本文選題：血壓 + 高血壓前期��； 參考：《第三軍醫(yī)大學(xué)》2016年博士論文

【摘要】：背景和目的:高血壓(Hypertension)是目前世界范圍內(nèi)影響人類健康的主要公共衛(wèi)生問題之一,估計(jì)有將近20%的人群受高血壓影響。目前關(guān)于高血壓具體的發(fā)病原因及機(jī)制還尚不清楚。2003年,由美國預(yù)防、檢測、評(píng)價(jià)與治療高血壓聯(lián)合委員會(huì)在第7次報(bào)告中首次提出了高血壓前期(Prehypertension)的概念,其具體是指在未使用降壓藥的情況下,兩次或者兩次以上不同時(shí)間測得的收縮壓(Systolic blood pressure,SBP)波動(dòng)于120-139mmHg和(或)舒張壓(Diastolic blood pressure,DBP)波動(dòng)于80-89mmHg的階段。相當(dāng)一部分高血壓前期患者在4年之內(nèi)將進(jìn)展為高血壓,尤其在中老年人這種現(xiàn)象更普遍。據(jù)估計(jì),目前大約有30%至50%人群處于高血壓前期的階段。高血壓前期常常伴隨其他心血管代謝危險(xiǎn)因素,并顯著增加冠狀動(dòng)脈心臟疾病、中風(fēng)和腎功能不全的患病風(fēng)險(xiǎn)。對(duì)于高血壓前期的患者早期干預(yù),可有效降預(yù)防高血壓的發(fā)病率,并對(duì)靶器官的損害起到早期預(yù)防的作用。目前,一些關(guān)于治療高血壓前期的策略已經(jīng)開始用于干預(yù)高血壓前期患者,包括生活方式的改變,如健康的飲食和規(guī)律體育運(yùn)動(dòng);以及使用降壓藥物,如血管緊張素Ⅱ受體阻滯劑。盡管這些干預(yù)措施可以改善高血壓前期狀態(tài),但依從性差和抗高血壓藥物相關(guān)的副作用阻礙了其在高血壓前期患者中的應(yīng)用。因此,目前迫切需要一種可靠而且副作用小的治療措施以防止高血壓前期向高血壓的發(fā)展。含硫氨基酸(Sulfur amino acid)是哺乳動(dòng)物體內(nèi)不可缺少的氨基酸之一,其代謝終產(chǎn)物包括�；撬�(Taurine),硫化氫(Hydrogen sulfide,H_2S)和二氧化硫(Sulfur dioxide,SO2)。�；撬嵩�150年前首次從牛膽汁中分離出來而得名。機(jī)體內(nèi)�；撬岬膩碓匆詳z取為主,可通過膳食動(dòng)物性食品如蛋、肉及海生動(dòng)物獲得。此外,�；撬嵋部梢宰陨砗铣�,其主要通過半胱氨酸或甲硫氨酸等含硫氨基酸經(jīng)一系列酶促反應(yīng)轉(zhuǎn)化而來。H_2S作為一種生物介質(zhì),在體內(nèi)許多生理及病理過程中均發(fā)揮潛在的作用。H_2S主要是以半胱氨酸和同型半胱氨酸為底物,由胱硫醚β合酶(Cystathionine-β-synthase,CBS)、胱硫醚γ裂解酶(Cystathionine-γ-lyase,CSE)和3-巰基丙酮酸轉(zhuǎn)硫酶(3-mercaptopyruvatesulfurtransferase,3-mst)促反應(yīng)生成。之前研究發(fā)現(xiàn),牛磺酸和H_2s在高血壓的發(fā)生發(fā)展中發(fā)揮重要的作用。例如,mozaffari等研究發(fā)現(xiàn)體內(nèi)低水平�；撬峥梢约又馗啕}引起的高血壓。此外,vandenberg等關(guān)于腎移植后患者的研究發(fā)現(xiàn),尿中低水平H_2s代謝產(chǎn)物與腎移植后患者收縮壓升高明顯相關(guān)。但含硫氨基酸是如何發(fā)揮抗高血壓作用的機(jī)制仍需進(jìn)一步探討。瞬時(shí)受體電位通道(transientreceptorpotentialchannels,trpcs)是結(jié)構(gòu)同源的一類細(xì)胞膜上的非選擇性陽離子通道家族。研究發(fā)現(xiàn),trpc3介導(dǎo)的細(xì)胞膜上鈣信號(hào)在高血壓發(fā)病過程中發(fā)揮重要的作用。此外,最近的一項(xiàng)研究發(fā)現(xiàn)H_2s具有影響小鼠骨髓間充質(zhì)干細(xì)胞胞膜trpcs并調(diào)節(jié)其胞內(nèi)Ca~(2+)平衡的作用。盡管基于目前研究結(jié)果并未發(fā)現(xiàn)含硫氨基酸、trpc3及鈣信號(hào)與高血壓之間的直接關(guān)系,但足以提醒我們四者之間存在密切的關(guān)系。因此,基于以上研究結(jié)果我們進(jìn)一步探討了�；撬嵩诟哐獕呵捌诩案纳蒲芄δ苤械淖饔眉捌渚唧w機(jī)制。材料與方法:本研究分為臨床試驗(yàn)和動(dòng)物實(shí)驗(yàn)兩大部分,第一部分的臨床研究方案經(jīng)第三軍醫(yī)大學(xué)大坪醫(yī)院論理委員會(huì)討論通過,并注冊(cè)u(píng)snationallibraryofmedicine(http://www.clinicaltrials.gov,identifier:nct01816698),所有志愿者簽署知情同意書。入選120名高血壓前期志愿者(男性51例,女性69例)隨機(jī)分配至牛磺酸顆粒組(60例)和安慰劑顆粒組(60例),及58名年齡匹配的正常血壓志愿者被納入我們的臨床試驗(yàn)研究。第二部分以自發(fā)性高血壓大鼠(shr)、trpc3-/-小鼠和wt小鼠為模型,分離人和小鼠的腸系膜動(dòng)脈及小鼠和大鼠的主動(dòng)脈應(yīng)用于分子機(jī)制的實(shí)驗(yàn)研究。1.�；撬岣深A(yù)對(duì)高血壓前期志愿者血壓的影響。應(yīng)用水銀血壓計(jì)測量�；撬岣深A(yù)期間志愿者的診室血壓;應(yīng)用動(dòng)態(tài)血壓計(jì)監(jiān)測牛磺酸干預(yù)前、后志愿者的24小時(shí)動(dòng)態(tài)血壓。2.�；撬岣深A(yù)對(duì)高血壓前期志愿者血管功能的影響。應(yīng)用高分辨率血管超聲技術(shù)檢測�；撬岣深A(yù)前、后志愿者內(nèi)皮依賴性血管舒張功能(flow-mediateddilation,fmd)和非內(nèi)皮依賴性血管舒張功能(nitroglycerin-mediateddilation,nmd)。3.�；撬岣深A(yù)對(duì)血漿硫化氫(H_2s)含量的影響。應(yīng)用反相高效液相色譜法檢測�；撬岣深A(yù)前后志愿者血漿中�；撬岷虷_2s水平。4.�；撬岣深A(yù)對(duì)血管組織H_2s合成酶和trpc3的表達(dá)的影響。以自發(fā)性高血壓大鼠(shr,4周齡)為模型,以2%�；撬犸嬘盟皩�(duì)照組干預(yù)12周,分離大鼠主動(dòng)脈應(yīng)用免疫熒光和免疫印跡(westernblot)技術(shù)檢測人和動(dòng)物血管壁的cbs,cse和trpc3的表達(dá)。5.�；撬岣深A(yù)對(duì)野生型小鼠(wt)及trpc3-/-小鼠血管功能的影響。分離小鼠的腸系膜動(dòng)脈應(yīng)用微血管張力測定系統(tǒng)檢測�；撬岣深A(yù)前、后血管的舒縮功能;6.�；撬釋�(duì)血管組織及血管平滑肌細(xì)胞[Ca~(2+)]i的影響。