that this effect is dependent on the release of atrial natriuretic peptide (ANP), since ANP does not cause significant increases in hindquarters blood flow in Brattleboro rats. The greater delayed pressor effect of endothelin‐1 is a
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Subsequently, in both strains, there was a rise in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstrictions. 5 The higher bolus dose of endothelin‐3 caused initial hypotension and hindquarters vasodilatation similar to those seen with endothelin‐1. However, the subsequent pressor effect was less with endothelin‐3, as was the renal vasoconstriction, and it did not cause any increase in hindquarters vascular resistance. 6 Infusion of endothelin‐1 at the lower rate (12 pmol h−1) caused renal and mesenteric vasoconstrictions in both strains of rat, whereas endothelin‐3 at this rate caused only mesenteric vasoconstriction. 7 Infusion of endothelin‐1 at the higher rate (120 pmol h−1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. Endothelin‐3 had a smaller pressor effect and a lesser constrictor action on the renal and mesenteric vascular beds; it did not constrict the hindquarters vascular bed. 8 These results show, that in conscious Long Evans and Brattleboro rats, the initial depressor effects of the higher bolus doses of endothelin‐1 and −3 were similar, and, hence, not influenced by the absence of endogenous vasopressin. Endothelin‐1 and −3 appear equipotent in their initial hyperaemic vasodilator effects in the hindquarters vasculature in both strains, making it unlikely that this effect is dependent on the release of atrial natriuretic peptide (ANP), since ANP does not cause significant increases in hindquarters blood flow in Brattleboro rats. The greater delayed pressor effect of endothelin‐1 is associated with its more marked vasoconstrictor effects on renal and mesenteric vascular beds and is accentuated, relative to endothelin‐3, by the lack of a constrictor effect of endothelin‐3 in the hindquarters vasculature.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.1990.tb14662.x</identifier><identifier>PMID: 2139584</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; Cardiovascular system ; Endothelins ; Heart Rate - drug effects ; Hindlimb - blood supply ; Male ; Medical sciences ; Miscellaneous ; Peptides - pharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Brattleboro ; Regional Blood Flow - drug effects ; Renal Circulation - drug effects ; Rheology ; Splanchnic Circulation - drug effects ; Vasoconstriction - drug effects</subject><ispartof>British journal of pharmacology, 1990-01, Vol.99 (1), p.107-112</ispartof><rights>1990 British Pharmacological Society</rights><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4222-efb7e54c448b44c8187790956804dc69184da3ed0712c144bd8390645d8d584d3</citedby><cites>FETCH-LOGICAL-c4222-efb7e54c448b44c8187790956804dc69184da3ed0712c144bd8390645d8d584d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1917519/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1917519/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=6685999$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2139584$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gardiner, S.M.</creatorcontrib><creatorcontrib>Compton, A.M.</creatorcontrib><creatorcontrib>Bennett, T.</creatorcontrib><title>Regional haemodynamic effects of endothelin‐1 and endothelin‐3 in conscious Long Evans and Brattleboro rats</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1 The regional haemodynamic effects of bolus doses (4 and 40 pmol) and infusions (12 and 120 pmol h−1) of endothelin‐1 and endothelin‐3 were assessed in conscious, Long Evans and Brattleboro (i.e. vasopressin‐deficient) rats, chronically‐instrumented with pulsed Doppler flow probes. 2 In both strains of rat the lower bolus dose of endothelin‐1 caused only a slight pressor effect, but there were marked renal and mesenteric vasoconstrictions and hindquarters vasodilatation. 