COPD患者血清ANP、BNP和CNP测定及其临床意义

目的：探讨慢性阻塞性肺疾病（COPD）患者血清心钠素（ANP）、脑钠肽（BNP）、C型钠尿肽（CNP）水平的变化及其临床意义。方法：采用放射免疫分析79例COPD患者和36例健康对照组血清ANP、BNP和CNP水平,并进行统计分析。结果：COPD组血清ANP、BNP和CNP水平显著地高于健康对照组（t=3.6841,P〈0.01;t=11.70,P〈0.01;t=2.177,P〈0.05）,但Ⅰ、Ⅱ、Ⅲ和Ⅳ级组间血清ANP、BNP和CNP水平方差检验无显著性意义（F=2.123、F=1.515、F=0.165,P均〉0.05）。相互间相关性分析揭示：ANP、BNP和CNP三者间均呈显著正相关（r=0.369,P〈0.01;r=0.354,P〈0.01;r=0.426,P〈0.01）。住院期间死亡的患者血清ANP、BNP和CNP水平显著地高于好转出院的患者（t=5.149,P〈0.01;t=4.875,P〈0.01;t=2.830,P〈0.01）。结论：COPD患者血清ANP、BNP和CNP显著升高,且与病人的稳定情况、肺动脉压力及预后相关。     

基质金属蛋白酶3和尿激酶型纤溶酶原激活物受体在2型糖尿病大血管病变中的变化

目的： 探讨基质金属蛋白酶3（MMP-3）和尿激酶型纤溶酶原激活物受体（uPAR）在2型糖尿病大血管病变中的变化。方法: 用ELISA双抗体夹心法测定26例正常对照和39例2型糖尿病患者（其中单纯2型糖尿病15例、合并大血管病变24例）的血浆MMP-3和uPAR水平。结果: 单纯糖尿病组uPAR高于正常对照（P<0.05）而MMP-3无显著差异；合并大血管病变组MMP-3显著高于正常对照和单纯糖尿病组（P<0.01，P<0.01），而uPAR亦高于正常对照及单纯病变组（P<0.01，P<0.05）。2型糖尿病血浆MMP-3水平和uPAR水平呈正相关， LDL-C与uPAR呈正相关且是uPAR主要影响因素。 结论: MMP-3和uPAR与2型糖尿病大血管病变发生密切相关，MMP-3可作为2型糖尿病血管病变的循环标志物。     

EH患者血清利钠多肽及血栓素B_2水平的分析

目的：探讨原发性高血压（EH）患者血清ANP、BNP、CNP及TXB2水平的变化及其临床意义。方法：30例EH患者和正常人对照组分为2组;不同EH分期Ⅰ、Ⅱ、Ⅲ期分为3组,将测定结果进行统计分析。四项血清标志物均采用放射免疫分析。结果：EH患者组ANP、BNP、CNP及TXB2四项血清指标水平均较对照组升高非常显著（P均〈0.01）。Ⅰ期组EH患者血清ANP、CNP及TXB2三项血清标志物与对照组比较差异均无显著性（P均〉0.05）,而血清BNP则显著高于对照组（P〈0.05）;Ⅱ期组患者ANP水平显著高于Ⅰ期组和对照组（P〈0.05）,而BNP、CNP和TXB2三项血清标志物则非常显著高于Ⅰ期组和对照组（P均〈0.01）。Ⅲ期组结果显示,ANP、BNP、CNP和TXB2四项血清标志物均非常显著地高于Ⅱ期组、Ⅰ期组及对照组（P均〈0.01）,相关分析结果显示,患者ANP、BNP和CNP三项指标与自身的平均动脉压呈显著正相关（r=0.298,P〈0.01;r=0.409,P〈0.01;r=0.412,P〈0.01）。结论：本文四项血清指标水平显著升高,测定数据的变化与EH的发病及病情进展有关。     

