盐敏感性高血压病患者血浆心钠素、血管紧张素Ⅱ和醛固酮水平测定及苯那普利治疗的初步观察(英文)

Decreases Plasma Atrial Natriuretic Peptide in Patients With Salt-sensitive Essential Hypertension and Increase After Benazepril Therapy

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 ,3 0例 )和非盐敏感性 (NSS ,3 4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。 3 0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( 10mg/d～ 2 0mg/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 2 8± 15 40 )pmol/L ,NSS( 14 5 52± 2 6 53 ) pmol/L和对照组 ( 197 74± 2 6 2 0 )pmol/L ,P均 <0 0 1]。盐负荷期SS组和NSS组血浆ANP水平均明显增高 [分别为 ( 13 3 56± 3 4 0 3 ) pmol/L和 ( 169 2 0± 3 5 91)pmol/L ,P均 <0 0 5]。增高的百分数两组间无显著性差异 (P >0 0 5)。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 0 5)。盐负荷期SS组和NSS组血浆AⅡ和ALD水平无明显改变 (P均 >0 0 5)。 ( 3 )SS组于苯那普利治疗后血压明显降低 (P <0 0 1) 。

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.