The Role of Atrial Natriuretic Peptide (ANP) in Cardiopulmonary Diseases

Atrial natriuretic peptide (ANP) is a peptide hormone that has potent natriuretic, diuretic, vasodilator, sympatholytic, and renin - and aldos-terone - suppressing activities and is involved in the regulation of volume and electrolyte balance and blood pressure. Further, ANP has also been shown to inhibit cellular growth, proliferation and induce apoptosis in a variety of cell lines, including vascular smooth muscle cells and cardiac myocytes. Recent studies have demonstrated that ANP is not only involved in blood pressure and volume homeostasis but also in the direct regulation of cardiac growth. We and other investigators have demonstrated the existence of natriuretic peptide receptors in the heart and cardiac cells, suggesting that ANP has direct actions on cardiac tissue. Several recent in vivo studies have suggested that statement of ANP is inversely related to cardiac growth/hypertrophy. Transgenic mice overexpressing ANP have lower heart weight and blood pressure than wild type mice. Conversely, we demonstrated that transgenic mice with homozygous disruption of the pro - ANP gene (Nppa) (ANP -/- mice) have no circulating or tissue ANP and exhibit significant cardiac hypertrophy and increased blood pressure. Further, transgenic mice lacking a functional natriuretic peptide receptor A (NPR-A) gene display elevated blood pressure and marked cardiac hypertrophy. The role of ANP in the development of cardiac hypertrophy in response to hemodynamic stress has not previously been studied. Our previous studies demonstrated that ANP - / -mice with hypoxia - induced pulmonary hypertension and high salt diet - induced systemic hypertension develop greater cardiac enlargement than their wild type controls under same experimental conditions, suggest-ing that cardiac enlargement in ANP -/- mice might, at least in part, be related to increased afterload. In a recent study, we used ANP -/- mice to further test the hypothesis that ANP plays an important role in protecting against the development of cardiac enlargement induced by volume overload stress. Adult (8-10 wk old) male ANP -/- and wild type ANP+/+ mice underwent an aorto - caval fistula (ACF) or sham surgery and were subjected to echocardiographic examination at 2 wks. Mean arterial pressure (MAP) and atrial, left ventricular (LV) and right ventricular (RV) mass were greater in sham - operated ANP-/-mice than in ANP+/+mice. MAP decreased following ACF to a similar extent in both genotypes. ACF induced significant concentric cardiac enlargement in both genotypes. Cardiac enlargement and lung weight increased to a greater extent in ANP - / - mice than in ANP+/ + mice, indicating that disrupted ANP statement worsens ACF- induced cardiac enlargement and pulmonary congestion. LV function (velocity of circumferential shortening [VCFr], circumferential stress, fraction shortening, fraction shortening, and e-jection time and fraction) assessed by echocardiography did not differ between sham - operated ANP + / + and ANP - / - mice and remained unchanged after ACF. These findings indicate that ANP deletion results in biventricular enlargement and an exaggerated response to the stress of volume overload. This support the hypothesis that ANP has direct antihypertrophic and car-dioprotective actions in heart. Further study is needed to dissect the contributions of increased afterload from those of removing the antihypertrophic effects of ANP to basal and stress induced cardiac enlargement in this animal model.

Atrial natriuretic peptide signal pathway upregulated in stomach of streptozotocin-induced diabetic mice

AIM:To investigate atrial natriuretic peptide(ANP) secretion from gastric mucosa and the relationship between the ANP/natriuretic peptide receptor type A (NPR-A)pathway and diabetic gastroparesis. METHODS:Male imprinting control region(ICR)mice (4 wk old)were divided into two groups:control mice, and streptozotocin-induced diabetic mice.Eight weeks after injection,spontaneous gastric contraction was recorded by using physiography in control and streptozotocin-induced diabetic mice.The ANP-positive cells in gastric mucosa and among dispersed gastric epithelial cells were detected by using immunohistochemistry and flow cytometry,respectively.ANP and natriureticpeptide receptor type A(NPR-A)gene expression in gastric tissue was observed by using the reverse transcriptase polymerase chain reaction. RESULTS:The frequency of spontaneous gastric contraction was reduced from 12.9±0.8 cycles/min in the control group to 8.4±0.6 cycles/min in the diabetic mice(n=8,P<0.05).However,the amplitude of contraction was not significantly affected in the diabetic group.The depletion of interstitial cells of Cajal in the gastric muscle layer was observed in the diabetic mice.ANP-positive cells were distributed in the gastric mucosal layer and the density index of ANP-positive cells was increased from 20.9±2.2 cells/field in control mice to 51.8±2.9 cells/field in diabetic mice(n=8, P<0.05).The percentage of ANP-positive cells among the dispersed gastric epithelial cells was increased from 10.0%±0.9%in the control mice to 41.2%± 1.0%in the diabetic mice(n=3,P<0.05).ANP and NPR-A genes were both expressed in mouse stomach, and the expression was significantly increased in the diabetic mice. CONCLUSION:These results suggest that the ANP/ NPR-A signaling pathway is upregulated in streptozotocin-induced diabetic mice,and contributes to the development of diabetic gastroparesis.

