Modulation of Angiotensin II Responses in Sympathetic Neurons by Cytosolic Calcium
ABSTRACT—Both stimulatory and suppressive responses of the sympathetic nervous system to angiotensin II (AII) have been reported in intact animals. To elucidate possible cellular mechanisms, we studied AII-induced changes in cytosolic Ca ([Ca]i) in primary cultures of rat stellate ganglion neurons....
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2003-01, Vol.41 (1), p.56-63 |
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| creator | Fernandez, Stanley F Huang, Ming-He Davidson, Bruce A Knight, Paul R Izzo, Joseph L |
| description | ABSTRACT—Both stimulatory and suppressive responses of the sympathetic nervous system to angiotensin II (AII) have been reported in intact animals. To elucidate possible cellular mechanisms, we studied AII-induced changes in cytosolic Ca ([Ca]i) in primary cultures of rat stellate ganglion neurons. Two different patterns of [Ca]i responses to AII were observeddose-dependent increases in [Ca]i in cells with intrinsically low baseline [Ca]i (n=64) and dose-dependent suppression of [Ca]i in neurons with intrinsically higher baseline [Ca]i (n=46). Individual neurons could express both response patterns to AII. In neurons with low basal [Ca]i, superfusion with Ca ionophore (ionomycin) increased [Ca]i and reversed the initial AII-induced stimulatory pattern. L-type Ca channel antagonism (nifedipine) in neurons with high baseline [Ca]i lowered [Ca]i and reversed the initial AII-induced suppressive response. Both stimulatory and suppressive responses were abolished by AT1 receptor antagonism (losartan). AII-induced stimulatory responses were blocked by IP3 receptor antagonism (2-APB) and by thapsigargin. AII-induced suppression of neuronal [Ca]i was blunted when Na-Ca exchange was impaired. We conclude that [Ca]i acts as a switch for AII-mediated stimulatory and suppressive responses in individual sympathetic neurons. AT1 receptor-mediated neuronal stimulation and suppression may allow local homeostatic adaptation to meet complex systemic needs. |
| doi_str_mv | 10.1161/01.HYP.0000047513.75459.7E |
| format | Article |
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To elucidate possible cellular mechanisms, we studied AII-induced changes in cytosolic Ca ([Ca]i) in primary cultures of rat stellate ganglion neurons. Two different patterns of [Ca]i responses to AII were observeddose-dependent increases in [Ca]i in cells with intrinsically low baseline [Ca]i (n=64) and dose-dependent suppression of [Ca]i in neurons with intrinsically higher baseline [Ca]i (n=46). Individual neurons could express both response patterns to AII. In neurons with low basal [Ca]i, superfusion with Ca ionophore (ionomycin) increased [Ca]i and reversed the initial AII-induced stimulatory pattern. L-type Ca channel antagonism (nifedipine) in neurons with high baseline [Ca]i lowered [Ca]i and reversed the initial AII-induced suppressive response. Both stimulatory and suppressive responses were abolished by AT1 receptor antagonism (losartan). AII-induced stimulatory responses were blocked by IP3 receptor antagonism (2-APB) and by thapsigargin. AII-induced suppression of neuronal [Ca]i was blunted when Na-Ca exchange was impaired. We conclude that [Ca]i acts as a switch for AII-mediated stimulatory and suppressive responses in individual sympathetic neurons. AT1 receptor-mediated neuronal stimulation and suppression may allow local homeostatic adaptation to meet complex systemic needs.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000047513.75459.7E</identifier><identifier>PMID: 12511530</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Angiotensin II - pharmacology ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Calcium - metabolism ; Calcium - physiology ; Calcium Channel Blockers - pharmacology ; Calcium Signaling ; Cardiology. Vascular system ; Cells, Cultured ; Cytosol - metabolism ; Dose-Response Relationship, Drug ; Experimental diseases ; Inositol 1,4,5-Trisphosphate - physiology ; Ion Transport ; Kinetics ; Medical sciences ; Neurons - drug effects ; Neurons - metabolism ; Nifedipine - pharmacology ; Norepinephrine - metabolism ; Rats ; Receptors, Angiotensin - physiology ; Sodium - metabolism ; Stellate Ganglion - drug effects ; Stellate Ganglion - metabolism ; Sympathetic Nervous System - cytology ; Sympathetic Nervous System - metabolism</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2003-01, Vol.41 (1), p.56-63</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. 