Juxtamedullary Afferent Arteriolar Responses to P1 and P2 Purinergic Stimulation
We assessed the responsiveness of rat juxtamedullary afferent arterioles to purinergic stimulation using the in vitro blood-perfused juxtamedullary nephron technique combined with videomicroscopy to allow direct measurement of arteriolar inside diameter. To minimize the contribution of endogenously...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1991-06, Vol.17 (6, Part 2), p.1033-1037 |
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| container_issue | 6, Part 2 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Inscho, Edward W Carmines, Pamela K Navar, L Gabriel |
| description | We assessed the responsiveness of rat juxtamedullary afferent arterioles to purinergic stimulation using the in vitro blood-perfused juxtamedullary nephron technique combined with videomicroscopy to allow direct measurement of arteriolar inside diameter. To minimize the contribution of endogenously formed angiotensin II, all rats were pretreated with enalaprilat (2 mg i.v.) for 3d minutes before the right kidney was isolated and prepared for study. Renal perfusion pressure was set at 110 mm Hg and held constant Afferent arteriolar diameter averaged 20.9±0.8 μm (n=41) under control conditions. Exposure to 1.0 μM 2-chloroadenosine induced a significant (11.1 ±3.2%) reduction in vessel diameter, whereas a 100 μ:M concentration induced an afferent vasodilation (7.6±1.5%;pμ0.05). These data are consistent with the preferential stimulation of high affinity constrictor adenosine receptors (A1) at lower concentrations and activation of lower affinity vasodilator adenosine receptors (A2) at higher concentrations. In contrast, ATP elicited a significant afferent vasoeonstriction of approximately 9.2%, 12.9%, and 10.0% at concentrations in the range of 1–100 μM (p |
| doi_str_mv | 10.1161/01.hyp.17.6.1033 |
| format | Article |
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To minimize the contribution of endogenously formed angiotensin II, all rats were pretreated with enalaprilat (2 mg i.v.) for 3d minutes before the right kidney was isolated and prepared for study. Renal perfusion pressure was set at 110 mm Hg and held constant Afferent arteriolar diameter averaged 20.9±0.8 μm (n=41) under control conditions. Exposure to 1.0 μM 2-chloroadenosine induced a significant (11.1 ±3.2%) reduction in vessel diameter, whereas a 100 μ:M concentration induced an afferent vasodilation (7.6±1.5%;pμ0.05). These data are consistent with the preferential stimulation of high affinity constrictor adenosine receptors (A1) at lower concentrations and activation of lower affinity vasodilator adenosine receptors (A2) at higher concentrations. In contrast, ATP elicited a significant afferent vasoeonstriction of approximately 9.2%, 12.9%, and 10.0% at concentrations in the range of 1–100 μM (p<0.05). Treatment with ADP, at concentrations up to 100 μM, failed to alter vessel caliber significantly. Furthermore, the nonhydrolyzable ATP analogue α,βmethylene ATP produced a rapid and potent vasoeonstriction, which mimicked the response to ATP. These data reveal the presence of both adenosine-sensitive P1 and ATP-sensitive P2 purinergic receptors on rat juxtamedullary afferent arterioles and demonstrate that ATP can induce afferent arteriolar vasoeonstriction directly without first requiring hydrolysis to adenosine.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.17.6.1033</identifier><identifier>PMID: 2045147</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>2-Chloroadenosine - pharmacology ; Adenosine Diphosphate - pharmacology ; Adenosine Triphosphate - analogs & derivatives ; Adenosine Triphosphate - pharmacology ; Animals ; Arterioles - drug effects ; Arterioles - physiology ; Biological and medical sciences ; Endocrine kidney. Renin-angiotensin-aldosterone system ; Fundamental and applied biological sciences. Psychology ; Male ; Purines - metabolism ; Rats ; Renal Circulation - drug effects ; Renal Circulation - physiology ; Time Factors ; Vasoconstriction ; Vertebrates: endocrinology</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1991-06, Vol.17 (6, Part 2), p.1033-1037</ispartof><rights>1991 American Heart Association, Inc.