Endogenous Endothelin-1 Regulates Hypoxia-Induced Atrial Natriuretic Peptide Secretion by Activating the MAPK/ERK and PI3K/Akt Signaling Pathways in Isolated Beating Rabbit Atria

The present study investigated a possible mechanism for endogenous endothelin-1 (ET-1) regulation of atrial natriuretic peptide (ANP) secretion in isolated perfused acute hypoxic rabbit atria. Acute hypoxia significantly enhanced the release of ET-1 and the expression of the ET receptor (ETR) type A and B (ETRA and ETRB) in atrial tissues, with a concomitant increase in ANP secretion. The ETRA or ETRB antagonist, BQ123 (0.3 μmol/L) or BQ788 (0.3 μmol/L), respectively attenuated hypoxia-induced ANP secretion. Both antagonists significantly attenuated the levels of hypoxiainduced atrial phosphorylated (p)-extracellular signal-regulated kinase (ERK) and p-protein kinase B (Akt). The ERK and Akt inhibitors, PD098059 (30 μmol/L) and LY294002 (30 μmol/L), respectively mimicked the effect of the ETR antagonists. These results demonstrated that acute hypoxia- mediated atrial ET-1 regulated ANP secretion through ETR and the subsequent mitogenactivated protein kinase (MAPK)/ERK and ETR-phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathways. These pathways may mediate atrial endocrine functions under hypoxic conditions.

p42/p44 mitogen-activated protein kinases inhibit atrial natriuretic peptide mRNA transcription in gp130-mediated hypertrophic ventricular myocytes

Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK,also called p42/p44 MAPK)signaling pathway.Methods:isolated neonatal ventricular myocytes were treated with different concentrations of CT-1(10^(-9),10^(-8)and 10^(-7)mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.

Effect of atrial natriuretic peptide on ischemia-reperfusion injury in a porcine total hepatic vascular exclusion model

AIM: To evaluate the effect of ANP on warm I/R injury in a porcine THVE model. METHODS: Miniature pigs (mini-pigs) weighing 16-24 kg were observed for 120 min after reperfusion following 120 min of THVE. The animals were divided into two groups. ANP (0.1 μg/kg per min) was administered to the ANP group (n = 7), and vehicle was administered to the control group (n = 7). Either vehicle or ANP was intravenously administered from 30 min before the THVE to the end of the experiment. Arterial blood was collected to measure AST, LDH, and TNF-α. Hepatic tissue blood ? ow (HTBF) was also measured. Liver specimens were harvested for p38 MAPK analysis and histological study. Those results were compared between the two groups. RESULTS: The AST and LDH levels were lower in the ANP group than in the control group; the AST levels were signifi cantly different between the two groups (60 min: 568.7 ± 113.3 vs 321.6 ± 60.1, P = 0.038 < 0.05, 120 min: 673.6 ± 148.2 vs 281.1 ± 44.8, P = 0.004 < 0.01). No signifi cant difference was observed in the TNF-α levels between the two groups. HTBF was higher in the ANP group, but the difference was not signif icant. A signifi cantly higher level of phosphorylated p38 MAPK was observed in the ANP group compared to the controlgroup (0 min: 2.92 ± 1.1 vs 6.38 ± 1.1, P = 0.011 < 0.05).Histological tissue damage was milder in the ANP group than in the control group. CONCLUSION: Our results show that ANP has a protective role in I/R injury with p38 MAPK activation in a porcine THVE model.

