The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit
1 A study was undertaken in the anaesthetized rabbit to classify the α‐adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, sig...
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| Veröffentlicht in: | British journal of pharmacology 1985-03, Vol.84 (3), p.715-724 |
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| description | 1
A study was undertaken in the anaesthetized rabbit to classify the α‐adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective α1‐adrenoceptor antagonist, prazosin, but not by the selective α2‐adrenoceptor antagonist, idazoxan.
2
Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan.
3
Intrarenal administration of the selective α‐adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%.
4
Infusion of guanabenz (selective α2‐adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11% to 15%, while at doses which decreased blood flow by 7%, these other variables did not change.
5
Administration of UK 14304 (selective α2‐adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%.
6
Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs.
7
These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of α1‐ but not α2‐adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either α1‐ or α2‐adrenoceptors. |
| doi_str_mv | 10.1111/j.1476-5381.1985.tb16154.x |
| format | Article |
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A study was undertaken in the anaesthetized rabbit to classify the α‐adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective α1‐adrenoceptor antagonist, prazosin, but not by the selective α2‐adrenoceptor antagonist, idazoxan.
2
Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan.
3
Intrarenal administration of the selective α‐adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%.
4
Infusion of guanabenz (selective α2‐adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11% to 15%, while at doses which decreased blood flow by 7%, these other variables did not change.
5
Administration of UK 14304 (selective α2‐adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%.
6
Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs.
7
These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of α1‐ but not α2‐adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either α1‐ or α2‐adrenoceptors.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.1985.tb16154.x</identifier><identifier>PMID: 2859065</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adrenergic alpha-Antagonists - pharmacology ; alpha -adrenergic ; Anesthesia ; Animals ; Antihypertensive Agents - pharmacology ; Biological and medical sciences ; Brimonidine Tartrate ; Dioxanes - pharmacology ; Fundamental and applied biological sciences. Psychology ; Guanabenz - pharmacology ; Hemodynamics - drug effects ; Idazoxan ; kidney ; Kidney - drug effects ; Kidney Tubules - metabolism ; Male ; Methoxamine - pharmacology ; Natriuresis - drug effects ; Norepinephrine - metabolism ; Norepinephrine - pharmacology ; Phenylephrine - pharmacology ; Prazosin - pharmacology ; Quinoxalines - pharmacology ; Rabbits ; Receptors, Adrenergic, alpha - physiology ; renin ; Renin - metabolism ; sodium ; Sodium - metabolism ; Vertebrates: urinary system</subject><ispartof>British journal of pharmacology, 1985-03, Vol.84 (3), p.715-724</ispartof><rights>1985 British Pharmacological Society</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5385-7697197bca1b286179df4f95eadb0d99773eca575b783e0ca8539441df9e5bba3</citedby><cites>FETCH-LOGICAL-c5385-7697197bca1b286179df4f95eadb0d99773eca575b783e0ca8539441df9e5bba3</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/PMC1987143/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1987143/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8481320$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2859065$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hesse, I.F.A.</creatorcontrib><creatorcontrib>Johns, Edward J.</creatorcontrib><title>The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
A study was undertaken in the anaesthetized rabbit to classify the α‐adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective α1‐adrenoceptor antagonist, prazosin, but not by the selective α2‐adrenoceptor antagonist, idazoxan.
2
Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan.
3
Intrarenal administration of the selective α‐adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%.
4
Infusion of guanabenz (selective α2‐adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11% to 15%, while at doses which decreased blood flow by 7%, these other variables did not change.
5
Administration of UK 14304 (selective α2‐adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%.
6
Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs.