2型糖尿病微血管病变患者血浆对氧磷酯酶-1活性与氧化应激的关系

目的探讨2型糖尿病微血管病变(DMPA)患者血浆对氧磷酯酶-1(PON-1)活性与氧化应激的关系。方法168例2型糖尿病根据微血管并发症情况分为无微血管并发症(NDC)组、糖尿病视网膜病变(DR)组和糖尿病肾病(DN)组,分别检测各组患者血浆PON-1、超氧化物歧化酶(SOD)和循环谷胱甘肽过氧化物酶(GSHPx)活性、丙二醛(MDA)含量,分析PON-1活性与SOD、MDA、GSHPx之间的关系。结果糖尿病各组患者血浆PON-1、SOD、GSHPx活性均明显低于对照组(P<0.01),DMPA组又低于NDC组(P<0.05),而血浆MDA含量与对照组比较显著升高(P<0.01),DMPA组又高于NDC组(P<0.05)。相关分析表明,糖尿病患者血浆PON-1活性与GSHPx、SOD呈正相关(r=0.774,P<0.01;r=0.801,P<0.01),与MDA呈负相关(r=-0.833,P<0.01)。结论在2型糖尿病DMPA中氧化应激增强及血浆PON-1活性显著降低,PON-1与氧化应激及其相互作用参与了2型糖尿病DM-PA的发生和发展。     

2型糖尿病患者C反应蛋白、脂联素和瘦素水平与胰岛素抵抗的相关性

目的探讨C反应蛋白(CRP)、脂联素(APN)、瘦素(Leptin)水平、胰岛素抵抗指数(HOMA-IR)与2型糖尿病(T2DM)病变易患因素的关系。方法用RIA法测定2型糖尿病患者血浆leptin和胰岛素(FINS),用ELSIA法测定血清ANP,用全自动生化分析仪常规测定血清CRP、空腹血糖(FPG),计算胰岛素抵抗指数(HOMA-IR,FPG×FINS/22.5),以正常健康体检者为对照组,进行对比分析。结果 CRP、leptin、HOMA-IR在2型糖尿病组显著高于对照组(P<0.01),ANP显著低于对照组(P<0.01);线性相关显示2型糖尿病HOMA-IR与CRP(r=0.36,P<0.05)、leptin(r=0.39,P<0.05)呈正相关,2型糖尿病HOMA-IR与APN(r=-0.32,P<0.05)呈负相关。结论低APN和高CRP、leptin血症可能是糖尿病的发病因子,它们的代谢紊乱与胰岛素抵抗有密切关系。     

原发性高血压患者血清利钠肽水平的变化

目的:研究原发性高血压(EH)患者血清利钠肽(ANP,BNP,CNP)水平的变化,及其与高血压分期和靶 器官损害间的关系。方法:放射免疫分析测定112例EH患者和47例非高血压患者的血清利钠肽(ANP,BNP, CNP)水平,并进行对照统计分析。结果:EH组血清ANP,BNP,CNP水平均较对照组显著增高(P均<0.01),而 且与平均动脉压成显著正相关(P均<0.01),但与体重指数无相关性意义,男女组间无统计学差异。Ⅰ、Ⅱ、Ⅲ期组 间平均血清ANP,BNP,CNP水平依次显著性递增(P均<0.05),不同分期的EH患者之间血清ANP,BNP,CNP水 平均有明显差异(P均<0.05)。EH患者中伴心脑肾并发症组血清ANP,BNP,CNP水平显著高于无并发症组(P 均<0.01)。结论:EH患者血清ANP,BNP,CNP水平显著增高,且与平均动脉压、高血压分期及是否伴有并发症 相关,提示ANP,BNP,CNP变化与病情严重程度及高血压的靶器官损害相关并有助于预后判断。     

