{"title":"支持钙敏感受体（CaSR）参与l -半胱氨酸介导的小鼠胸主动脉血管松弛的证据。","authors":"Nuran Ogulener, Busra Akarsakarya, Fatma Aydinoglu","doi":"10.1159/000548774","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>In our study, the possible role of the calcium-sensing receptor (CaSR) pathway in L-cysteine/Hydrogen sulfide (H2S)-induced vasorelaxations was investigated in isolated mouse thoracic aorta tissue.</p><p><strong>Methods: </strong>For this purpose, vasorelaxations to L-cysteine (H2S substrate; 1 µM -10 mM) and calindol (CaSR agonist; 0.3-10 M) were measured in endothelial-intact and denuded-thoracic aorta segments contracted with phenylephrine (5 M). Also, the effects of propargylglycine (PAG) and calhex-231, cystathionine-gamma-lyase (CSE) and CaSR inhibitor, respectively, on L-cysteine- and calindol-induced vasorelaxations were investigated in thoracic aorta segments. In addition, the effects of L-cysteine, calindol and endothelium on H2S generation in mouse aorta segments were investigated.</p><p><strong>Results: </strong>L-cysteine- and calindol-induced vasorelaxations were reduced in the presence of PAG and calhex231. Furthermore, in endothelium-denuded tissues, the vasorelaxations to calindol and L-cysteine were reduced compared to endothelium-intact tissues. Also, calindol increased basal H2S generation, and PAG and Calhex-231 reduced the increase in H2S production stimulated with calindol. Calhex-231 reduced the increase in H2S production in the presence of L-cysteine. Also, H2S production decreased in endothelium-denuded tissues.</p><p><strong>Conclusion: </strong>In conclusion, endogenous hydrogen sulfide generated by CSE produces endothelium-dependent relaxation by activating CaSR in mouse thoracic aorta tissue.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-19"},"PeriodicalIF":2.3000,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Evidence in Favour of Calcium-Sensing Receptor(CaSR) in L-cysteine-mediated Vasorelaxation of Mouse Thoracic Aorta.\",\"authors\":\"Nuran Ogulener, Busra Akarsakarya, Fatma Aydinoglu\",\"doi\":\"10.1159/000548774\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>In our study, the possible role of the calcium-sensing receptor (CaSR) pathway in L-cysteine/Hydrogen sulfide (H2S)-induced vasorelaxations was investigated in isolated mouse thoracic aorta tissue.</p><p><strong>Methods: </strong>For this purpose, vasorelaxations to L-cysteine (H2S substrate; 1 µM -10 mM) and calindol (CaSR agonist; 0.3-10 M) were measured in endothelial-intact and denuded-thoracic aorta segments contracted with phenylephrine (5 M). Also, the effects of propargylglycine (PAG) and calhex-231, cystathionine-gamma-lyase (CSE) and CaSR inhibitor, respectively, on L-cysteine- and calindol-induced vasorelaxations were investigated in thoracic aorta segments. In addition, the effects of L-cysteine, calindol and endothelium on H2S generation in mouse aorta segments were investigated.</p><p><strong>Results: </strong>L-cysteine- and calindol-induced vasorelaxations were reduced in the presence of PAG and calhex231. Furthermore, in endothelium-denuded tissues, the vasorelaxations to calindol and L-cysteine were reduced compared to endothelium-intact tissues. Also, calindol increased basal H2S generation, and PAG and Calhex-231 reduced the increase in H2S production stimulated with calindol. Calhex-231 reduced the increase in H2S production in the presence of L-cysteine. Also, H2S production decreased in endothelium-denuded tissues.</p><p><strong>Conclusion: </strong>In conclusion, endogenous hydrogen sulfide generated by CSE produces endothelium-dependent relaxation by activating CaSR in mouse thoracic aorta tissue.</p>\",\"PeriodicalId\":17530,\"journal\":{\"name\":\"Journal of Vascular Research\",\"volume\":\" \",\"pages\":\"1-19\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2025-10-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Vascular Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1159/000548774\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Vascular Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000548774","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
Evidence in Favour of Calcium-Sensing Receptor(CaSR) in L-cysteine-mediated Vasorelaxation of Mouse Thoracic Aorta.
Introduction: In our study, the possible role of the calcium-sensing receptor (CaSR) pathway in L-cysteine/Hydrogen sulfide (H2S)-induced vasorelaxations was investigated in isolated mouse thoracic aorta tissue.
Methods: For this purpose, vasorelaxations to L-cysteine (H2S substrate; 1 µM -10 mM) and calindol (CaSR agonist; 0.3-10 M) were measured in endothelial-intact and denuded-thoracic aorta segments contracted with phenylephrine (5 M). Also, the effects of propargylglycine (PAG) and calhex-231, cystathionine-gamma-lyase (CSE) and CaSR inhibitor, respectively, on L-cysteine- and calindol-induced vasorelaxations were investigated in thoracic aorta segments. In addition, the effects of L-cysteine, calindol and endothelium on H2S generation in mouse aorta segments were investigated.
Results: L-cysteine- and calindol-induced vasorelaxations were reduced in the presence of PAG and calhex231. Furthermore, in endothelium-denuded tissues, the vasorelaxations to calindol and L-cysteine were reduced compared to endothelium-intact tissues. Also, calindol increased basal H2S generation, and PAG and Calhex-231 reduced the increase in H2S production stimulated with calindol. Calhex-231 reduced the increase in H2S production in the presence of L-cysteine. Also, H2S production decreased in endothelium-denuded tissues.
Conclusion: In conclusion, endogenous hydrogen sulfide generated by CSE produces endothelium-dependent relaxation by activating CaSR in mouse thoracic aorta tissue.
期刊介绍：
The ''Journal of Vascular Research'' publishes original articles and reviews of scientific excellence in vascular and microvascular biology, physiology and pathophysiology. The scope of the journal covers a broad spectrum of vascular and lymphatic research, including vascular structure, vascular function, haemodynamics, mechanics, cell signalling, intercellular communication, growth and differentiation. JVR''s ''Vascular Update'' series regularly presents state-of-the-art reviews on hot topics in vascular biology. Manuscript processing times are, consistent with stringent review, kept as short as possible due to electronic submission. All articles are published online first, ensuring rapid publication. The ''Journal of Vascular Research'' is the official journal of the European Society for Microcirculation. A biennial prize is awarded to the authors of the best paper published in the journal over the previous two years, thus encouraging young scientists working in the exciting field of vascular biology to publish their findings.
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