</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5191-400ad5eccab9e87b9893f3e22554d8bd8c35d94c8be2c41d2bb688ec852f4fbb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,776,780,785,786,3673,23910,23911,25119,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19795037$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2045147$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Inscho, Edward W</creatorcontrib><creatorcontrib>Carmines, Pamela K</creatorcontrib><creatorcontrib>Navar, L Gabriel</creatorcontrib><title>Juxtamedullary Afferent Arteriolar Responses to P1 and P2 Purinergic Stimulation</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>We assessed the responsiveness of rat juxtamedullary afferent arterioles to purinergic stimulation using the in vitro blood-perfused juxtamedullary nephron technique combined with videomicroscopy to allow direct measurement of arteriolar inside diameter. To minimize the contribution of endogenously formed angiotensin II, all rats were pretreated with enalaprilat (2 mg i.v.) for 3d minutes before the right kidney was isolated and prepared for study. Renal perfusion pressure was set at 110 mm Hg and held constant Afferent arteriolar diameter averaged 20.9±0.8 μm (n=41) under control conditions. Exposure to 1.0 μM 2-chloroadenosine induced a significant (11.1 ±3.2%) reduction in vessel diameter, whereas a 100 μ:M concentration induced an afferent vasodilation (7.6±1.5%;pμ0.05). These data are consistent with the preferential stimulation of high affinity constrictor adenosine receptors (A1) at lower concentrations and activation of lower affinity vasodilator adenosine receptors (A2) at higher concentrations. In contrast, ATP elicited a significant afferent vasoeonstriction of approximately 9.2%, 12.9%, and 10.0% at concentrations in the range of 1–100 μM (p<0.05). Treatment with ADP, at concentrations up to 100 μM, failed to alter vessel caliber significantly. Furthermore, the nonhydrolyzable ATP analogue α,βmethylene ATP produced a rapid and potent vasoeonstriction, which mimicked the response to ATP. These data reveal the presence of both adenosine-sensitive P1 and ATP-sensitive P2 purinergic receptors on rat juxtamedullary afferent arterioles and demonstrate that ATP can induce afferent arteriolar vasoeonstriction directly without first requiring hydrolysis to adenosine.</description><subject>2-Chloroadenosine - pharmacology</subject><subject>Adenosine Diphosphate - pharmacology</subject><subject>Adenosine Triphosphate - analogs & derivatives</subject><subject>Adenosine Triphosphate - pharmacology</subject><subject>Animals</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - physiology</subject><subject>Biological and medical sciences</subject><subject>Endocrine kidney. Renin-angiotensin-aldosterone system</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Male</subject><subject>Purines - metabolism</subject><subject>Rats</subject><subject>Renal Circulation - drug effects</subject><subject>Renal Circulation - physiology</subject><subject>Time Factors</subject><subject>Vasoconstriction</subject><subject>Vertebrates: endocrinology</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE2L1EAQhhtR1tnVuxchF70lVvVH0n0cFnVXFgx-gJ6a7k7FiWaSsTth3X9vDzNoQVFQ9dZL1cPYC4QKscY3gNXu4VBhU9UVghCP2AYVl6VUtXjMNoBGlgbx21N2mdJPAJRSNhfsgoNUKJsNaz-sfxa3p24dRxcfim3fU6RpKbZxoTjMuVl8onSYp0SpWOaixcJNXdHyol3jMFH8MYTi8zLs19Etwzw9Y096NyZ6fq5X7Ou7t1-ub8q7j-9vr7d3ZVBosJQArlMUgvOGdOONNqIXxLlSstO-00GozsigPfEgsePe11pT0Ir3svdeXLHXJ99DnH-vlBa7H1Kg_MVE85qshhpQSMhCOAlDnFOK1NtDHPb5V4tgjxAtoL353lpsbG2PEPPKy7P36jOafwtnann-6jx3Kbixj24KQ_rvaxqjQBx18qS7n8dMM_0a13uKdkduXHYWckhe6xKNwXwtQJlToPgLelGKhA</recordid><startdate>199106</startdate><enddate>199106</enddate><creator>Inscho, Edward W</creator><creator>Carmines, Pamela K</creator><creator>Navar, L Gabriel</creator><general>American Heart Association, Inc</general><general>Lippincott</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>199106</creationdate><title>Juxtamedullary Afferent Arteriolar Responses to P1 and P2 