糖尿病患者血浆CRP浓度与糖尿病血管病变的相关分析

目的:揭示2型糖尿病(DM2)患者血浆C-反应蛋白(CRP)浓度,探讨其对糖尿病血管病变的诊断价值。方法:对50例健康体检正常者和126例DM2患者,用ELISA检测血浆CRP浓度,统计分析其与糖尿病血管病变的相关性。结果:糖尿病患者血浆CRP浓度(7.48±3.26)mg/L较健康体检正常者(1.41±0.71)mg/L显著升高(P<0.01);糖尿病血管病变患者血浆CRP浓度(11.27±3.19)mg/L较糖尿病非血管病变患者(5.61±2.26)mg/L显著升高(P<0.01)。Logistic回归显示,血浆CRP浓度(OR=3.141,95%CI=1.431～11.316,P<0.01)是糖尿病并发血管病变的独立危险因素。ROC曲线分析显示,血浆CRP浓度对糖尿病并发血管病变有显著诊断价值(曲线下面积=0.849,95%CI=0.779～0.902,P<0.01),且判定血浆CRP浓度>8.36 mg/L,对诊断糖尿病并发血管病变有85.7%的灵敏度和76.9%的特异度。结论:CRP可能参与糖尿病血管病变的血管内皮损伤过程,血浆CRP浓度对于DM2并发血管病变,可提供作为一敏感的诊断标志物。     

2型糖尿病微血管病变患者血浆同型半胱氨酸、胱抑素C水平及血液流变学指标变化

目的:观察2型糖尿病(T2DM)微血管病变患者血浆同型半胱氨酸(Hcy)、胱抑素C(CysC)水平及血液流变学指标的变化。方法:T2DM患者120例,按有无微血管病变分为糖尿病无微血管病变组(A组,62例)和糖尿病并微血管病变组(B组,58例),检测两组病人的血浆Hcy、CysC水平和血液流变学指标并进行组间比较分析。结果:与A组比较,B组血浆Hcy、CysC、全血粘度、血浆粘度、红细胞压积、红细胞聚集指数均明显升高,差异有统计学意义(P<0.01)。结论:高Hcy、CysC及高粘血症参与了糖尿病微血管病变的发生和发展。     

冠状动脉病变程度与血浆B型利钠肽对冠心病的影响因素

目的 探讨冠心病患者冠状动脉病变程度与血浆B型利钠肽的关系。方法 选择我院2017年1月~8月住院的冠心病患者54例为A组,同时选择冠脉血管无狭窄的患者26例作为B组,收集所有研究对象的年龄、性别、血糖、血脂、血压、血浆脑钠肽（BNP）浓度、冠状动脉的病变部位及程度等临床资料,观察不同程度冠状动脉病变患者的血浆BNP水平。结果 血浆BNP水平A组较B组升高,统计学意义显著（P＜0.001）。Logistic回归分析显示,年龄、BNP水平、舒张压是冠状动脉狭窄的独立危险因素。在A1、A2及A3组中随着Gensini评分增加,血浆BNP水平逐渐升高,Gensini评分与血浆BNP水平呈明显的正相关（r=0.594,P＜0.05）。结论 血浆BNP参与了冠状动脉狭窄的病理生理过程,是冠状动脉病变的独立危险因素之一;血浆BNP的水平能一定程度上的反映冠脉病变程度。     

糖尿病视网膜病变患者血浆Hcy、CEC和ET水平的检测分析

目的:分析糖尿病视网膜病变患者血浆同型半胱氨酸(Hcy)、外周血循环内皮细胞(CEC)和血浆内皮素(ET)水平及其相互关系。方法:将80例2型糖尿病(T2DM)患者分为2组:无糖尿病视网膜病变(NDR)组50例,糖尿病视网膜病变(DR)组30例,以我院健康体检正常者30例为对照(NC)组。分别测定Hcy、CEC、ET水平。结果:T2DM患者Hcy、CEC和ET水平均明显高于对照组(P<0.01);DR组Hcy、CEC、ET明显高于NDR组(P<0.01)。DR组血浆CEC计数和ET浓度呈正相关(r=0.839,P<0.05),Hcy浓度与CEC计数呈正相关(r=0.615,P<0.05),Hcy与ET浓度亦呈正相关(r=0.642,P<0.05)。结论:T2DM患者血浆Hcy、CEC、ET水平升高与DR有密切关系,血浆Hcy升高及内皮损伤可能在糖尿病患者视网膜病变的发生和发展中起重要作用。     

Regional cardiac expression and concentration of natriuretic peptides in patients with severe chronic heart failure

