Pentosan polysulfate preserves renal microvascular P2X1 receptor reactivity and autoregulatory behavior in DOCA-salt hypertensive rats
Inflammation contributes to ANG II-associated impairment of renal autoregulation and microvascular P2X1 receptor signaling, but its role in renal autoregulation in mineralocorticoid-induced hypertension is unknown. Autoregulatory behavior was assessed using the blood-perfused juxtamedullary nephron...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2016-03, Vol.310 (6), p.F456-F465 |
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| container_title | American journal of physiology. Renal physiology |
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| creator | Guan, Zhengrong Singletary, Sean T Cha, Haword Van Beusecum, Justin P Cook, Anthony K Pollock, Jennifer S Pollock, David M Inscho, Edward W |
| description | Inflammation contributes to ANG II-associated impairment of renal autoregulation and microvascular P2X1 receptor signaling, but its role in renal autoregulation in mineralocorticoid-induced hypertension is unknown. Autoregulatory behavior was assessed using the blood-perfused juxtamedullary nephron preparation. Hypertension was induced in uninephrectomized control rats (UNx) by subcutaneous implantation of a DOCA pellet plus administration of 1% NaCl in the drinking water (DOCA-salt) for 3 wk. DOCA-salt rats developed hypertension that was unaltered by anti-inflammatory treatment with pentosan polysulfate (DOCA-salt+PPS) but was suppressed with "triple therapy" (hydrochlorothiazide, hydralazine, and reserpine; DOCA-salt+TTx). Baseline arteriolar diameters were similar across all groups. UNx rats exhibited pressure-dependent vasoconstriction with diameters declining to 69 ± 2% of control at 170 mmHg, indicating intact autoregulation. DOCA-salt treatment significantly blunted this pressure-mediated vasoconstriction. Diameters remained between 91 ± 4 and 98 ± 3% of control over 65-170 mmHg, indicating impaired autoregulation. In contrast, pressure-mediated vasoconstriction was preserved in DOCA-salt+PPS and DOCA-salt+TTx rats, reaching 77 ± 7 and 75 ± 3% of control at 170 mmHg, respectively. ATP is required for autoregulation via P2X1 receptor activation. ATP- and β,γ-methylene ATP (P2X1 receptor agonist)-mediated vasoconstriction were markedly attenuated in DOCA-salt rats compared with UNx (P < 0.05), but significantly improved by PPS or TTx (P < 0.05 vs. DOCA-salt) treatment. Arteriolar responses to adenosine and UTP (P2Y2 receptor agonist) were unaffected by DOCA-salt treatment. PPS and TTx significantly reduced MCP-1 and protein excretion in DOCA-salt rats. These results support the hypothesis that hypertension triggers inflammatory cascades but anti-inflammatory treatment preserves renal autoregulation in DOCA-salt rats, most likely by normalizing renal microvascular reactivity to P2X1 receptor activation. |
| doi_str_mv | 10.1152/ajprenal.00110.2015 |
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Autoregulatory behavior was assessed using the blood-perfused juxtamedullary nephron preparation. Hypertension was induced in uninephrectomized control rats (UNx) by subcutaneous implantation of a DOCA pellet plus administration of 1% NaCl in the drinking water (DOCA-salt) for 3 wk. DOCA-salt rats developed hypertension that was unaltered by anti-inflammatory treatment with pentosan polysulfate (DOCA-salt+PPS) but was suppressed with "triple therapy" (hydrochlorothiazide, hydralazine, and reserpine; DOCA-salt+TTx). Baseline arteriolar diameters were similar across all groups. UNx rats exhibited pressure-dependent vasoconstriction with diameters declining to 69 ± 2% of control at 170 mmHg, indicating intact autoregulation. DOCA-salt treatment significantly blunted this pressure-mediated vasoconstriction. Diameters remained between 91 ± 4 and 98 ± 3% of control over 65-170 mmHg, indicating impaired autoregulation. In contrast, pressure-mediated vasoconstriction was preserved in DOCA-salt+PPS and DOCA-salt+TTx rats, reaching 77 ± 7 and 75 ± 3% of control at 170 mmHg, respectively. ATP is required for autoregulation via P2X1 receptor activation. ATP- and β,γ-methylene ATP (P2X1 receptor agonist)-mediated vasoconstriction were markedly attenuated in DOCA-salt rats compared with UNx (P < 0.05), but significantly improved by PPS or TTx (P < 0.05 vs. DOCA-salt) treatment. Arteriolar responses to adenosine and UTP (P2Y2 receptor agonist) were unaffected by DOCA-salt treatment. PPS and TTx significantly reduced MCP-1 and protein excretion in DOCA-salt rats. These results support the hypothesis that hypertension triggers inflammatory cascades but anti-inflammatory treatment preserves renal autoregulation in DOCA-salt rats, most likely by normalizing renal microvascular reactivity to P2X1 receptor activation.