以應(yīng)用fura-2am/Ca~(2+)熒光探針技術(shù)檢測�；撬岣深A(yù)前、后血管組織及平滑肌細(xì)胞內(nèi)[Ca~(2+)]i的變化及trpc3的影響。結(jié)果:1.與正常血壓對(duì)照組相比較,高血壓前期志愿者診室血壓和24h動(dòng)態(tài)血壓顯著增高,其脈搏波傳導(dǎo)速度(cm/s)及餐后血糖也明顯升高。高血壓前期志愿者安慰劑組和�；撬峤M的基線特征無顯著性差異。2.與基線血壓相比較,長期�；撬岣深A(yù)顯著降低高血壓前期志愿者的診室血壓和24h動(dòng)態(tài)血壓,且白天平均動(dòng)態(tài)血壓下降顯著,夜間平均動(dòng)態(tài)血壓無明顯影響。長期�；撬岣深A(yù)對(duì)高血壓前期志愿者正常高值組的血壓下降幅值比正常低值組更為明顯。3.長期�；撬岣深A(yù)對(duì)高血壓前期志愿者內(nèi)皮依賴性血管舒張(fmd)和非內(nèi)皮依賴性血管舒張(nmd)功能均有顯著的改善,而安慰劑干預(yù)無作用。4.長期�；撬岣深A(yù)對(duì)高血壓前期志愿者血漿�；撬岷虷_2s水平均有顯著升高,且血漿�；撬岷虷_2s水平與收縮壓和舒張壓下降幅值呈負(fù)相關(guān)。5.人腸系膜動(dòng)脈(mas)及野生型小鼠(wt)主動(dòng)脈有cbs、cse和trpc3共表達(dá),trpc3-/-基因敲除小鼠的主動(dòng)脈cbs、cse表達(dá)比同窩野生型trpc3+/+小鼠表達(dá)顯著增強(qiáng)。6.長期牛磺酸干預(yù)顯著上調(diào)自發(fā)性高血壓大鼠(shr)主動(dòng)脈cbs、cse的表達(dá),而抑制trpc3的表達(dá)。離體實(shí)驗(yàn)顯示,�；撬岱跤四c系膜動(dòng)脈(mas)能顯著增加cbs、cse表達(dá),而抑制trpc3的表達(dá),且呈劑量依賴的關(guān)系。7.利用毒胡蘿卜素(thapsigargin,tg)耗竭細(xì)胞內(nèi)Ca~(2+)后,H_2s的供體硫氫化鈉(nahs)顯著改善腸系膜動(dòng)脈kcl誘導(dǎo)的血管收縮反應(yīng),而trpc3-/-基因敲除小鼠比同窩野生型trpc3+/+小鼠nahs的作用明顯增強(qiáng)。8.nahs能抑制苯腎上腺素(pe)誘導(dǎo)的腸系膜動(dòng)脈Ca~(2+)內(nèi)流;trpc3-/-基因敲除或trpc3抑制劑(pyr3)均能顯著減少tg誘導(dǎo)的腸系膜動(dòng)脈Ca~(2+)內(nèi)流,nahs能顯著抑制同窩野生型trpc3+/+小鼠tg誘導(dǎo)的腸系膜動(dòng)脈Ca~(2+)內(nèi)流,而trpc3-/-基因敲除小鼠無此作用。結(jié)論:1.長期�；撬岣深A(yù)可降低高血壓前期志愿者的診室血壓和24h動(dòng)態(tài)血壓,且白天平均動(dòng)態(tài)血壓下降顯著,高血壓前期志愿者在正常高值時(shí)血壓下降更明顯。2.長期�；撬岣深A(yù)能顯著改善高血壓前期志愿者的內(nèi)皮依賴性和非內(nèi)皮依賴性血管舒張功能。3.長期�；撬岣深A(yù)能增加高血壓前期志愿者血漿�；撬岷虷_2S水平,且血漿�；撬岷虷_2S濃度越高,血壓下降越顯著。4.CBS、CSE和TRPC3在人、動(dòng)物的腸系膜動(dòng)脈和主動(dòng)脈存在共表達(dá),TRPC3基因敲除或�；撬峋茱@著增加CBS、CSE表達(dá),而抑制TRPC3表達(dá)。長期�；撬岣深A(yù)降低血壓與抑制血管組織TRPC3,減少血管平滑肌[Ca2+]i有關(guān)。長期�；撬岣深A(yù)可上調(diào)CBS、CSE表達(dá),促進(jìn)H_2S生成,改善高血壓前期血壓及血管功能。
[Abstract]:Background and purpose: hypertension (Hypertension) is one of the major public health problems affecting human health worldwide. It is estimated that nearly 20% of the population is affected by hypertension. The current causes and mechanisms of hypertension are still not clear for.2003, the United States Joint Committee for the prevention, detection, evaluation and treatment of hypertension. For the first time in the seventh report, the concept of prehypertension (Prehypertension) was first proposed. It specifically refers to the fluctuation of the Systolic blood pressure (SBP) in the 120-139mmHg and / or diastolic pressure (Diastolic blood pressure, DBP) fluctuating in the 80-89mmHg order without the use of antihypertensive drugs at different times. A considerable portion of prehypertensive patients will progress into high blood pressure within 4 years, especially in middle aged and elderly people. It is estimated that about 30% to 50% people are at the stage of prehypertension. Prehypertension is often associated with other cardiovascular metabolic risk factors and significantly increases coronary heart disease, stroke, and stroke. The risk of renal insufficiency. Early intervention in patients with prehypertension can effectively reduce the incidence of hypertension and play an early preventive effect on target organ damage. At present, some strategies for the treatment of prehypertension have begun to intervene in prehypertensive patients, including lifestyle changes, such as health. Diet