The purpose of this study was to examine the regional cardiac mRNA expression and concentration of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) in relation to the circulating peptide concentrations in patients with chronic heart failure (CHF). The myocardial mRNA levels and peptide concentrations of BNP and ANP were analysed in seven different regions of the heart from patients undergoing cardiac transplantation. Autopsy samples from individuals without known cardiovascular disease were used as controls. The plasma levels of natriuretic peptides and their N‐terminal propeptides, Nt‐proBNP and Nt‐proANP, were measured in the CHF patients and healthy volunteers. In the autopsy specimens, the atrial regions appeared to contain the highest peptide levels for BNP as well as ANP, the atrioventricular ratio being 12–262 and 72–637‐fold, respectively. In the CHF patients there was a relative shift towards the ventricle for BNP, reducing the atrioventricular ratio to 6–16‐fold. The circulating concentrations of BNP/Nt‐proBNP in the CHF patients correlated closely to the BNP mRNA expression in most myocardial regions including the left ventricle (r=0.72, P < 0.001). For circulating concentrations of ANP/Nt‐proANP, such correlation were limited to the left atrium free wall (r=0.66, P < 0.002). Thus, of the two natriuretic peptides, BNP/Nt‐proBNP may be a better reflector of left ventricular overload.     

Expression patterns of natriuretic peptides in pre-hibernating and hibernating anatolian ground squirrel (Spermophilus xanthoprymnus) lung

Anatolian ground squirrel (Spermophilus xanthoprymnus) is a true hibernator. This animal transiently reduces pulmonary function during hibernation. Continuance of pulmonary function is very important to survive ground squirrels during the hibernation. Natriuretic peptides may be key players in the modulation of pulmonary hemostasis. However, NPs’ role in pulmonary function during hibernation remains unclear. We aimed to investigate the localization and distribution of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) in squirrel lungs during pre-hibernation and hibernation periods using immunohistochemistry. Our immunohistochemical data indicate that ANP, BNP, and CNP were produced by the mucosal epithelium of terminal and respiratory bronchioles, smooth muscle cells in the lamina propria of terminal bronchioles and vascular smooth muscle cells, alveolar type II cells, and macrophages. ANP immunoreactivity was weaker than BNP and CNP immunoreactivities in these cells. The results also demonstrate that the number of ANP, BNP and CNP positive alveolar type II cells tended to increase, although statistically non-significant, during the hibernation period, but the expression of NPs in other pulmonary cells is unaffected by hibernation. This study firstly investigates ANP, BNP and CNP distribution in the Anatolian ground squirrel lung. However, further studies are required to dissect their functional roles during the hibernation.     

Polymyxin B-immobilized fiber hemoperfusion attenuates increased plasma atrial natriuretic peptide and brain natriuretic Peptide levels in patients with septic shock

Polymyxin B-immobilized fiber (PMX-F) hemoperfusion is reported to be safe and effective in septic shock patients. Because atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) may have pathophysiologic significance in the cardiac dysfunction of septic shock patients, we conducted a study to determine whether PMX-F treatment affects plasma ANP and BNP levels in patients with septic shock. Fifty septic shock patients (34 men and 16 women; mean age 60.0 years) and 30 healthy volunteers (18 men and 12 women; mean age 56.0 years) were included in this study. Polymyxin B-immobilized fiber treatment was performed twice, separated by an interval of 24 hours. Blood endotoxin, interleukin (IL)-6, ANP, and BNP levels were measured before, immediately after the second PMX-F treatment, and the following day. In comparing patients with septic shock with healthy control subjects, we found significant increases in plasma endotoxin (p < 0.001), IL-6 (p < 0.001), ANP (p < 0.001), and BNP (p < 0.001). After the second PMX-F treatment, plasma levels of endotoxin (p < 0.01), IL-6 (p < 0.01), ANP (p < 0.01), and BNP (p < 0.01) were reduced significantly. Values decreased further the following day. Both plasma ANP and BNP levels are increased in septic shock patients and PMX-F treatment is effective in reducing these natriuretic peptide levels.     

Functional contribution of voltage-dependent and Ca2+ activated K+ (BK(Ca)) channels to the relaxation of guinea-pig aorta in response to natriuretic peptides.