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00110.2015</identifier><identifier>PMID: 26697978</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Adenosine Triphosphate - analogs & derivatives ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Antihypertensive Agents - pharmacology ; Antihypertensive Agents - therapeutic use ; Arterioles - drug effects ; Arterioles - metabolism ; Blood Pressure ; Chemokine CCL2 - urine ; Disease Models, Animal ; Homeostasis - drug effects ; Hydralazine - pharmacology ; Hydralazine - therapeutic use ; Hydrochlorothiazide - pharmacology ; Hydrochlorothiazide - therapeutic use ; Hypertension - drug therapy ; Hypertension - etiology ; Hypertension - metabolism ; Hypertension - physiopathology ; In Vitro Techniques ; Kidney - blood supply ; Kidney - drug effects ; Kidney - metabolism ; Male ; Pentosan Sulfuric Polyester - pharmacology ; Pentosan Sulfuric Polyester - therapeutic use ; Proteinuria - drug therapy ; Rats, Sprague-Dawley ; Receptors, Purinergic P2X1 - metabolism ; Reserpine - pharmacology ; Reserpine - therapeutic use ; Vasoconstriction</subject><ispartof>American journal of physiology. Renal physiology, 2016-03, Vol.310 (6), p.F456-F465</ispartof><rights>Copyright © 2016 the American Physiological Society.</rights><rights>Copyright © 2016 the American Physiological Society 2016 American Physiological Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27925,27926</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26697978$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guan, Zhengrong</creatorcontrib><creatorcontrib>Singletary, Sean T</creatorcontrib><creatorcontrib>Cha, Haword</creatorcontrib><creatorcontrib>Van Beusecum, Justin P</creatorcontrib><creatorcontrib>Cook, Anthony K</creatorcontrib><creatorcontrib>Pollock, Jennifer S</creatorcontrib><creatorcontrib>Pollock, David M</creatorcontrib><creatorcontrib>Inscho, Edward W</creatorcontrib><title>Pentosan polysulfate preserves renal microvascular P2X1 receptor reactivity and autoregulatory behavior in DOCA-salt hypertensive rats</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Inflammation contributes to ANG II-associated impairment of renal autoregulation and microvascular P2X1 receptor signaling, but its role in renal autoregulation in mineralocorticoid-induced hypertension is unknown. Autoregulatory behavior was assessed using the blood-perfused juxtamedullary nephron preparation. Hypertension was induced in uninephrectomized control rats (UNx) by subcutaneous implantation of a DOCA pellet plus administration of 1% NaCl in the drinking water (DOCA-salt) for 3 wk. DOCA-salt rats developed hypertension that was unaltered by anti-inflammatory treatment with pentosan polysulfate (DOCA-salt+PPS) but was suppressed with "triple therapy" (hydrochlorothiazide, hydralazine, and reserpine; DOCA-salt+TTx). Baseline arteriolar diameters were similar across all groups. UNx rats exhibited pressure-dependent vasoconstriction with diameters declining to 69 ± 2% of control at 170 mmHg, indicating intact autoregulation. DOCA-salt treatment significantly blunted this pressure-mediated vasoconstriction. Diameters remained between 91 ± 4 and 98 ± 3% of control over 65-170 mmHg, indicating impaired autoregulation. In contrast, pressure-mediated vasoconstriction was preserved in DOCA-salt+PPS and DOCA-salt+TTx rats, reaching 77 ± 7 and 75 ± 3% of control at 170 mmHg, respectively. ATP is required for autoregulation via P2X1 receptor activation. ATP- and β,γ-methylene ATP (P2X1 receptor agonist)-mediated vasoconstriction were markedly attenuated in DOCA-salt rats compared with UNx (P < 0.05), but significantly improved by PPS or TTx (P < 0.05 vs. DOCA-salt) treatment. Arteriolar responses to adenosine and UTP (P2Y2 receptor agonist) were unaffected by DOCA-salt treatment. PPS and TTx significantly reduced MCP-1 and protein excretion in DOCA-salt rats. These results support the hypothesis that hypertension triggers inflammatory cascades but anti-inflammatory treatment preserves renal autoregulation in DOCA-salt rats, most likely by normalizing renal microvascular reactivity to P2X1 receptor activation.