Hamish A L Lemmey, Christopher J Garland, Kim A Dora
{"title":"肌内皮反馈回路对微血管张力的内在调节。","authors":"Hamish A L Lemmey, Christopher J Garland, Kim A Dora","doi":"10.1016/bs.ctm.2020.01.004","DOIUrl":null,"url":null,"abstract":"<p><p>The endothelium is an important regulator of arterial vascular tone, acting to release nitric oxide (NO) and open Ca<sup>2+</sup>-activated K<sup>+</sup> (K<sub>Ca</sub>) channels to relax vascular smooth muscle cells (VSMCs). While agonists acting at endothelial cell (EC) receptors are widely used to assess the ability of the endothelium to reduce vascular tone, the intrinsic EC-dependent mechanisms are less well characterized. In small resistance arteries and arterioles, the presence of heterocellular gap junctions termed myoendothelial gap junctions (MEGJs) allows the passage of not only current, but small molecules including Ca<sup>2+</sup> and inositol trisphosphate (IP<sub>3</sub>). When stimulated to contract, the increase in VSM Ca<sup>2+</sup> and IP<sub>3</sub> can therefore potentially pass through MEGJs to activate adjacent ECs. This activation releases NO and opens K<sub>Ca</sub> channels, which act to limit contraction. This myoendothelial feedback (MEF) is amplified by EC Ca<sup>2+</sup> influx and release pathways, and is dynamically modulated by processes regulating gap junction conductance. There is a remarkable localization of key signaling and regulatory proteins within the EC projection toward VSM, and the intrinsic EC-dependent signaling pathways occurring with this highly specialized microdomain are reviewed.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Intrinsic regulation of microvascular tone by myoendothelial feedback circuits.\",\"authors\":\"Hamish A L Lemmey, Christopher J Garland, Kim A Dora\",\"doi\":\"10.1016/bs.ctm.2020.01.004\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The endothelium is an important regulator of arterial vascular tone, acting to release nitric oxide (NO) and open Ca<sup>2+</sup>-activated K<sup>+</sup> (K<sub>Ca</sub>) channels to relax vascular smooth muscle cells (VSMCs). While agonists acting at endothelial cell (EC) receptors are widely used to assess the ability of the endothelium to reduce vascular tone, the intrinsic EC-dependent mechanisms are less well characterized. In small resistance arteries and arterioles, the presence of heterocellular gap junctions termed myoendothelial gap junctions (MEGJs) allows the passage of not only current, but small molecules including Ca<sup>2+</sup> and inositol trisphosphate (IP<sub>3</sub>). When stimulated to contract, the increase in VSM Ca<sup>2+</sup> and IP<sub>3</sub> can therefore potentially pass through MEGJs to activate adjacent ECs. This activation releases NO and opens K<sub>Ca</sub> channels, which act to limit contraction. This myoendothelial feedback (MEF) is amplified by EC Ca<sup>2+</sup> influx and release pathways, and is dynamically modulated by processes regulating gap junction conductance. There is a remarkable localization of key signaling and regulatory proteins within the EC projection toward VSM, and the intrinsic EC-dependent signaling pathways occurring with this highly specialized microdomain are reviewed.</p>\",\"PeriodicalId\":11029,\"journal\":{\"name\":\"Current topics in membranes\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current topics in membranes\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.ctm.2020.01.004\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/3/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current topics in membranes","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/bs.ctm.2020.01.004","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/3/6 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
Intrinsic regulation of microvascular tone by myoendothelial feedback circuits.
The endothelium is an important regulator of arterial vascular tone, acting to release nitric oxide (NO) and open Ca2+-activated K+ (KCa) channels to relax vascular smooth muscle cells (VSMCs). While agonists acting at endothelial cell (EC) receptors are widely used to assess the ability of the endothelium to reduce vascular tone, the intrinsic EC-dependent mechanisms are less well characterized. In small resistance arteries and arterioles, the presence of heterocellular gap junctions termed myoendothelial gap junctions (MEGJs) allows the passage of not only current, but small molecules including Ca2+ and inositol trisphosphate (IP3). When stimulated to contract, the increase in VSM Ca2+ and IP3 can therefore potentially pass through MEGJs to activate adjacent ECs. This activation releases NO and opens KCa channels, which act to limit contraction. This myoendothelial feedback (MEF) is amplified by EC Ca2+ influx and release pathways, and is dynamically modulated by processes regulating gap junction conductance. There is a remarkable localization of key signaling and regulatory proteins within the EC projection toward VSM, and the intrinsic EC-dependent signaling pathways occurring with this highly specialized microdomain are reviewed.
期刊介绍:
Current Topics in Membranes provides a systematic, comprehensive, and rigorous approach to specific topics relevant to the study of cellular membranes. Each volume is a guest edited compendium of membrane biology.