{"title":"胆骨化醇治疗原发性高血压合并维生素D缺乏症患者肾素-血管紧张素系统钝化。","authors":"Davide Carrara, Matteo Bernini, Alessandra Bacca, Ilaria Rugani, Emiliano Duranti, Agostino Virdis, Lorenzo Ghiadoni, Stefano Taddei, Giampaolo Bernini","doi":"10.1177/1470320312471149","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Vitamin D plasma levels are negatively associated with blood pressure and cardiovascular mortality, and vitamin D supplementation reduces cardiovascular events. Renin-angiotensin system (RAS) suppression may be one of the mechanisms involved. However, there are no interventional prospective studies demonstrating a reduction in circulating RAS components after vitamin D treatment.</p><p><strong>Methods: </strong>Fifteen consecutive drug-free patients with essential hypertension and hypovitaminosis D underwent therapy with an oral dose of 25000 I.U. of cholecalciferol once a week for two months, while maintaining a constant-salt diet. In basal conditions and at the end of the study, RAS activity (plasma angiotensinogen, renin, PRA, angiotensin II, aldosterone and urinary angiotensinogen) was investigated, in addition to blood pressure and plasma vitamin D levels (25(OH)D).</p><p><strong>Results: </strong>After cholecalciferol administration, all patients exhibited normalized plasma 25(OH)D values. At the end of the study, a reduction (p < 0.05) in plasma renin and aldosterone, and a decrement, although not significant, of PRA and angiotensin II, was observed. No difference was found in plasma and urinary angiotensinogen or blood pressure values.</p><p><strong>Conclusions: </strong>Our data indicate that in essential hypertensives with hypovitaminosis D, pharmacological correction of vitamin D levels can blunt systemic RAS activity.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"82-7"},"PeriodicalIF":0.0000,"publicationDate":"2014-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312471149","citationCount":"49","resultStr":"{\"title\":\"Cholecalciferol administration blunts the systemic renin-angiotensin system in essential hypertensives with hypovitaminosis D.\",\"authors\":\"Davide Carrara, Matteo Bernini, Alessandra Bacca, Ilaria Rugani, Emiliano Duranti, Agostino Virdis, Lorenzo Ghiadoni, Stefano Taddei, Giampaolo Bernini\",\"doi\":\"10.1177/1470320312471149\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Vitamin D plasma levels are negatively associated with blood pressure and cardiovascular mortality, and vitamin D supplementation reduces cardiovascular events. Renin-angiotensin system (RAS) suppression may be one of the mechanisms involved. However, there are no interventional prospective studies demonstrating a reduction in circulating RAS components after vitamin D treatment.</p><p><strong>Methods: </strong>Fifteen consecutive drug-free patients with essential hypertension and hypovitaminosis D underwent therapy with an oral dose of 25000 I.U. of cholecalciferol once a week for two months, while maintaining a constant-salt diet. In basal conditions and at the end of the study, RAS activity (plasma angiotensinogen, renin, PRA, angiotensin II, aldosterone and urinary angiotensinogen) was investigated, in addition to blood pressure and plasma vitamin D levels (25(OH)D).</p><p><strong>Results: </strong>After cholecalciferol administration, all patients exhibited normalized plasma 25(OH)D values. At the end of the study, a reduction (p < 0.05) in plasma renin and aldosterone, and a decrement, although not significant, of PRA and angiotensin II, was observed. No difference was found in plasma and urinary angiotensinogen or blood pressure values.</p><p><strong>Conclusions: </strong>Our data indicate that in essential hypertensives with hypovitaminosis D, pharmacological correction of vitamin D levels can blunt systemic RAS activity.</p>\",\"PeriodicalId\":520698,\"journal\":{\"name\":\"Journal of the renin-angiotensin-aldosterone system : JRAAS\",\"volume\":\" \",\"pages\":\"82-7\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1177/1470320312471149\",\"citationCount\":\"49\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of the renin-angiotensin-aldosterone system : JRAAS\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1177/1470320312471149\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2013/1/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the renin-angiotensin-aldosterone system : JRAAS","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/1470320312471149","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/1/2 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 49
摘要
维生素D血浆水平与血压和心血管死亡率呈负相关,补充维生素D可减少心血管事件。肾素-血管紧张素系统(RAS)抑制可能是其机制之一。然而,没有前瞻性干预性研究证明维生素D治疗后循环RAS成分减少。方法:连续15例无药物治疗的原发性高血压合并维生素D缺乏症患者,给予胆骨化醇25000 iu /周口服1次,疗程2个月,同时保持不变的盐饮食。在基础条件下和研究结束时,除了血压和血浆维生素D水平(25(OH)D)外,还研究了RAS活性(血浆血管紧张素原、肾素、PRA、血管紧张素II、醛固酮和尿血管紧张素原)。结果:经胆骨化醇治疗后,所有患者血浆25(OH)D值均恢复正常。在研究结束时,观察到血浆肾素和醛固酮含量降低(p < 0.05), PRA和血管紧张素II含量下降(尽管不显著)。血浆和尿血管紧张素原或血压值没有发现差异。结论:我们的数据表明,在合并维生素D缺乏症的原发性高血压患者中,维生素D水平的药物纠正可以减弱全身RAS活性。
Cholecalciferol administration blunts the systemic renin-angiotensin system in essential hypertensives with hypovitaminosis D.
Introduction: Vitamin D plasma levels are negatively associated with blood pressure and cardiovascular mortality, and vitamin D supplementation reduces cardiovascular events. Renin-angiotensin system (RAS) suppression may be one of the mechanisms involved. However, there are no interventional prospective studies demonstrating a reduction in circulating RAS components after vitamin D treatment.
Methods: Fifteen consecutive drug-free patients with essential hypertension and hypovitaminosis D underwent therapy with an oral dose of 25000 I.U. of cholecalciferol once a week for two months, while maintaining a constant-salt diet. In basal conditions and at the end of the study, RAS activity (plasma angiotensinogen, renin, PRA, angiotensin II, aldosterone and urinary angiotensinogen) was investigated, in addition to blood pressure and plasma vitamin D levels (25(OH)D).
Results: After cholecalciferol administration, all patients exhibited normalized plasma 25(OH)D values. At the end of the study, a reduction (p < 0.05) in plasma renin and aldosterone, and a decrement, although not significant, of PRA and angiotensin II, was observed. No difference was found in plasma and urinary angiotensinogen or blood pressure values.
Conclusions: Our data indicate that in essential hypertensives with hypovitaminosis D, pharmacological correction of vitamin D levels can blunt systemic RAS activity.