and regular physical exercise; and the use of antihypertensive drugs, such as angiotensin II receptor blockers. Although these interventions can improve prehypertension, side effects associated with poor compliance and antihypertensive drugs have hindered their application in prehypertensive patients. Small side effects to prevent the development of prehypertension to hypertension. Sulfur amino acid is one of the essential amino acids in mammals, its metabolic products include taurine (Taurine), hydrogen sulfide (Hydrogen sulfide, H_2S) and sulfur dioxide (Sulfur dioxide, SO2). Taurine was first 150 years ago. The source of taurine is derived from the body of the body. The source of taurine is derived mainly through dietary animal foods such as eggs, meat and marine animals. In addition, taurine can also be synthesized by its own, which is converted to.H_2S by a series of enzymatic reactions mainly through a series of sulfur-containing amino acids such as cysteine or methionine. Mediators, which play a potential role in many physiological and pathological processes in the body,.H_2S mainly take cysteine and homocysteine as substrates, cystathine beta synthase (Cystathionine- beta -synthase, CBS), cystathion gamma lyase (Cystathionine- gamma -lyase, CSE) and 3- mercapto pyruvate thiotransferase (3-mercaptopyruvatesulfurtransferase, 3-m). St) promote the formation of the reaction. Previous studies have found that taurine and H_2s play an important role in the development of hypertension. For example, mozaffari and other studies have found that low levels of taurine in the body can aggravate high salt induced hypertension. In addition, the study of Vandenberg and other patients after renal transplantation has found that low levels of H_2s metabolites in urine and renal migration The increase in systolic blood pressure in patients with post implantation is obviously related. But the mechanism of how sulfur containing amino acids play an antihypertensive role still needs to be further explored. The transient receptor potential channel (transientreceptorpotentialchannels, TRPCs) is a non selective cation channel family on a kind of cell membrane of structure homologous. The study found that TRPC3 mediated cell membrane Calcium signals play an important role in the pathogenesis of hypertension. In addition, a recent study found that H_2s has an effect on the cell membrane TRPCs of mouse bone marrow mesenchymal stem cells and regulates its intracellular Ca~ (2+) balance. Although the current research results have not found the direct correlation between amino acid, TRPC3 and calcium signals and hypertension It is enough to remind us that there is a close relationship between the four. Therefore, based on the above results, we further explore the role and specific mechanisms of taurine in prehypertension and the improvement of vascular function. Materials and methods: This study is divided into two parts of clinical trial and animal testing, and the first part of the clinical research program Through the discussion of the theory Committee of Daping Hospital of Third Military Medical University, and registered usnationallibraryofmedicine (http://www.clinicaltrials.gov, identifier:nct01816698), all volunteers signed the informed consent. 