3 The lower bolus dose of endothelin‐3 did not affect blood pressure significantly, although the changes in regional haemodynamics were qualitatively similar to those seen following endothelin‐1 in Long Evans and Brattleboro rats. 4 The higher dose of endothelin‐1 caused an initial hypotension accompanied by substantial hindquarters vasodilatations in Long Evans and Brattleboro rats. Subsequently, in both strains, there was a rise in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstrictions. 5 The higher bolus dose of endothelin‐3 caused initial hypotension and hindquarters vasodilatation similar to those seen with endothelin‐1. However, the subsequent pressor effect was less with endothelin‐3, as was the renal vasoconstriction, and it did not cause any increase in hindquarters vascular resistance. 6 Infusion of endothelin‐1 at the lower rate (12 pmol h−1) caused renal and mesenteric vasoconstrictions in both strains of rat, whereas endothelin‐3 at this rate caused only mesenteric vasoconstriction. 7 Infusion of endothelin‐1 at the higher rate (120 pmol h−1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. Endothelin‐3 had a smaller pressor effect and a lesser constrictor action on the renal and mesenteric vascular beds; it did not constrict the hindquarters vascular bed. 8 These results show, that in conscious Long Evans and Brattleboro rats, the initial depressor effects of the higher bolus doses of endothelin‐1 and −3 were similar, and, hence, not influenced by the absence of endogenous vasopressin. Endothelin‐1 and −3 appear equipotent in their initial hyperaemic vasodilator effects in the hindquarters vasculature in both strains, making it unlikely that this effect is dependent on the release of atrial natriuretic peptide (ANP), since ANP does not cause significant increases in hindquarters blood flow in Brattleboro rats. The greater delayed pressor effect of endothelin‐1 is associated with its more marked vasoconstrictor effects on renal and mesenteric vascular beds and is accentuated, relative to endothelin‐3, by the lack of a constrictor effect of endothelin‐3 in the hindquarters vasculature.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiovascular system</subject><subject>Endothelins</subject><subject>Heart Rate - drug effects</subject><subject>Hindlimb - blood supply</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Peptides - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Brattleboro</subject><subject>Regional Blood Flow - drug effects</subject><subject>Renal Circulation - drug effects</subject><subject>Rheology</subject><subject>Splanchnic Circulation - drug effects</subject><subject>Vasoconstriction - drug effects</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkc1u1DAUhS1EVYbCIyBZCLFLsBPHPywQtGpppZFACNaWYzszHjl2sTOls-MR-ox9kiadaESXeOMrn3OP79UHwFuMSjyeD5sSE0aLpua4xEKgcmgxobQqb5-BxUF6DhYIIVZgzPkL8DLnDUKjyJpjcFzhWjScLED8YVcuBuXhWtk-ml1QvdPQdp3VQ4axgzaYOKytd-H-7x2GKpinTzV0AeoYsnZxm-EyhhU8v1EhP1pPkxoGb9uYIhzL_Aocdcpn-3q-T8Cvi_OfZ5fF8tvXq7Mvy0KTqqoK27XMNkQTwltCNMecMYFEQzkiRlOBOTGqtgYxXGlMSGt4LRAljeFm3MvUJ-DTPvd62_bWaBuGpLy8Tq5XaSejcvKpEtxaruKNxAKzBosx4P0ckOLvrc2D7F3W1nsV7LinZIIRWldkNH7cG3WKOSfbHT7BSE645EZOTOTERE645IxL3o7Nb_4d89A68xn1d7Ousla-Sypolw82SnkjxDTs573tj_N29x8DyNPvl49l_QCmabXk</recordid><startdate>199001</startdate><enddate>199001</enddate><creator>Gardiner, S.M.</creator><creator>Compton, A.M.</creator><creator>Bennett, T.</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</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><scope>5PM</scope></search><sort><creationdate>199001</creationdate><title>Regional haemodynamic effects of endothelin‐1 and endothelin‐3 in conscious Long Evans and Brattleboro rats</title><author>Gardiner, S.M. ; Compton, A.M. ; Bennett, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4222-efb7e54c448b44c8187790956804dc69184da3ed0712c144bd8390645d8d584d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiovascular system</topic><topic>Endothelins</topic><topic>Heart Rate - drug effects</topic><topic>Hindlimb - blood supply</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Peptides - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Brattleboro</topic><topic>Regional Blood Flow - drug effects</topic><topic>Renal Circulation - drug effects</topic><topic>Rheology</topic><topic>Splanchnic Circulation - drug effects</topic><topic>Vasoconstriction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gardiner, S.M.