Purinergic Stimulation</title><author>Inscho, Edward W ; Carmines, Pamela K ; Navar, L Gabriel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5191-400ad5eccab9e87b9893f3e22554d8bd8c35d94c8be2c41d2bb688ec852f4fbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>2-Chloroadenosine - pharmacology</topic><topic>Adenosine Diphosphate - pharmacology</topic><topic>Adenosine Triphosphate - analogs & derivatives</topic><topic>Adenosine Triphosphate - pharmacology</topic><topic>Animals</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - physiology</topic><topic>Biological and medical sciences</topic><topic>Endocrine kidney. Renin-angiotensin-aldosterone system</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Male</topic><topic>Purines - metabolism</topic><topic>Rats</topic><topic>Renal Circulation - drug effects</topic><topic>Renal Circulation - physiology</topic><topic>Time Factors</topic><topic>Vasoconstriction</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Inscho, Edward W</creatorcontrib><creatorcontrib>Carmines, Pamela K</creatorcontrib><creatorcontrib>Navar, L Gabriel</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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Inscho, Edward W</au><au>Carmines, Pamela K</au><au>Navar, L Gabriel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Juxtamedullary Afferent Arteriolar Responses to P1 and P2 Purinergic Stimulation</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1991-06</date><risdate>1991</risdate><volume>17</volume><issue>6, Part 2</issue><spage>1033</spage><epage>1037</epage><pages>1033-1037</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>We assessed the responsiveness of rat juxtamedullary afferent arterioles to purinergic stimulation using the in vitro blood-perfused juxtamedullary nephron technique combined with videomicroscopy to allow direct measurement of arteriolar inside diameter. To minimize the contribution of endogenously formed angiotensin II, all rats were pretreated with enalaprilat (2 mg i.v.) for 3d minutes before the right kidney was isolated and prepared for study. Renal perfusion pressure was set at 110 mm Hg and held constant Afferent arteriolar diameter averaged 20.9±0.8 μm (n=41) under control conditions. Exposure to 1.0 μM 2-chloroadenosine induced a significant (11.1 ±3.2%) reduction in vessel diameter, whereas a 100 μ:M concentration induced an afferent vasodilation (7.6±1.5%;pμ0.05). These data are consistent with the preferential stimulation of high affinity constrictor adenosine receptors (A1) at lower concentrations and activation of lower affinity vasodilator adenosine receptors (A2) at higher concentrations. In contrast, ATP elicited a significant afferent vasoeonstriction of approximately 9.2%, 12.9%, and 10.0% at concentrations in the range of 1–100 μM (p<0.05). Treatment with ADP, at concentrations up to 100 μM, failed to alter vessel caliber significantly. Furthermore, the nonhydrolyzable ATP analogue α,βmethylene ATP produced a rapid and potent vasoeonstriction, which mimicked the response to ATP. These data reveal the presence of both adenosine-sensitive P1 and ATP-sensitive P2 purinergic receptors on rat juxtamedullary afferent arterioles and demonstrate that ATP can induce afferent arteriolar vasoeonstriction directly without first requiring hydrolysis to adenosine.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>2045147</pmid><doi>10.1161/01.hyp.17.6.1033</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | 2-Chloroadenosine - pharmacology Adenosine Diphosphate - pharmacology Adenosine Triphosphate - analogs & derivatives Adenosine Triphosphate - pharmacology Animals Arterioles - drug effects Arterioles - physiology Biological and medical sciences Endocrine kidney. Renin-angiotensin-aldosterone system Fundamental and applied biological sciences. Psychology Male Purines - metabolism Rats Renal Circulation - drug effects Renal Circulation - physiology Time Factors Vasoconstriction Vertebrates: endocrinology |
| title | Juxtamedullary Afferent Arteriolar Responses to P1 and P2 Purinergic Stimulation |
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