</description><subject>Adenosine Triphosphate - analogs & derivatives</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - metabolism</subject><subject>Blood Pressure</subject><subject>Chemokine CCL2 - urine</subject><subject>Disease Models, Animal</subject><subject>Homeostasis - drug effects</subject><subject>Hydralazine - pharmacology</subject><subject>Hydralazine - therapeutic use</subject><subject>Hydrochlorothiazide - pharmacology</subject><subject>Hydrochlorothiazide - therapeutic use</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - etiology</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Kidney - blood supply</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Pentosan Sulfuric Polyester - pharmacology</subject><subject>Pentosan Sulfuric Polyester - therapeutic use</subject><subject>Proteinuria - drug therapy</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Purinergic P2X1 - metabolism</subject><subject>Reserpine - pharmacology</subject><subject>Reserpine - therapeutic use</subject><subject>Vasoconstriction</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkEuLFTEQhYMozkN_gSBZuukxj86jN8JwfYwwMLNQmF1TndSdmyG3u03SDf0H_N1GHUVXdahz-A5VhLzi7IJzJd7Cw5xwhHjBGK87wbh6Qk6rIxreav206k7yxipzd0LOcn5gP4OCPycnQuvOdMaeku-3OJYpw0jnKW55iXsoSCs4Y1ox018N9BhcmlbIbomQ6K2449VwOJcpVQGuhDWUjcLoKSx1ifc1WOdGBzzAGmosjPT9ze6yyRALPWwzpoJjDivSBCW_IM_2EDO-fJzn5OvHD192V831zafPu8vrZuaWl8Z5IRmgd5Jzbr0zvPWKDV5py6wElOitHYyXrd4jUwKV0h3TrHWIng97eU7e_ebOy3CsnHp8gtjPKRwhbf0Eof_fGcOhv5_WvjWdFoZVwJtHQJq-LZhLfwzZYYww4rTknhvTcmWl7Wr09b9df0v-PF_-AEyXjhA</recordid><startdate>20160315</startdate><enddate>20160315</enddate><creator>Guan, Zhengrong</creator><creator>Singletary, Sean T</creator><creator>Cha, Haword</creator><creator>Van Beusecum, Justin P</creator><creator>Cook, Anthony K</creator><creator>Pollock, Jennifer S</creator><creator>Pollock, David M</creator><creator>Inscho, Edward W</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160315</creationdate><title>Pentosan polysulfate preserves renal microvascular P2X1 receptor reactivity and autoregulatory behavior in DOCA-salt hypertensive rats</title><author>Guan, Zhengrong ; Singletary, Sean T ; Cha, Haword ; Van Beusecum, Justin P ; Cook, Anthony K ; Pollock, Jennifer S ; Pollock, David M ; Inscho, Edward W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p181t-cd230aedc31118dc714d50bd568083ae3ed88b7d346fe052e55690604ceed1bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenosine Triphosphate - analogs & derivatives</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - metabolism</topic><topic>Blood Pressure</topic><topic>Chemokine CCL2 - urine</topic><topic>Disease Models, Animal</topic><topic>Homeostasis - drug effects</topic><topic>Hydralazine - pharmacology</topic><topic>Hydralazine - therapeutic use</topic><topic>Hydrochlorothiazide - pharmacology</topic><topic>Hydrochlorothiazide - therapeutic use</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - etiology</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Kidney - blood supply</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Pentosan Sulfuric Polyester - pharmacology</topic><topic>Pentosan Sulfuric Polyester - therapeutic use</topic><topic>Proteinuria - drug therapy</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Purinergic P2X1 - metabolism</topic><topic>Reserpine - pharmacology</topic><topic>Reserpine - therapeutic use</topic><topic>Vasoconstriction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guan, Zhengrong</creatorcontrib><creatorcontrib>Singletary, Sean T</creatorcontrib><creatorcontrib>Cha, Haword</creatorcontrib><creatorcontrib>Van Beusecum, Justin P</creatorcontrib><creatorcontrib>Cook, Anthony K</creatorcontrib><creatorcontrib>Pollock, Jennifer