Effect of acupuncture on the genetic expression of myocardial endothelin-1 and atrial natriuretic peptide in rats with stress-induced prehypertension

Objective:To explore the protective effect of acupuncture against myocardial injury in rats with stress-induced prehypertension (SIPH) by observing the genetic expression of myocardial endothelin-1 (ET-1) and atrial natriuretic peptide (ANP).Methods:Thirty-six Wistar rats were randomized into three groups:the control group,model group,and model + acupuncture (AP) group (n =12 rats per group).During the 11-day modeling period,the model group and the model + AP group experienced plantar electric stimulation in combination with noise exposure,and daily acupuncture intervention was applied simultaneously in the model + AP group;the control group did not experience modeling or acupuncture.Systolic pressure (SP) was measured the day before modeling began,and on the 3rd,5th,7th,9th,and 11th day after modeling initiation.On the 12th day,histopathological observation of the left ventricle was made with hematoxylin-eosin staining and quantitative genetic expression of myocardial ET-1,and ANP was tested by quantitative real-time polymerase chain reaction (PCR).Results:SP was higher in the model group than the control group on the 3rd,5th,7th,9th,and 11th days (all P <.01).SP in the model + AP group was lower than that in the control group on the 5th and 7th days (respectively,P =.008,P =.002) and on the 9th and 11th days (P =.029,P =.039).Hematoxylin-eosin staining showed normal myocardial cellular structure in the control group.The model group showed disordered arrangement of cardiac cells with morphological changes in some nuclei,including enlargement or dissolution;there was also infiltration of inflammatory cells and proliferation of collagen fibers.In the model + AP group,most of the myocardial cells were normally structured,and only part of the cells had morphological changes with enlarged nuclei or dissolution.Real-time PCR showed that expression of ET-1 and ANP mRNA in the model group was greater than the control group (respectively,P =.024,P =.000101).The model + AP group had lower expression of ET-1 and ANP mRNA compared with the model group (respectively,P =.033,P =.043).Conclusion:Acupuncture may lower blood pressure and downregulate the genetic expression of myocardial ET-1 and ANP in SIPH rats,suggesting a protective effect of acupuncture against myocardial damage.

Relationship between contents of plasma atrial natriuretic peptide and serum lipids of atherosclerosis in rabbits

Changes in plasma atrial natriuretic peptide(ANP)and serum lipids were observed us-ing dietetic atherosclerosis(AS)models.The results showed that plasma ANP level of the ASgroup was significantly higher than that of the control group(14.33±3.58μg/L vs 9.43±3.14μg/L).There was also a marked increase in serum Tch,TG,LDL-ch and VLDL-ch comparedwith the control group(P【0.01),suggesting that release of ANP increased with disturbance ofthe serum lipids and during AS formation,and that change in ANP was closely related to Tchand LDL-ch(P【0.05).Possible mechanisms causing these changes are also discussed.

Effects of highly potent atrial natriuretic peptide on circulating reninangiotensin-aldosterone system and cardiac function in dogs with ischemic heart failure

The effects of highly-potent atrial natriuretic peptide (HPANP) on circulating re nin-angiotensin-aldos-terone system (RAAS) and cardiac function were studied in an acute ischemic heart failure model. HPANP (6 μg/kg and 3 μg/kg) was infused intracoronarily. It was found that both doses of HPANP could cause significant decrease in plasma renin activity (PRA), angiotensin II (AII) and aldosterone (Ald). After the administraticn of HPANP, PRA, AII and Ald in the coronary sinus were decreased by 73. 2% (P<0.01), 68. o% (P<0.01) and 73. 6% (P<0.01), and the hormones in peripheral venous blood by 63. 3% (P<0.01), 53. 3% (P<0.01) and 64. 9% (P<0.01), respectively at the dose of 6 μg/kg. While PRA, AII and Ald in the coronary sinus and in peripheral venous blood decreased by 55. 9%, 55. 3%, 61. 9%, and 54. 0%, 42. 3%, 53, 3%, respectively at the 3μg/kg dose level. At the higher dose, HPANP increased left ventricular systolic pressure (LVSP, +13. 1%, P<0. 05), +dP/dtmax(+24.1 %, P<0.01), -dp/dtmax (+35.9%, P<0.01), and VCE(+28.9%, P<0.05). Mean arterial pressure and left ventricular end-diastolic pressure (LVEDP) were decreased (-15.0%, P<0.01, and 29. 6%, P<0.01, respectively). In contrast, the lower dose caused no significant changes of LVSP, +dp/dtmex,dp/dtmax and VCE(not including LVEDP, - 20. 5 %, P<0.05). Neither of the doses caused significant changes in heart rate and T value- Normal saline infusion has no effects on cardiac function and circulating RAAS- We conclude that in ischemic heart failure, intracoronary administration of HPANP can significantly suppress the activity of circulating RAAS, and improve cardiac function by reducing pre- and after-load of the heart, but has no direct myocardial effects.

