{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:00:34Z","timestamp":1718654434638},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[1997,2,1]]},"abstract":"<jats:p> Metabolic pathways in vascular smooth muscles (VSM) appear to be functionally compartmentalized such that glycolysis fuels membrane-related processes, whereas oxidative processes fuel actin-myosin interaction. Because ATP influences Ca2+ channel activity, we examined the effects of ATP and metabolic substrates on Ca2+ channel activity with patch-clamp techniques in VSM cells isolated from rat portal vein. The peak magnitude of the Ca2+ channel currents was found to depend on the ATP concentration in the patch pipette. Cells perfused with 1, 3, and 5 mMATP had mean peak currents of 4.7 +\/- 0.6, 12.2 +\/- 1.9, and 17.6 +\/- 2.0 pA\/pF, respectively, and all currents showed substantial rundown. In separate experiments performed in the absence of intracellular ATP, provision of glycolytic but not oxidative substrates was able to maintain Ca2+ channel currents at levels comparable with those seen in the presence of 1 mM ATP. In the presence of 5 mM ATP, provision of glycolytic substrates resulted in a high peak current amplitude that was also very stable. Finally, metabolic inhibition with cyanide and iodoacetate caused a significant increase in the rate of current rundown, even in the presence of 5 mM ATP. These findings indicate that Ca2+ channel current is strongly dependent on ATP and that the source of ATP can also be an important factor. Compared with exogenous provision of ATP, endogenous metabolism preferentially maintained Ca2+ channel currents, consistent with the hypothesis of a functionally separate subsarcolemmal compartment. This provides an effective pathway for linking E-C coupling and vascular contractility to the metabolic state of the vascular cell. <\/jats:p>","DOI":"10.1152\/ajpheart.1997.272.2.h987","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T04:32:51Z","timestamp":1513917171000},"page":"H987-H994","source":"Crossref","is-referenced-by-count":4,"title":["Dependence of Ca2+ channel currents on endogenous and exogenous sources of ATP in portal vein smooth muscle"],"prefix":"10.1152","volume":"272","author":[{"given":"J. N.","family":"Lorenz","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University ofCincinnati, Ohio 45267-0576, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. J.","family":"Paul","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University ofCincinnati, Ohio 45267-0576, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajpheart.1997.272.2.H987","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:02:50Z","timestamp":1567962170000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajpheart.1997.272.2.H987"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1997,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1997,2,1]]}},"alternative-id":["10.1152\/ajpheart.1997.272.2.H987"],"URL":"https:\/\/doi.org\/10.1152\/ajpheart.1997.272.2.h987","relation":{},"ISSN":["0363-6135","1522-1539"],"issn-type":[{"value":"0363-6135","type":"print"},{"value":"1522-1539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1997,2,1]]}}}