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To elucidate possible cellular mechanisms, we studied AII-induced changes in cytosolic Ca ([Ca]i) in primary cultures of rat stellate ganglion neurons. Two different patterns of [Ca]i responses to AII were observeddose-dependent increases in [Ca]i in cells with intrinsically low baseline [Ca]i (n=64) and dose-dependent suppression of [Ca]i in neurons with intrinsically higher baseline [Ca]i (n=46). Individual neurons could express both response patterns to AII. In neurons with low basal [Ca]i, superfusion with Ca ionophore (ionomycin) increased [Ca]i and reversed the initial AII-induced stimulatory pattern. L-type Ca channel antagonism (nifedipine) in neurons with high baseline [Ca]i lowered [Ca]i and reversed the initial AII-induced suppressive response. Both stimulatory and suppressive responses were abolished by AT1 receptor antagonism (losartan). AII-induced stimulatory responses were blocked by IP3 receptor antagonism (2-APB) and by thapsigargin. AII-induced suppression of neuronal [Ca]i was blunted when Na-Ca exchange was impaired. We conclude that [Ca]i acts as a switch for AII-mediated stimulatory and suppressive responses in individual sympathetic neurons. AT1 receptor-mediated neuronal stimulation and suppression may allow local homeostatic adaptation to meet complex systemic needs.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Calcium - metabolism</subject><subject>Calcium - physiology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Signaling</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Cytosol - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Experimental diseases</subject><subject>Inositol 1,4,5-Trisphosphate - physiology</subject><subject>Ion Transport</subject><subject>Kinetics</subject><subject>Medical sciences</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Nifedipine - pharmacology</subject><subject>Norepinephrine - metabolism</subject><subject>Rats</subject><subject>Receptors, Angiotensin - physiology</subject><subject>Sodium - metabolism</subject><subject>Stellate Ganglion - drug effects</subject><subject>Stellate Ganglion - metabolism</subject><subject>Sympathetic Nervous System - cytology</subject><subject>Sympathetic Nervous System - metabolism</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkFtr2zAUgMXYWNNuf2GYwvZmT0cXy95bCWkb6NbSbbA9CUU5WtzJVibZlPz7qk0gMIEkjvSdCx8h50ArgBo-U6iuf99V9HkJJYFXSgrZVmrxisxAMlEKWfPXZEahFWUL8OuEnKb0QCkIIdRbcgJMAkhOZ-T-a1hP3oxdGIrgiovhTxdGHFI3FMtlcY9pG4aEqcjx912_NeMGx84W33CK-aNY7Yr5bgwp-Pw4N952U_-OvHHGJ3x_uM_Iz8vFj_l1eXN7tZxf3JRWKklLxdfOUXRSMamEY6ZVprGGG4c1Iq3zrBxlsxLWAM9HI13DHUgw68wLx8_Ip33dbQz_Jkyj7rtk0XszYJiSVqwVTS1lBs__Ax_CFIc8m2ZUsoYpJTL0ZQ_ZGFKK6PQ2dr2JOw1UP2vXFHTWro_a9Yt2rRY5-cOhw7TqcX1MPXjOwMcDYJI13kUz2C4dOSHqXJFlTuy5x-BHjOmvnx4x6g0aP25eWgtWNyWjlFPIUZk3UP4EtkKaeA</recordid><startdate>200301</startdate><enddate>200301</enddate><creator>Fernandez, Stanley F</creator><creator>Huang, Ming-He</creator><creator>Davidson, Bruce A</creator><creator>Knight, Paul R</creator><creator>Izzo, Joseph L</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200301</creationdate><title>Modulation of Angiotensin II Responses in Sympathetic Neurons by Cytosolic Calcium</title><author>Fernandez, Stanley F ; Huang, Ming-He ; Davidson, Bruce A ; Knight, Paul R ; Izzo, Joseph L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5750-73dff0ef572574f2a97a8ca3afe6ee061443e58b4ca134ca85f83f151ad5744f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Calcium - metabolism</topic><topic>Calcium - physiology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Signaling</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Cytosol - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Experimental diseases</topic><topic>Inositol 1,4,5-Trisphosphate - physiology</topic><topic>Ion Transport</topic><topic>Kinetics</topic><topic>Medical sciences</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Nifedipine - pharmacology</topic><topic>Norepinephrine - metabolism</topic><topic>Rats</topic><topic>Receptors, Angiotensin - physiology</topic><topic>Sodium - metabolism</topic><topic>Stellate Ganglion - drug effects</topic><topic>Stellate Ganglion - metabolism</topic><topic>Sympathetic Nervous System - cytology</topic><topic>Sympathetic Nervous System - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fernandez, Stanley F</creatorcontrib><creatorcontrib>Huang, Ming-He</creatorcontrib><creatorcontrib>Davidson, Bruce A</creatorcontrib><creatorcontrib>Knight, Paul R</creatorcontrib><creatorcontrib>Izzo, Joseph L</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fernandez, Stanley F</au><au>Huang, Ming-He</au><au>Davidson, Bruce A</au><au>Knight, Paul R</au><au>Izzo, Joseph L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of Angiotensin II Responses in Sympathetic Neurons by Cytosolic Calcium</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2003-01</date><risdate>2003</risdate><volume>41</volume><issue>1</issue><spage>56</spage><epage>63</epage><pages>56-63</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>ABSTRACT—Both stimulatory and suppressive responses of the sympathetic nervous system to angiotensin II (AII) have been reported in intact animals. To elucidate possible cellular mechanisms, we studied AII-induced changes in cytosolic Ca ([Ca]i) in primary cultures of rat stellate ganglion neurons. Two different patterns of [Ca]i responses to AII were observeddose-dependent increases in [Ca]i in cells with intrinsically low baseline [Ca]i (n=64) and dose-dependent suppression of [Ca]i in neurons with intrinsically higher baseline [Ca]i (n=46). Individual neurons could express both response patterns to AII. In neurons with low basal [Ca]i, superfusion with Ca ionophore (ionomycin) increased [Ca]i and reversed the initial AII-induced stimulatory pattern. L-type Ca channel antagonism (nifedipine) in neurons with high baseline [Ca]i lowered [Ca]i and reversed the initial AII-induced suppressive response. Both stimulatory and suppressive responses were abolished by AT1 receptor antagonism (losartan). AII-induced stimulatory responses were blocked by IP3 receptor antagonism (2-APB) and by thapsigargin. AII-induced suppression of neuronal [Ca]i was blunted when Na-Ca exchange was impaired. We conclude that [Ca]i acts as a switch for AII-mediated stimulatory and suppressive responses in individual sympathetic neurons. AT1 receptor-mediated neuronal stimulation and suppression may allow local homeostatic adaptation to meet complex systemic needs.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12511530</pmid><doi>10.1161/01.HYP.0000047513.75459.7E</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 2003-01, Vol.41 (1), p.56-63 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Angiotensin II - pharmacology Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Calcium - metabolism Calcium - physiology Calcium Channel Blockers - pharmacology Calcium Signaling Cardiology. Vascular system Cells, Cultured Cytosol - metabolism Dose-Response Relationship, Drug Experimental diseases Inositol 1,4,5-Trisphosphate - physiology Ion Transport Kinetics Medical sciences Neurons - drug effects Neurons - metabolism Nifedipine - pharmacology Norepinephrine - metabolism Rats Receptors, Angiotensin - physiology Sodium - metabolism Stellate Ganglion - drug effects Stellate Ganglion - metabolism Sympathetic Nervous System - cytology Sympathetic Nervous System - metabolism |
| title | Modulation of Angiotensin II Responses in Sympathetic Neurons by Cytosolic Calcium |
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