CAJ | 학술논문

目的探讨心钠素(ANP)和肾素-血管紧张素-醛固酮系统(RAAS)在盐敏感性高血压病发病中的作用及苯那普利的降压作用和ANP的关系.方法采用改良的Sullivan急性口服盐水负荷试验的方法将64例高血压病患者分为盐敏感性(SS, 30例)和非盐敏感性(NSS,34例)高血压病组,测定盐负荷前与盐负荷期间血浆ANP、血管紧张素Ⅱ(AⅡ)和醛固酮(ALD)水平.30例正常人为对照组.SS组患者采用自身对照的方法予以口服安慰剂和苯那普利(10 mg/d～20 mg/d),观察治疗前后血压及血浆ANP水平的变化.结果 (1)基础血浆ANP水平,SS组显著低于NSS组,NSS组显著低于正常组[分别为SS(110.28±15.40)pmol/L,NSS(145.52±26.53)pmol/L和对照组(197.74±26.20)pmol/L, P均<0.01].盐负荷期SS组和NSS组血浆ANP水平均明显增高[分别为(133.56±34.03)pmol/L和(169.20±35.91)pmol/L,P均<0.05].增高的百分数两组间无显著性差异(P>0.05).但SS组血浆ANP仍低于正常水平.(2)基础血浆AⅡ和ALD水平在SS组与NSS组间无明显差异(P均>0.05).盐负荷期SS组和NSS组血浆AⅡ和ALD水平无明显改变(P均>0.05).(3)SS组于苯那普利治疗后血压明显降低(P<0.01),血浆ANP水平显著增高[(146.74±31.86)pmol/L,P<0.01].(4)基础血浆ANP水平与盐负荷引起的平均动脉压增高的幅值呈显著负相关( b=-0.06,P<0.05).结论循环内源性ANP的不足可能是SS高血压病的一个重要发生机制.苯那普利显著升高血浆ANP水平,能够有效降低SS高血压病患者的血压.
목적탐토심납소(ANP)화신소-혈관긴장소-철고동계통(RAAS)재염민감성고혈압병발병중적작용급분나보리적강압작용화ANP적관계.방법채용개량적Sullivan급성구복염수부하시험적방법장64례고혈압병환자분위염민감성(SS, 30례)화비염민감성(NSS,34례)고혈압병조,측정염부하전여염부하기간혈장ANP、혈관긴장소Ⅱ(AⅡ)화철고동(ALD)수평.30례정상인위대조조.SS조환자채용자신대조적방법여이구복안위제화분나보리(10 mg/d～20 mg/d),관찰치료전후혈압급혈장ANP수평적변화.결과 (1)기출혈장ANP수평,SS조현저저우NSS조,NSS조현저저우정상조[분별위SS(110.28±15.40)pmol/L,NSS(145.52±26.53)pmol/L화대조조(197.74±26.20)pmol/L, P균<0.01].염부하기SS조화NSS조혈장ANP수평균명현증고[분별위(133.56±34.03)pmol/L화(169.20±35.91)pmol/L,P균<0.05].증고적백분수량조간무현저성차이(P>0.05).단SS조혈장ANP잉저우정상수평.(2)기출혈장AⅡ화ALD수평재SS조여NSS조간무명현차이(P균>0.05).염부하기SS조화NSS조혈장AⅡ화ALD수평무명현개변(P균>0.05).(3)SS조우분나보리치료후혈압명현강저(P<0.01),혈장ANP수평현저증고[(146.74±31.86)pmol/L,P<0.01].(4)기출혈장ANP수평여염부하인기적평균동맥압증고적폭치정현저부상관( b=-0.06,P<0.05).결론순배내원성ANP적불족가능시SS고혈압병적일개중요발생궤제.분나보리현저승고혈장ANP수평,능구유효강저SS고혈압병환자적혈압.
Objective To study the role of atrial natriuretic peptide (ANP) and renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of salt-sensitive (SS) hypertension and mechanism of the hypotensive effect of benazepril and ANP in patients with SS essential hypertension. Methods Sixty-four patients with essential hypertension were divided into SS (n=30) and non-salt-sensitive (NSS, n=34) groups by modified Sulliran's method. Plasma ANP, angiotensin Ⅱ (AⅡ) and aldosterone (ALD) were determined before and during the period of salt loading test. Thirty healthy subjects as controls were also enrolled. A self-comparative study of benazepril with the placebo was performed in SS group. Before and after the placebo and benazepril therapy, blood pressure (BP) and plasma ANP were determined. Results (1)Basal plasma ANP level in the SS group was significantly lower than that in the NSS group. Basal plasma ANP level in the NSS group was also significantly lower than that in the control group [(110.28±15.40) pmol/L vs NSS (145.52±26.53) pmol/L and control (197.74±26.20) pmol/L]. Plasma ANP in both SS and NSS groups [(133.56±34.03) pmol/L and (169.20±35.91) pmol/L respectively, both P<0.05 vs control]. Percentage of increase of plasma ANP in SS and NSS groups was of no difference (P>0.05) . (2) No significant difference of basal plasma AⅡ and ALD levels were found between SS and NSS groups (P>0.05). There were no significant changes of plasma AⅡ and ALD during salt loading in both SS and NSS groups ( both P>0.05). (3) After the benazepril treatment, plasma ANP was increased significantly [(146.74±31.86) pmol/L , P<0.01]; both systolic and diastolic BP were reduced significantly in SS group. (4) Basal plasma ANP level was negatively correlated with the magnitude of increase of mean arterial pressure (MAP) by salt loading (b=-0.06, P<0.05). Conclusion Deficiency of circulating endogenous ANP may play an important role in the pathogenesis of SS hypertension. Benazepril could reduce BP and increase plasma ANP significantly in patients with SS hypertension.