Contribution of Estrogen to Sex Dimorphic Expression of Cardiac Natriuretic Peptide and Nitric Oxide Synthase Systems in ANP Gene-Disrupted Mice

Background: Sex dimorphism in the prevalence, onset, development and progression of cardiovascular disease (CVD) is well recognized, but the mechanisms whereby sex hormones are believed to confer cardioprotection are still not fully understood. Objective: This study more closely delineates the effect of 17β-Estradiol (E2) on the expression and signaling of the cardiac NP and NOS systems, well-known cardioprotective modulators of the cardiac hypertrophy (CH) response, that both contribute to downstream production of cyclic guanosine 3’,5’-monophosphate (cGMP). Materials and Methods: Ovariectomized (OVX) female ANP+/+ and ANP-/- mice, 6 - 7 weeks old, were subjected to a five-week treatment with E2 (100 μg/100 μL/day) or vehicle (VEH). Left ventricle from these treatment groups, along with that from age-matched male ANP+/+ and ANP-/- mice was used to assess expression of these systems by real-time quantitative PCR (qPCR). Left ventricle tissue and plasma cGMP were measured by enzyme immunoassay to assess alterations in resultant downstream signaling. Results: NP system expression was unchanged across genotype, sex and E2 treatment. Sex-specific differences in NOS system expression were observed;female mice showed an increased expression of NOS system genes that were significantly elevated in all but one of the E2 treatment groups. Left ventricle tissue cGMP remained unchanged across genotype, sex and E2 treatment. Plasma cGMP levels were unchanged in ANP+/+ treatment groups. In ANP-/- treatment groups, plasma cGMP in the female OVX-E2 mice was significantly higher compared to male and female OVX-VEH mice. Conclusion: These findings demonstrate that in the absence of ANP, E2 upregulates cardiac NOS system expression to produce cGMP. This study confirms the importance of the cardiac NOS system in females;this particular system may be a promising future target for sex-specific treatments and therapies for CVD in women.

ANP及KIM-1在脓毒症患者发生急性肾损伤中的变化及意义

目的探讨血心钠肽（ANP）及尿肾损伤分子-1（KIM-1）在脓毒症发生急性肾损伤（AKI）中的动态变化及意义。方法选取自2012—01～2012—09在我院ICU收治的60例脓毒症患者为研究对象，分别在0、2、6、24、48h采集血液及尿液标本，用ELISA法分别检测ANP和KIM-1。根据脓毒症患者是否在住院期间发生AKI，分为脓毒症AKI组、脓毒症非AKI组进行对比分析。结果在ICU住院期间28例患者发生AKI，AKI发生率46．67％。AKI组血ANP在2、6、24、48h和尿KIM-1在6、24、48h高于非AKI组（P〈0．05）；2h血ANP和6h尿KIM-1与确诊AKI时24h血清肌酐（sCr）呈正相关（r=0．959，P=0．000；r=0．938，P=0．000）。2h血ANP和6h尿KIM-1的ROC曲线下面积（AUC）分别为0．865（95％C10．772～0．957）和0．923（95％C10．854～0．992）。结论血ANP和尿KIM-1较sCr更早出现升高，其水平变化可以反映肾损害的严重程度，可以预测脓毒症是否发生AKI。

跳伞应激对空降兵情绪及ANP、AngⅡ、ET的影响

Objective: To study the change o f ANP,AngⅡ,ET and psychological reaction during military parachute jumping. Methods: Fifty-four new airborne were randomly divided into control group,experiment gro up one and experiment group two.10ml blood of median were col lect ed.The ANP,AngⅡand ET level were tested with RIA,and the level of emotion arous al was estimated with questionnaire.R esults : (1)There was a significant increase of plasma ANP,AngⅡ,ET durin g parachute jumping stress. (2) The score of anxiety 24 hour before jumpingwas significantly different from that of immediately after landing.Conclusion: Some kinds of psychological intervene was needed in preventing psychosomatic desease and neuroses during parachute jumping.