We examined the relaxant effects of natriuretic peptide family on the isolated guinea-pig aorta to determine the receptor subtype which primarily mediates this vascular relaxation, with particular attention to the apparent contribution of voltage-dependent and Ca2+-activated KS (BK(Ca)) channels to the response. Three endogenous natriuretic peptide ligands (natriuretic peptide, ANP; brain natriuretic peptide, BNP; C-type natriuretic peptide, CNP) produced a concentration-dependent relaxation in de-endothelialized guinea-pig aorta pre-contracted by noradrenaline (NA), with a potency order of ANP > or = BNP > CNP. Although the relaxations elicited by these three natriuretic peptide ligands were significantly diminished by iberiotoxin (IbTx, 10(-7) M), a selective BK(Ca) channel blocker, the inhibitory effect of IbTx was most pronounced for the CNP-induced relaxation; when estimated at 10(-7) M of each peptide, the apparent extent of BK(Ca) channel contribution to the total relaxant response was approximately 60% for CNP > approximately 20% for either ANP or BNP. Supporting the substantial role of BK(Ca) channels in the vascular responses, high-KCl (80 mM) potently suppressed the relaxations induced by these natriuretic peptide ligands. The relaxant response to 8-Bromo-cyclic GMP, a membrane permeable cyclic GMP analogue, was also diminished by IbTx (10(-7) M) and high-KCl (80 mM), which indicates the key role of cyclic GMP in the BK(Ca) channel-mediated, natriuretic peptide-elicited vascular relaxation. These results indicate that the A-type receptor (NPR-A, which is more selective for ANP and BNP) rather than the B-type receptor (NPR-B, which is more selective for CNP) predominates in the guinea-pig aorta as the natriuretic peptide receptor which mediates this vascular smooth muscle relaxation. Although activation of BK(Ca) channels substantially contributes to both NPR-A- and NPR-B-activated relaxations, particularly in the NPR-B-activated relaxation, this K channel may function as a primary relaxant mediator in this conduit artery.     

The nocturnal secretion of cardiac natriuretic peptides during obstructive sleep apnoea and its response to therapy with nasal continuous positive airway pressure

The nocturnal secretion profile of the newly identified natriuretic peptide (NP), brain natriuretic peptide (BNP), was studied in 14 patients with obstructive sleep apnoea syndrome (OSAS) (apnoea hypopnoea index: 60.5±3.4, mean±SE) during two separate nights before and during nasal continuous positive airway pressure (NCPAP) therapy. Plasma levels of NPs (atrial natriuretic peptides; ANP and BNP) were measured at 2-h intervals during sleep. Simultaneously, blood pressure was measured by a non-invasive method (Finapres^®, Ohmeda, Englewood, CO, USA) and urine was collected for determing volume and catecholamine levels. Urinary and serum sodium concentration were determined before and after the study. Eight non-snoring subjects were also studied for the investigation of normal nocturnal profiles of BNP levels. To understand the discrete secretion profiles of the two NPs during sleep, blood was sampled from an additional seven patients every 5 min over a 30-min period around 00.00 and 04.00 hours before NCPAP. In patients with OSAS, plasma BNP levels increased from the beginning of sleep (22:00 h) to the morning (06:00 h) before NCPAP therapy (P< 0.01, anova ). Baseline BNP levels were not significantly correlated with patient's clinical and poly- somnographic parameters. However, in the latter half of the sleep period (02:00–06:00 h), increases in BNP levels during the night before NCPAP therapy were significantly correlated with blood pressure elevations (systolic: r=0.784 P< 0.01, diastolic: r=0.587 P< 0.01) and with apnoea duration (r=0.582 P< 0.01). In normal subjects BP and BNP levels were not changed significantly during sleep. Plasma BNP levels were well correlated with concomitant ANP levels (P< 0.001). NCPAP therapy reduced ANP and BNP levels during sleep and in the morning (P< 0.01). Plasma levels of BNP at 5 min intervals before NCPAP therapy revealed few variations. On the other hand, ANP levels fluctuated over the 30-min period. Changes in BNP levels during sleep in the patients with OSAS may be related to blood pressure variations, but may be too small to play a significant physiological role in regulating diuresis in OSAS. Further work is required to determine the precise role of dual natriuretic system in cardiovascular load and natriuresis in OSAS.     