</creatorcontrib><creatorcontrib>Compton, A.M.</creatorcontrib><creatorcontrib>Bennett, 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><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gardiner, S.M.</au><au>Compton, A.M.</au><au>Bennett, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regional haemodynamic effects of endothelin‐1 and endothelin‐3 in conscious Long Evans and Brattleboro rats</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1990-01</date><risdate>1990</risdate><volume>99</volume><issue>1</issue><spage>107</spage><epage>112</epage><pages>107-112</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1 The regional haemodynamic effects of bolus doses (4 and 40 pmol) and infusions (12 and 120 pmol h−1) of endothelin‐1 and endothelin‐3 were assessed in conscious, Long Evans and Brattleboro (i.e. vasopressin‐deficient) rats, chronically‐instrumented with pulsed Doppler flow probes. 2 In both strains of rat the lower bolus dose of endothelin‐1 caused only a slight pressor effect, but there were marked renal and mesenteric vasoconstrictions and hindquarters vasodilatation. 3 The lower bolus dose of endothelin‐3 did not affect blood pressure significantly, although the changes in regional haemodynamics were qualitatively similar to those seen following endothelin‐1 in Long Evans and Brattleboro rats. 4 The higher dose of endothelin‐1 caused an initial hypotension accompanied by substantial hindquarters vasodilatations in Long Evans and Brattleboro rats. Subsequently, in both strains, there was a rise in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstrictions. 5 The higher bolus dose of endothelin‐3 caused initial hypotension and hindquarters vasodilatation similar to those seen with endothelin‐1. However, the subsequent pressor effect was less with endothelin‐3, as was the renal vasoconstriction, and it did not cause any increase in hindquarters vascular resistance. 6 Infusion of endothelin‐1 at the lower rate (12 pmol h−1) caused renal and mesenteric vasoconstrictions in both strains of rat, whereas endothelin‐3 at this rate caused only mesenteric vasoconstriction. 7 Infusion of endothelin‐1 at the higher rate (120 pmol h−1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. Endothelin‐3 had a smaller pressor effect and a lesser constrictor action on the renal and mesenteric vascular beds; it did not constrict the hindquarters vascular bed. 8 These results show, that in conscious Long Evans and Brattleboro rats, the initial depressor effects of the higher bolus doses of endothelin‐1 and −3 were similar, and, hence, not influenced by the absence of endogenous vasopressin. Endothelin‐1 and −3 appear equipotent in their initial hyperaemic vasodilator effects in the hindquarters vasculature in both strains, making it unlikely that this effect is dependent on the release of atrial natriuretic peptide (ANP), since ANP does not cause significant increases in hindquarters blood flow in Brattleboro rats. The greater delayed pressor effect of endothelin‐1 is associated with its more marked vasoconstrictor effects on renal and mesenteric vascular beds and is accentuated, relative to endothelin‐3, by the lack of a constrictor effect of endothelin‐3 in the hindquarters vasculature.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>2139584</pmid><doi>10.1111/j.1476-5381.1990.tb14662.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Biological and medical sciences
Blood Pressure - drug effects
Cardiovascular system
Endothelins
Heart Rate - drug effects
Hindlimb - blood supply
Male
Medical sciences
Miscellaneous
Peptides - pharmacology
Pharmacology. Drug treatments
Rats
Rats, Brattleboro
Regional Blood Flow - drug effects
Renal Circulation - drug effects
Rheology
Splanchnic Circulation - drug effects
Vasoconstriction - drug effects
title Regional haemodynamic effects of endothelin‐1 and endothelin‐3 in conscious Long Evans and Brattleboro rats
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