糖尿病肾病患者治疗前后AT-Ⅱ,VEGF,ET和ANP水平变化

目的 :检测糖尿病肾病 (DN)患者治疗前后血管紧张素Ⅱ (AT -Ⅱ )、血管内皮生长因子(VEGF)、内皮素 (ET)和心钠素 (ANP)含量变化 ,以比较不同药物的治疗效果。方法 :对象为DN患者分为 2组 :中药治疗观察组 35例 ;对照组 35例 ;正常对照组 35例。用放免法和ELISA法分别测定治疗前后血浆AT -Ⅱ、VEGF、ET和ANP水平。结果 :2组DN患者治疗前AT -Ⅱ、VEGF、ET和ANP含量均明显高于正常对照组 (p <0 0 5～ 0 0 1) ,治疗后较治疗前明显降低 (p<0 0 5～ 0 0 1)。观察组治疗后各含量下降较对照组明显。糖尿病肾病患者AT -Ⅱ含量与VEGF呈正相关 (r=0 4 6 5 ,p<0 0 5 ) ,血浆ET含量与ANP呈正相关 (r=0 6 1,p <0 0 5 ) ,观察组疗效稍好于对照组。结论 :AT -Ⅱ、VEGF、ET和ANP与DN的发生发展和病情的严重程度有关 ,它们之间可相互作用共同参与DN病变过程。以它们的指标作为疗效观察 ,中西药结合治疗糖尿病肾病患者效果较好。

经导管房间隔缺损封堵术对血清ANP、ET及心腔大小的影响

目的通过观察房间隔缺损(ASD)封堵术前、后血清ANP、ET及各心腔大小的变化,探讨经导管ASD封堵术对血清ANP、ET及心脏大小的影响。方法对29例成功行经导管ASD封堵术的患者,分别于封堵术前、术后24、72h取静脉血,采用放射免疫法测定血清ANP、ET的浓度;并于术前及术后第4天行心脏超声检查,测量各房室腔大小。结果ASD封堵术后24h及72h血清ANP浓度较术前明显降低,差异有统计学意义(P<0.01);封堵术后血清ET浓度与术前比较无显著差异。封堵术后第4天右室、右房内径较术前明显缩小,差异有统计学意义(P<0.01)。结论ASD封堵术后血清ANP浓度明显降低,右房、右室内径明显缩小。

动脉导管未闭封堵术前后血清ANP、ET的动态观察

目的通过观察动脉导管未闭(PDA)封堵术前后血清ANP、ET的变化,探讨经导管封堵PDA对血清ANP、ET的影响及意义。方法对35例成功进行封堵术的PDA患者,分别于封堵术前及术后24、72h取静脉血,采用放射免疫法测定ANP及ET浓度。结果与PDA患者管封堵术前比较,封堵术后24h及72h血清ANP、ET浓度均显示下降,ANP由(144.20±76.84)ng/L下降为(101.74±61.76)ng/L与(86.4±41.6)ng/L,ET由(88.33±60.13)ng/L下降为(80.96±59.16)ng/L与(61.77±37.93)ng/L,且术后72h下降差异具有统计学意义(P<0.05)。结论PDA封堵术后血清ANP、ET显示明显下降,而检测血清ANP及ET浓度可以间接了解心脏功能及肺动脉压力的变化。

急性脑梗死患者血浆ET、ANP水平的相关性研究

采用均相竞争法直接测定急性脑梗死患者的血浆内皮素 (ET)、心钠素 (ANP)含量 ,并动态观察其变化。结果显示 ,脑梗死患者急性期血浆 ET、ANP含量明显高于对照组 (P<0 .0 1) ,随着时间的延长 ,二者含量均逐渐降低 ,但于发病半个月后仍高于正常。经对患者发病后第 2、6、10、15天的 ET、ANP结果作相关分析 ,发现四个时段的ET、ANP含量均呈正相关关系。认为脑梗死急性期血浆 ET与 ANP之间存在相互促进、相互抑制的关系。

ANP和CGRP对油酸型急性肺损伤家兔细胞因子的影响

目的:研究心钠素(ANP)和降钙素基因相关肽(CGRP)对油酸型急性肺损伤(AL I)家兔血及支气管肺泡灌洗液(BAL F)中TNF- α、IL- 8和ET- 1含量的影响。方法:观察油酸型AL I家兔ANP+CGRP治疗前、后不同时间静脉血和BAL F中上述3种细胞因子浓度的变化,并于实验结束后测定肺水质量分数。结果:油酸致伤后30、6 0和12 0 min血及BAL F中TNF- α、IL- 8和ET- 1浓度显著增高(P<0 .0 5～0 .0 1) ,尤其以TNF- α增幅最大,ANP+CGRP治疗后各因子浓度明显降低(P<0 .0 5～0 .0 1) ,肺水质量分数也显著降低(P<0 .0 5 )。结论:静脉注射ANP+CGRP可有效降低油酸致伤后血和BAL F中TNF- α、IL- 8及ET- 1含量,抑制肺内炎症反应,减轻肺损伤。

