{"title":"镍诱导的冠状血管收缩对电致钠钾泵活性的依赖性。","authors":"G Rubányi, M Bakos, K Hajdu, T Pataki","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The possible interactions between the vasoactive trace metal nickel ion (Ni2+) and membrane Na-K-ATPase in the isolated perfused rat heart and in the isolated canine coronary artery have been studied. The characteristic features of 1 microM Ni2+-induced contractile response in the canine coronary artery strip were similar to those evoked by the inhibition of Na-K-ATPase. Inhibition of the pump activity by ouabain (10(-4)M) or by K+-deficient Krebs solution prevented Ni2+-action both in the canine coronary artery strip and in the perfused rat heart, indicating that when Ni2+ causes coronary vasoconstriction the Na, K-exchange is influenced. Further studies are needed to clarify whether Ni2+ acts directly on the enzyme, or the vascular action of this trace metal depends on the ionic gradients maintained by the electrogenic Na-K-pump.</p>","PeriodicalId":7049,"journal":{"name":"Acta physiologica Academiae Scientiarum Hungaricae","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Dependence of nickel-induced coronary vasoconstriction on the activity of the electrogenic Na+, K+-pump.\",\"authors\":\"G Rubányi, M Bakos, K Hajdu, T Pataki\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The possible interactions between the vasoactive trace metal nickel ion (Ni2+) and membrane Na-K-ATPase in the isolated perfused rat heart and in the isolated canine coronary artery have been studied. The characteristic features of 1 microM Ni2+-induced contractile response in the canine coronary artery strip were similar to those evoked by the inhibition of Na-K-ATPase. Inhibition of the pump activity by ouabain (10(-4)M) or by K+-deficient Krebs solution prevented Ni2+-action both in the canine coronary artery strip and in the perfused rat heart, indicating that when Ni2+ causes coronary vasoconstriction the Na, K-exchange is influenced. Further studies are needed to clarify whether Ni2+ acts directly on the enzyme, or the vascular action of this trace metal depends on the ionic gradients maintained by the electrogenic Na-K-pump.</p>\",\"PeriodicalId\":7049,\"journal\":{\"name\":\"Acta physiologica Academiae Scientiarum Hungaricae\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1982-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta physiologica Academiae Scientiarum Hungaricae\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta physiologica Academiae Scientiarum Hungaricae","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
本文研究了大鼠离体灌注心脏和犬离体冠状动脉中具有血管活性的微量金属镍离子(Ni2+)与细胞膜na - k - atp酶之间可能的相互作用。1微米Ni2+诱导犬冠状动脉条带收缩反应的特征与na - k - atp酶抑制引起的收缩反应相似。沃阿因(10(-4)M)或K+缺陷克雷布斯溶液抑制泵活性,可阻止Ni2+在犬冠状动脉条和灌注的大鼠心脏中的作用,表明当Ni2+引起冠状动脉收缩时,Na, K交换受到影响。需要进一步的研究来阐明Ni2+是否直接作用于酶,或者这种微量金属的血管作用取决于电致na - k泵维持的离子梯度。
Dependence of nickel-induced coronary vasoconstriction on the activity of the electrogenic Na+, K+-pump.
The possible interactions between the vasoactive trace metal nickel ion (Ni2+) and membrane Na-K-ATPase in the isolated perfused rat heart and in the isolated canine coronary artery have been studied. The characteristic features of 1 microM Ni2+-induced contractile response in the canine coronary artery strip were similar to those evoked by the inhibition of Na-K-ATPase. Inhibition of the pump activity by ouabain (10(-4)M) or by K+-deficient Krebs solution prevented Ni2+-action both in the canine coronary artery strip and in the perfused rat heart, indicating that when Ni2+ causes coronary vasoconstriction the Na, K-exchange is influenced. Further studies are needed to clarify whether Ni2+ acts directly on the enzyme, or the vascular action of this trace metal depends on the ionic gradients maintained by the electrogenic Na-K-pump.