120 pre hypertensive volunteers (51 male and 69 female) were randomly assigned to the Taurine Granules group (60 cases) and consolation. The drug granule group (60 cases) and 58 age matched normal blood pressure volunteers were included in our clinical trial. The second part was a model of spontaneously hypertensive rats (SHR), trpc3-/- mice and WT mice. The experimental study of the molecular mechanisms of the mesenteric artery and the main arteries of mice and rats and the main arteries of mice and rats was applied to the molecular mechanism of.1. taurine. Effect of pre hypertensive blood pressure in pre hypertensive volunteers. Using a mercury sphygmomanometer to measure the blood pressure of the volunteers in the taurine intervention period; the effect of the 24 hour ambulatory blood pressure.2. taurine intervention on the vascular function of prehypertensive volunteers before the intervention of taurine intervention. High resolution vascular ultrasound was applied. The effects of endothelium-dependent vasodilatation (flow-mediateddilation, FMD) and non endothelium-dependent vasodilatation (nitroglycerin-mediateddilation, NMD).3. taurine on plasma hydrogen sulfide (H_2s) content before and after taurine intervention. The effect of taurine and H_2s level.4. taurine on the expression of H_2s synthetase and TRPC3 in vascular tissue was used in the volunteers. The rats of spontaneously hypertensive rats (SHR, 4 weeks old) were used as models, the drinking water of 2% taurine and the control group were intervened for 12 weeks. The isolated rat aorta was separated by immunofluorescence and Western blot (Westernblot) to detect human and animal. The expression of CBS, CSE and TRPC3 of the vascular wall on the effects of.5. taurine on the vascular function of wild type mice (WT) and trpc3-/- mice. The vasomotor function of the posterior vessels before taurine intervention was detected by the microvascular tension measurement system in the mesenteric artery of mice and the effect of 6. taurine on the blood tube tissue and the]i of vascular smooth muscle cells [Ca~ (2+). Fura-2am/Ca~ (2+) fluorescence probe was used to detect the changes of [Ca~ (2+)]i in the posterior vascular tissue and smooth muscle cells before taurine intervention and the effect of TRPC3. Results: 1. compared with the normal blood pressure control group, the blood pressure and 24h dynamic blood pressure in the early hypertensive volunteers were significantly increased, and the pulse wave conduction velocity (cm/s) and postprandial blood glucose were also observed in the pre hypertensive volunteers. There was no significant difference in baseline characteristics between the placebo group and the taurine group at prehypertension. Compared with the baseline blood pressure,.2. was significantly lower in the consulting room and the ambulatory blood pressure in the pre hypertensive volunteers, and the mean daytime ambulatory blood pressure decreased significantly and the mean nocturnal ambulatory blood pressure had no significant influence. The decrease of the blood pressure in the normal high value