從血管內皮細胞角度解析高血壓的成因、預防與治療

Causes, Prevention, and Treatment of Hypertension from the Vascular Endothelial cell Perspective

高血壓是一種常見的心血管疾病，長期未控制可能導致嚴重併發症，如心臟病、中風和腎功能衰竭。血管內皮細胞在調節血壓和血管張力方面扮演關鍵角色，當內皮功能受損時，血管收縮異常、血流阻力增加，進而促使高血壓的發生與惡化。本研究旨在探討內皮功能障礙與高血壓的關聯，並分析內皮健康對預防與治療高血壓的重要性。本文回顧血管內皮細胞的生理功能及其對血管張力的調控，以高血壓（Hypertension）、內皮細胞（Endothelial Cells）、內皮功能障礙（Endothelial Dysfunction）為關鍵詞於PubMed、Embase與華藝線上圖書館搜尋品質良好的相關文獻，分析高血壓患者內皮功能障礙的病理機轉、影響內皮功能的因素，包括高血糖、胰島素阻抗、脂肪代謝異常與肥胖，並探討運動、飲食與藥物治療對內皮功能的影響。內皮功能障礙是高血壓發展的核心病理機制，主要由一氧化氮（NO）生成減少、氧化壓力增加、慢性發炎與內皮素-1（ET-1）過度表達導致。高血糖與AGEs（糖化終產物）透過RAGE受體誘導氧化壓力與發炎反應，降低NO生成；胰島素阻抗改變血管舒張與收縮因子的平衡，使血管持續收縮；氧化型低密度脂蛋白（Ox-LDL）促進內皮發炎與動脈粥樣硬化；肥胖則透過精氨酸酶活化與脂肪組織釋放促炎因子，進一步損害內皮功能。預防內皮功能障礙的策略包括有氧運動與阻力運動，可提升流量介導擴張（FMD）並減少周邊血管阻力；飲食方面，攝取L-精氨酸、抗氧化物（如維生素C、多酚類）與Omega-3有助於保護內皮功能。藥物治療則可透過血管張力素轉化酶抑制劑（ACEIs）、血管收縮素II受體阻斷劑（ARBs）、β-受體阻滯劑、鈣通道阻滯劑等，改善NO生成、減少內皮素-1與氧化壓力，修復受損的內皮功能。此外，內皮前驅幹細胞移植技術也成為未來治療的潛在選項。血管內皮功能障礙是高血壓發病的關鍵病理機轉，與一氧化氮生成減少、氧化壓力與慢性發炎增加密切相關。代謝異常如高血糖、胰島素阻抗與肥胖會加劇內皮損傷。生活型態介入（如運動與抗氧化飲食）及藥物治療（如ACEIs、ARBs、β-阻斷劑與CCBs）可有效改善內皮功能並降低血壓。內皮前驅幹細胞移植則為未來高血壓治療的新方向。針對內皮功能的早期介入有助於提升高血壓整體治療成效與預後。

Hypertension is a common cardiovascular disease that leads to serious complications such as heart disease, stroke, and kidney failure if left uncontrolled. Vascular endothelial cells play a key role in regulating blood pressure and vascular tone; their dysfunction is a central pathological mechanism in the development of hypertension. Endothelial dysfunction is characterized by the reduced production of nitric oxide (NO), increased oxidative stress, chronic inflammation, and the overexpression of endothelin-1 (ET 1), which contribute to abnormal vasoconstriction and elevated vascular resistance, promoting the onset and progression of hypertension. Various metabolic abnormalities impair endothelial function, such as hyperglycemia, insulin resistance, high cholesterol, and obesity. Hyperglycemia and advanced glycation end products trigger oxidative stress and inflammation through the RAGE receptor, reducing NO production. Insulin resistance disrupts the balance between vasodilatory and vasoconstrictive factors, leading to sustained vasoconstriction. Oxidized low-density lipoprotein promotes endothelial inflammation and atherosclerosis. Additionally, obesity exacerbates endothelial dysfunction through activating arginase and stimulating the release of proinflammatory cytokines from adipose tissue. Prevention and treatment strategies for hypertension involve lifestyle interventions and pharmacological approaches. Aerobic exercise and resistance training increase flow-mediated dilation and reduce peripheral vascular resistance. Dietary interventions, such as increasing the intake of L-arginine, antioxidants (such as vitamin C and polyphenols), and omega-3 fatty acids, also protect endothelial function. Pharmacologically, agents such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers, and calcium channel blockers can increase NO production, reduce ET-1 levels, and decrease oxidative stress, helping to restore damaged endothelial cells. In addition, endothelial progenitor stem cell transplantation is a promising future therapeutic approach. In conclusion, endothelial dysfunction is closely related to the onset of hypertension. Early intervention can effectively increase endothelial function, lower blood pressure, as well as enhance treatment outcomes and prognosis.