{"title":"肾素血管紧张素醛固酮系统在肾血管性高血压中的作用","authors":"J. A. Gomez","doi":"10.5772/intechopen.97491","DOIUrl":null,"url":null,"abstract":"The renin angiotensin aldosterone system (RAAS) plays a key function in renovascular hypertension induced by renal artery stenosis (RAS). RAS causes a decrease in renal perfusion in the stenosed kidney which in turn stimulates renin the rate limiting enzyme in RAAS. This stimulation triggers a series of events starting with renin release leading to Ang II production, decrease in sodium excretion, increase sympathetic tone; all contributing to the development of renovascular hypertension. In RAS increase of superoxide reduce nitric oxide in the afferent arteriole increasing vasoconstriction and a marked decrease in glomerular filtration rate. In renovascular hypertension prostaglandins mediate renin release in the stenosed kidney. Targeting different RAAS components is part of the therapy for renovascular hypertension, with other options including renal nerves denervation and revascularization. Different clinical studies had explored revascularization, RAAS blocking and renal nerves denervation as a therapy. We will discuss organ, cellular and molecular components of this disease.","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"71 1","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2021-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Renin Angiotensin Aldosterone System Functions in Renovascular Hypertension\",\"authors\":\"J. A. Gomez\",\"doi\":\"10.5772/intechopen.97491\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The renin angiotensin aldosterone system (RAAS) plays a key function in renovascular hypertension induced by renal artery stenosis (RAS). RAS causes a decrease in renal perfusion in the stenosed kidney which in turn stimulates renin the rate limiting enzyme in RAAS. This stimulation triggers a series of events starting with renin release leading to Ang II production, decrease in sodium excretion, increase sympathetic tone; all contributing to the development of renovascular hypertension. In RAS increase of superoxide reduce nitric oxide in the afferent arteriole increasing vasoconstriction and a marked decrease in glomerular filtration rate. In renovascular hypertension prostaglandins mediate renin release in the stenosed kidney. Targeting different RAAS components is part of the therapy for renovascular hypertension, with other options including renal nerves denervation and revascularization. Different clinical studies had explored revascularization, RAAS blocking and renal nerves denervation as a therapy. We will discuss organ, cellular and molecular components of this disease.\",\"PeriodicalId\":17330,\"journal\":{\"name\":\"Journal of the Renin-Angiotensin-Aldosterone System\",\"volume\":\"71 1\",\"pages\":\"\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2021-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of the Renin-Angiotensin-Aldosterone System\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5772/intechopen.97491\",\"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 the Renin-Angiotensin-Aldosterone System","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5772/intechopen.97491","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
Renin Angiotensin Aldosterone System Functions in Renovascular Hypertension
The renin angiotensin aldosterone system (RAAS) plays a key function in renovascular hypertension induced by renal artery stenosis (RAS). RAS causes a decrease in renal perfusion in the stenosed kidney which in turn stimulates renin the rate limiting enzyme in RAAS. This stimulation triggers a series of events starting with renin release leading to Ang II production, decrease in sodium excretion, increase sympathetic tone; all contributing to the development of renovascular hypertension. In RAS increase of superoxide reduce nitric oxide in the afferent arteriole increasing vasoconstriction and a marked decrease in glomerular filtration rate. In renovascular hypertension prostaglandins mediate renin release in the stenosed kidney. Targeting different RAAS components is part of the therapy for renovascular hypertension, with other options including renal nerves denervation and revascularization. Different clinical studies had explored revascularization, RAAS blocking and renal nerves denervation as a therapy. We will discuss organ, cellular and molecular components of this disease.
期刊介绍:
JRAAS is a peer-reviewed, open access journal, serving as a resource for biomedical professionals, primarily with an active interest in the renin-angiotensin-aldosterone system in humans and other mammals. It publishes original research and reviews on the normal and abnormal function of this system and its pharmacology and therapeutics, mostly in a cardiovascular context but including research in all areas where this system is present, including the brain, lungs and gastro-intestinal tract.