S</creatorcontrib><creatorcontrib>Pollock, David M</creatorcontrib><creatorcontrib>Inscho, Edward W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guan, Zhengrong</au><au>Singletary, Sean T</au><au>Cha, Haword</au><au>Van Beusecum, Justin P</au><au>Cook, Anthony K</au><au>Pollock, Jennifer S</au><au>Pollock, David M</au><au>Inscho, Edward W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pentosan polysulfate preserves renal microvascular P2X1 receptor reactivity and autoregulatory behavior in DOCA-salt hypertensive rats</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2016-03-15</date><risdate>2016</risdate><volume>310</volume><issue>6</issue><spage>F456</spage><epage>F465</epage><pages>F456-F465</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Inflammation contributes to ANG II-associated impairment of renal autoregulation and microvascular P2X1 receptor signaling, but its role in renal autoregulation in mineralocorticoid-induced hypertension is unknown. Autoregulatory behavior was assessed using the blood-perfused juxtamedullary nephron preparation. Hypertension was induced in uninephrectomized control rats (UNx) by subcutaneous implantation of a DOCA pellet plus administration of 1% NaCl in the drinking water (DOCA-salt) for 3 wk. DOCA-salt rats developed hypertension that was unaltered by anti-inflammatory treatment with pentosan polysulfate (DOCA-salt+PPS) but was suppressed with "triple therapy" (hydrochlorothiazide, hydralazine, and reserpine; DOCA-salt+TTx). Baseline arteriolar diameters were similar across all groups. UNx rats exhibited pressure-dependent vasoconstriction with diameters declining to 69 ± 2% of control at 170 mmHg, indicating intact autoregulation. DOCA-salt treatment significantly blunted this pressure-mediated vasoconstriction. Diameters remained between 91 ± 4 and 98 ± 3% of control over 65-170 mmHg, indicating impaired autoregulation. In contrast, pressure-mediated vasoconstriction was preserved in DOCA-salt+PPS and DOCA-salt+TTx rats, reaching 77 ± 7 and 75 ± 3% of control at 170 mmHg, respectively. ATP is required for autoregulation via P2X1 receptor activation. ATP- and β,γ-methylene ATP (P2X1 receptor agonist)-mediated vasoconstriction were markedly attenuated in DOCA-salt rats compared with UNx (P < 0.05), but significantly improved by PPS or TTx (P < 0.05 vs. DOCA-salt) treatment. Arteriolar responses to adenosine and UTP (P2Y2 receptor agonist) were unaffected by DOCA-salt treatment. PPS and TTx significantly reduced MCP-1 and protein excretion in DOCA-salt rats. These results support the hypothesis that hypertension triggers inflammatory cascades but anti-inflammatory treatment preserves renal autoregulation in DOCA-salt rats, most likely by normalizing renal microvascular reactivity to P2X1 receptor activation.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>26697978</pmid><doi>10.1152/ajprenal.00110.2015</doi></addata></record> |
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| ispartof | American journal of physiology. Renal physiology, 2016-03, Vol.310 (6), p.F456-F465 |
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| subjects | Adenosine Triphosphate - analogs & derivatives Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Antihypertensive Agents - pharmacology Antihypertensive Agents - therapeutic use Arterioles - drug effects Arterioles - metabolism Blood Pressure Chemokine CCL2 - urine Disease Models, Animal Homeostasis - drug effects Hydralazine - pharmacology Hydralazine - therapeutic use Hydrochlorothiazide - pharmacology Hydrochlorothiazide - therapeutic use Hypertension - drug therapy Hypertension - etiology Hypertension - metabolism Hypertension - physiopathology In Vitro Techniques Kidney - blood supply Kidney - drug effects Kidney - metabolism Male Pentosan Sulfuric Polyester - pharmacology Pentosan Sulfuric Polyester - therapeutic use Proteinuria - drug therapy Rats, Sprague-Dawley Receptors, Purinergic P2X1 - metabolism Reserpine - pharmacology Reserpine - therapeutic use Vasoconstriction |
| title | Pentosan polysulfate preserves renal microvascular P2X1 receptor reactivity and autoregulatory behavior in DOCA-salt hypertensive rats |
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