ANG-Ⅱ、ANP对培养的人血管内皮细胞bFGF表达的影响

目的 了解血管紧张素 Ⅱ (Ang Ⅱ ) ,心钠素 (ANP)对人内皮细胞碱性成纤维细胞生长因子 (bFGF)表达的影响。方法 采用培养的人脐静脉内皮细胞 ,将Ang Ⅱ和ANP分别加入培养液内 ,通过免疫组织化学方法 ,原位杂交技术 ,结合图像分析法 ,测定各组内皮细胞bFGF蛋白及mRNA的表达变化。结果 Ang Ⅱ (10 8mol/L)对内皮细胞bFGF表达有明显促进作用 ,蛋白合成比对照组增加 5 9 3% (P <0 0 1) ;ANP (10 -7mol/L)对培养的内皮细胞bFGF表达有明显抑制作用 ,蛋白合成可减少 71 3% ;二者同时加入 ,蛋白合成比正常对照组减少 32 8% (P <0 0 1) ,各组间比较 ,差异具有统计学显著性意义 (P <0 0 1)。内皮细胞bFGFmRNA的变化与蛋白合成的改变基本相似。结论 ANP能拮抗AngⅡ对培养的人内皮细胞bFGF表达的促进作用 ,其作用可能是通过减少mRNA。

尿激酶对急性心肌梗死患者ERAANPS的影响

目的 观察尿激酶对急性心肌梗死 (AMI)患者血浆 -内皮素 -肾素 -血管紧张素 -心钠素系统(ERAANPS)的影响。方法 用放射免疫法测定AMI患者和正常对照组的血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素Ⅱ (ATⅡ )、心钠素 (ANP)的浓度。结果 与对照组相比 ,AMI后ERAANPS活性明显增强 ;尿激酶可使ET、PRA、ATⅡ浓度升高 ,与对照组相比具有显著性差异 (P <0 0 5 )。结论 急性心肌缺血坏死可激活ERAANPS ;

共染ANP对GH_4和AtT_（20）细胞肾素基因表达分泌的影响

本文应用现代基因共同转染技术，首次对ＧＨ４和ＡｔＴ２０细胞进行了重组大鼠ＡＮＰ和人肾素基因的共同转染，建立了表达细胞模型。并对其表达产物进行分析研究。文章着重分析研究了ＡＮＰ对肾素基因的表达产物的形成与分泌的调节作用。ＡＩ形成放免检测结果表明：转染细胞的表达是有效的。转染的ＧＨ４能有效地表达分泌肾素原；转染的ＡｔＴ２０细胞则不仅能形成肾素原，而且能分泌具有活性的肾素。ＡＮＰ转染的实验组不仅显示有明显的拮抗Ｆｏｒｓｋｏｌｉｎ的刺激作用，而且ＡＮＰ对肾素与肾素原的形成分泌有抑制作用，其中抑制肾素分泌的效能大于肾素原的分泌。实验证明，转染基因的表达细胞是有效研究肾素基因表达、分泌等调节的细胞模型。

羟乙基淀粉预扩容对剖宫产手术病人循环及ET、ANP的影响

目的观察羟乙基淀粉预扩容对联合腰麻下剖宫产手术病人循环和血浆内皮素(ET)、心钠素(ANP)的影响。方法30例剖宫产手术病人随机分为两组:羟乙基淀粉组(HES组)和复方乳酸钠组(LR组),每组15例。病人进入手术室开放外周静脉后快速输注两种液体各1000ml,并同时施行联合腰麻,记录BP、HR、SpO2的数值并分别于输液前(T0)、输液结束后(T1)、手术结束后30min(T2)抽静脉血测定血浆中ET、ANP的含量。结果两组病人麻醉后的BP较麻醉前均有明显下降(P<0.05);HES组ET、ANP的浓度没有明显的变化,而LR组ET、ANP的浓度较输液前明显增加并持续到手术结束(P<0.05)。结论羟乙基淀粉预扩容处理不但能维持联合腰麻下行剖宫产手术病人的循环稳定,而且能有效的减少ET、ANP等应激激素的释放。