高血压机制及并发症（Hypertension mechanism and complication）.docVIP

下载本文档

7
0
约1.26万字
约 9页
2017-09-13 发布于河南
举报
版权申诉

高血压机制及并发症（Hypertension mechanism and complication）.doc

1、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。。
2、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
3、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
4、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
5、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
6、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
7、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

高血压机制及并发症（Hypertension mechanism and complication）

高血压机制及并发症（Hypertension mechanism and complication） A) increased sympathetic nervous system activity of various etiological factors causing nerve function of cerebral cortex changes, various neurotransmitter concentration and abnormal activity, including norepinephrine, epinephrine, dopamine, serotonin and neuropeptide Y 5-, vasopressin, enkephalin, brain natriuretic peptide and central renin-angiotensin system, leading to increased sympathetic nervous system activity, plasma catecholamine concentration, resistance arteriolar constriction is enhanced. (two) renal sodium retention caused by renal sodium retention, the body in order to avoid excessive cardiac output increase tissue perfusion, systemic arteriolar constriction resistance increased, resulting in peripheral vascular resistance increased, the pressure natriuresis (pressure-natriuresis) mechanism can be out of retention of water and sodium excretion. It may also be increased by the release of natriuretic hormone, such as endogenous digitalis like substances, which excrete water and sodium and increase peripheral vascular resistance. The theoretical significance of this theory is that the elevation of blood pressure is a compensatory way to maintain the balance of water and sodium in the body, while the retention of water and sodium is the basic pathophysiological change. There are many factors can cause renal sodium retention, such as hyperactivity of the sympathetic activity of the renal vascular resistance increased slightly; glomerular structural changes; renal sodium excretion (hormone prostaglandin, kininogenase, renal medulla) secretion, or renal sodium excretion (endogenous hormone class Yang yellow substance, ANP secretion) abnormal or sodium retention hormone (18- hydroxy deoxy corticosterone and aldosterone release.). (three) the renin angiotensin aldosterone system (RAAS) activates the classical RAAS, including the secretion of renin by the afferent cells of the glomerular afferent artery, Activat