group of prehypertensive volunteers was more obvious than that of the normal low value group..3. long-term taurine intervention improved the function of endothelium-dependent vasodilatation (FMD) and non endothelium-dependent vasodilatation (NMD) in pre hypertensive volunteers, while placebo intervention had no effect on.4. long-term cows. The levels of taurine and H_2s in patients with prehypertension were significantly increased by sulfonic acid intervention, and the levels of plasma taurine and H_2s were negatively correlated with.5. human mesenteric artery (MAS) and wild type mouse (WT) aorta CBS, CSE and TRPC3 co expression, trpc3-/- knockout mice's aorta CBS, CSE table. The expression of Dabi fossa trpc3+/+ mice significantly enhanced.6. long-term taurine intervention significantly up-regulated the expression of CBS and CSE in the aorta of spontaneously hypertensive rats (SHR), and inhibited the expression of TRPC3. In vitro experiments showed that taurine incubated the mesenteric artery (MAS) to significantly increase CBS, CSE expression and inhibit the expression of TRPC3 in a dose dependent manner. Relationship.7. using Ca~ (2+) in the depleted cells of thapsigargin (TG), H_2s donor sodium hydrogen sulfide (NaHS) significantly improved the vasoconstrictor response induced by the mesenteric artery KCl, while trpc3-/- knockout mice significantly enhanced the inhibition of phenylephrine induced intestines than the NaHS of the same nest wild type trpc3+/+ mice. Ca~ (2+) internal flow, trpc3-/- gene knockout or TRPC3 inhibitor (pyr3) can significantly reduce the Ca~ (2+) flow in the mesenteric artery induced by TG, and NaHS can significantly inhibit the TG induced mesenteric artery Ca~ (trpc3-/-) flow in the same nest wild type trpc3+/+ mice, but there is no effect in the knockout mice. Conclusion: 1. long-term taurine intervention can reduce the high blood pressure. The blood pressure and 24h dynamic blood pressure in the consulting room in the pre pressure volunteers and the daytime mean ambulatory blood pressure decreased significantly. The decrease of blood pressure in the pre hypertensive volunteers was more obvious at the normal high value..2. long-term taurine intervention could significantly improve the endothelium-dependent and non endothelium dependent vasodilatation function.3. long-term taurine intervention in prehypertensive volunteers. The plasma taurine and H_2S levels were increased in pre hypertensive volunteers, and the higher the concentration of taurine and H_2S in plasma, the more significant the blood pressure decreased.4.CBS, CSE and TRPC3 were co expressed in human mesenteric arteries and aorta. TRPC3 gene knockout or taurine could significantly increase the expression of CBS, CSE, and inhibit the expression of TRPC3. Predescending hypotension is related to inhibiting vascular tissue TRPC3 and reducing vascular smooth muscle [Ca2+]i. Long-term taurine intervention can increase CBS, CSE expression, promote H_2S production, improve blood pressure and vascular function in prehypertensive period.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類號(hào)】：R544.1

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