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Morphine and Anandamide Stimulate Intracellular Calcium Transients in Human Arterial Endothelial Cells: Coupling to Nitric Oxide Release
Both morphine and anandamide significantly stimulated cultured endothelial intracellular calcium level increases in a concentration-dependent manner in cells pre-loaded with fura 2/AM. Morphine is more potent than anandamide (approximately 275 vs. 135 nM [Ca] i), and the [Ca] i for both ligands was...
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Published in: | Cellular signalling 1999-03, Vol.11 (3), p.189-193 |
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container_title | Cellular signalling |
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creator | Fimiani, Caterina Mattocks, Dwight Cavani, Francesco Salzet, Michel Deutsch, Dale G. Pryor, Stephen Bilfinger, Thomas V. Stefano, George B. |
description | Both morphine and anandamide significantly stimulated cultured endothelial intracellular calcium level increases in a concentration-dependent manner in cells pre-loaded with fura 2/AM. Morphine is more potent than anandamide (approximately 275
vs. 135 nM [Ca]
i), and the [Ca]
i for both ligands was blocked by prior exposure of the cells to their respective receptor antagonist, i.e., naloxone and SR 171416A. Various opioid peptides did not exhibit this ability, indicating a morphine-μ
3-mediated process. In comparing the sequence of events concerning morphine's and anandamide's action in stimulating both [Ca]
i and nitric oxide (NO) production in endothelial cells, we found that the first event precedes the second by 40±8 sec. The opiate and cannabinoid stimulation of [Ca]
i was attenuated in cells leeched of calcium, strongly suggesting that intracellular calcium levels regulate NOS activity. |
doi_str_mv | 10.1016/S0898-6568(98)00060-6 |
format | article |
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vs. 135 nM [Ca]
i), and the [Ca]
i for both ligands was blocked by prior exposure of the cells to their respective receptor antagonist, i.e., naloxone and SR 171416A. Various opioid peptides did not exhibit this ability, indicating a morphine-μ
3-mediated process. In comparing the sequence of events concerning morphine's and anandamide's action in stimulating both [Ca]
i and nitric oxide (NO) production in endothelial cells, we found that the first event precedes the second by 40±8 sec. The opiate and cannabinoid stimulation of [Ca]
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vs. 135 nM [Ca]
i), and the [Ca]
i for both ligands was blocked by prior exposure of the cells to their respective receptor antagonist, i.e., naloxone and SR 171416A. Various opioid peptides did not exhibit this ability, indicating a morphine-μ
3-mediated process. In comparing the sequence of events concerning morphine's and anandamide's action in stimulating both [Ca]
i and nitric oxide (NO) production in endothelial cells, we found that the first event precedes the second by 40±8 sec. The opiate and cannabinoid stimulation of [Ca]
i was attenuated in cells leeched of calcium, strongly suggesting that intracellular calcium levels regulate NOS activity.</description><subject>Analgesics, Opioid - pharmacology</subject><subject>Arachidonic Acids - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocannabinoids</subject><subject>Endothelia, morphine, anadamide, calcium transients, nitric oxide, μ 3 receptor</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Humans</subject><subject>Morphine - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Polyunsaturated Alkamides</subject><subject>Signal Transduction</subject><issn>0898-6568</issn><issn>1873-3913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNqFkV1PFTEQhhuigSP6EzC9Mnix2o9zelpuyMkGhQQlEbxuZrdzoKbbPbRdo__An20XkFtv5iN5ZibvvIQccfaBM64-XjNtdKNWSh8b_Z4xplij9siC67VspOHyBVk8IwfkVc4_GOMrpsQ-OeBMrqQyckH-fBnT7s5HpBAd3cQaYfAO6XXxwxSgIL2IJUGPIdQ20RZC76eB3iSI2WMsmfpIz6cBIt2kgslDoGfRjeUOw1y3dTKf0HacdsHHW1pG-tWX5Ht69Ws-9A0DQsbX5OUWQsY3T_mQfP90dtOeN5dXny_azWWDwixL03HFpJOd0so53ArhmBZSaycUg-3SCOBdp8xKAXdmuQUmOOs74zQYcFBVH5J3j3t3abyfMBc7-Dyrg4jjlK0ya8OFMf8F-VoshdC6gm-fwKkb0Nld8gOk3_bfkytw-ghg1fXTY7K5r5_r0fmEfbFu9BW2s632wVY7e2ZrfrDVKvkX0EWVXw</recordid><startdate>19990301</startdate><enddate>19990301</enddate><creator>Fimiani, Caterina</creator><creator>Mattocks, Dwight</creator><creator>Cavani, Francesco</creator><creator>Salzet, Michel</creator><creator>Deutsch, Dale G.</creator><creator>Pryor, Stephen</creator><creator>Bilfinger, Thomas V.</creator><creator>Stefano, George B.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope><scope>7X8</scope></search><sort><creationdate>19990301</creationdate><title>Morphine and Anandamide Stimulate Intracellular Calcium Transients in Human Arterial Endothelial Cells: Coupling to Nitric Oxide Release</title><author>Fimiani, Caterina ; 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Morphine is more potent than anandamide (approximately 275
vs. 135 nM [Ca]
i), and the [Ca]
i for both ligands was blocked by prior exposure of the cells to their respective receptor antagonist, i.e., naloxone and SR 171416A. Various opioid peptides did not exhibit this ability, indicating a morphine-μ
3-mediated process. In comparing the sequence of events concerning morphine's and anandamide's action in stimulating both [Ca]
i and nitric oxide (NO) production in endothelial cells, we found that the first event precedes the second by 40±8 sec. The opiate and cannabinoid stimulation of [Ca]
i was attenuated in cells leeched of calcium, strongly suggesting that intracellular calcium levels regulate NOS activity.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>10353693</pmid><doi>10.1016/S0898-6568(98)00060-6</doi><tpages>5</tpages></addata></record> |
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subjects | Analgesics, Opioid - pharmacology Arachidonic Acids - pharmacology Calcium - metabolism Calcium Channel Blockers - pharmacology Cells, Cultured Dose-Response Relationship, Drug Endocannabinoids Endothelia, morphine, anadamide, calcium transients, nitric oxide, μ 3 receptor Endothelium, Vascular - metabolism Humans Morphine - pharmacology Nitric Oxide - metabolism Polyunsaturated Alkamides Signal Transduction |
title | Morphine and Anandamide Stimulate Intracellular Calcium Transients in Human Arterial Endothelial Cells: Coupling to Nitric Oxide Release |
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