7
These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of α1‐ but not α2‐adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either α1‐ or α2‐adrenoceptors.</description><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>alpha -adrenergic</subject><subject>Anesthesia</subject><subject>Animals</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brimonidine Tartrate</subject><subject>Dioxanes - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guanabenz - pharmacology</subject><subject>Hemodynamics - drug effects</subject><subject>Idazoxan</subject><subject>kidney</subject><subject>Kidney - drug effects</subject><subject>Kidney Tubules - metabolism</subject><subject>Male</subject><subject>Methoxamine - pharmacology</subject><subject>Natriuresis - drug effects</subject><subject>Norepinephrine - metabolism</subject><subject>Norepinephrine - pharmacology</subject><subject>Phenylephrine - pharmacology</subject><subject>Prazosin - pharmacology</subject><subject>Quinoxalines - pharmacology</subject><subject>Rabbits</subject><subject>Receptors, Adrenergic, alpha - physiology</subject><subject>renin</subject><subject>Renin - metabolism</subject><subject>sodium</subject><subject>Sodium - metabolism</subject><subject>Vertebrates: urinary system</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkcFu1DAQhi0EKtvCIyBFCHFLsDdxbHNAhYrSSpXgUM7W2Jm0XmXjxU5oe-sj8Cq8CA_RJ8Hppis4IXyxNP83v2bmJ-QlowVL782qYJWoc15KVjAleTEYVjNeFdePyGInPSYLSqnIGZPyKdmPcUVpEgXfI3tLyRWt-YJcnV9iFnyHmW-zXz_vbn9AE7D3FjeDDzFzfTZMBF6MHQzO9xOXAOiyYTSpFrLoGzeuUxFM9GFzD0HfTFTqjmgD3tcerMAYNzwjT1roIj6f_wPy9fjj-dFJfvb50-nR-7PcphV4LmolmBLGAjNLWTOhmrZqFUdoDG2UEqJEC1xwI2SJ1ILkpaoq1rQKuTFQHpB3W9_NaNbYWOyHAJ3eBLeGcKM9OP230rtLfeG_63RXwaoyGbyeDYL_NmIc9NpFi10HPfoxalHTWlJV_xNkFZW1qngC325BG3yMAdvdNIzqKV-90lOIegpxmoPrOV99nZpf_LnPrnUONOmvZh2iha4N0FsXd5isJCuXNGGHW-zKdXjzHwPoD19OWAqFl78Bb5THvA</recordid><startdate>198503</startdate><enddate>198503</enddate><creator>Hesse, I.F.A.</creator><creator>Johns, Edward J.</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><general>Nature Publishing Group</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>7SQ</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>198503</creationdate><title>The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit</title><author>Hesse, I.F.A. ; Johns, Edward J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5385-7697197bca1b286179df4f95eadb0d99773eca575b783e0ca8539441df9e5bba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>alpha -adrenergic</topic><topic>Anesthesia</topic><topic>Animals</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brimonidine Tartrate</topic><topic>Dioxanes - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guanabenz - pharmacology</topic><topic>Hemodynamics - drug effects</topic><topic>Idazoxan</topic><topic>kidney</topic><topic>Kidney - drug effects</topic><topic>Kidney Tubules - metabolism</topic><topic>Male</topic><topic>Methoxamine - pharmacology</topic><topic>Natriuresis - drug effects</topic><topic>Norepinephrine - metabolism</topic><topic>Norepinephrine - pharmacology</topic><topic>Phenylephrine - pharmacology</topic><topic>Prazosin - pharmacology</topic><topic>Quinoxalines - pharmacology</topic><topic>Rabbits</topic><topic>Receptors, Adrenergic, alpha - physiology</topic><topic>renin</topic><topic>Renin - metabolism</topic><topic>sodium</topic><topic>Sodium - metabolism</topic><topic>Vertebrates: urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hesse, I.F.A.</creatorcontrib><creatorcontrib>Johns, Edward J.</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>Endocrinology Abstracts</collection><collection>Neurosciences Abstracts</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>Hesse, I.F.A.</au><au>Johns, Edward J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1985-03</date><risdate>1985</risdate><volume>84</volume><issue>3</issue><spage>715</spage><epage>724</epage><pages>715-724</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
A study was undertaken in the anaesthetized rabbit to classify the α‐adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective α1‐adrenoceptor antagonist, prazosin, but not by the selective α2‐adrenoceptor antagonist, idazoxan.
2
Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan.
3
Intrarenal administration of the selective α‐adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%.
4
Infusion of guanabenz (selective α2‐adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11% to 15%, while at doses which decreased blood flow by 7%, these other variables did not change.
5
Administration of UK 14304 (selective α2‐adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%.
6
Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs.
7
These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of α1‐ but not α2‐adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either α1‐ or α2‐adrenoceptors.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>2859065</pmid><doi>10.1111/j.1476-5381.1985.tb16154.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenergic alpha-Antagonists - pharmacology alpha -adrenergic Anesthesia Animals Antihypertensive Agents - pharmacology Biological and medical sciences Brimonidine Tartrate Dioxanes - pharmacology Fundamental and applied biological sciences. Psychology Guanabenz - pharmacology Hemodynamics - drug effects Idazoxan kidney Kidney - drug effects Kidney Tubules - metabolism Male Methoxamine - pharmacology Natriuresis - drug effects Norepinephrine - metabolism Norepinephrine - pharmacology Phenylephrine - pharmacology Prazosin - pharmacology Quinoxalines - pharmacology Rabbits Receptors, Adrenergic, alpha - physiology renin Renin - metabolism sodium Sodium - metabolism Vertebrates: urinary system |
| title | The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit |
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