Atrial amyloid deposits in the failing human heart display both atrial and brain natriuretic peptide-like immunoreactivity

Atrial amyloid deposits are common in the ageing human heart and contain alpha-atrial natriuretic peptide (proANP99-126) immunoreactivity. However, atrial myocytes secrete both amino and carboxy terminal fragments of the ANP prohormone (proANP1-126) and also express an homologous, but separate brain natriuretic peptide (BNP). Characteristic amyloid deposits were identified in the atria of 9/22 patients (26-63 years of age) with end-stage heart failure. Amyloid fibrils displayed immunoreactivity for both amino and carboxy terminal fragments of proANP1-126 and for the distinct BNP sequence. As in other endocrine organs, both mature and precursor peptide sequences appear to be constituents of amyloid fibrils. Whilst immunoreactivity for cardiac peptide hormones is co-localized in atrial amyloid deposits, it is uncertain whether the increase in natriuretic peptide expression which accompanies cardiac failure contributes to the incidence of isolated atrial amyloidosis.     

急性心肌梗死患者血浆BNP、ANP、ET和CRP水平变化

为观察急性心肌梗死(AMI)患者血浆中脑钠肽(BNP)、内皮素(ET)、C-反应蛋白(CRP)和心钠素(ANP)水平变化, 探讨AMI发病机制,为诊断、治疗及预后判断提供依据, 应用酶联免疫及免疫放射分析法对46例AMI患者治疗前后和30名对照者血浆中的BNP、ET、CRP、ANP水平进行检测.结果显示, AMI患者血浆中BNP、ET、CRP、ANP治疗后均明显下降, 与治疗前比较有显著性差异(P＜0.01); AMI患者BNP、ET、CRP、ANP水平明显高于对照组(P＜0.01); BNP与CRP治疗前水平变化比较呈正相关r=0.847, 治疗后呈明显的下降趋势, 其相关系数为r=0.654; AMI患者治疗前后ANP与ET比较呈正相关, 但经溶栓和相应的支持治疗后ANP基本恢复到正常水平(P＞0.05),而BNP、ET、CRP水平虽然下降明显, 但与对照组比较仍有明显差异(P＜0.05).结论: AMI患者血浆中BNP、ANP、ET、CRP水平的变化说明其参与了急性心肌梗死发生、发展, 特别是冠状动脉粥样斑块的形成和(或)破裂及血栓形成, 其炎症因子是主要因素.因此, 四项指标的观察分析对AMI诊断、治疗、预后判断具有重要意义.     

Increased brain natriuretic peptide and atrial natriuretic peptide plasma concentrations in dialysis-dependent chronic renal failure and in patients with elevated left ventricular filling pressure

Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations were measured in patients with dialysis-dependent chronic renal failure and in patients with coronary artery disease exhibiting normal or elevated left ventricular end-diastolic pressure (LVEDP) (n = 30 each). Blood samples were obtained from the arterial line of the arteriovenous shunt before, 2 h after the beginning of, and at the end of hemodialysis in patients with chronic renal failure. In patients with coronary artery disease arterial blood samples were collected during cardiac catheterization. BNP and ANP concentrations were determined by radioimmunoassay after Sep Pak C₁₈ extraction. BNP and ANP concentrations decreased significantly (P < 0.001) during hemodialysis (BNP: 192.1 ± 24.9, 178.6 ± 23.0, 167.2 ± 21.8 pg/ml; ANP: 240.2 ± 28.7, 166.7 ± 21.3, 133.0 ± 15.5 pg/ml). The decrease in BNP plasma concentrations, however, was less marked than that in ANP plasma levels (BNP 13.5 ± 1.8%, ANP 40.2 ± 3.5%; P < 0.001). Plasma BNP and ANP concentrations were 10.7 ± 1.0 and 60.3 ± 4. 0 pg/ml in patients with normal LVEDP and 31.7 ± 3.6 and 118.3 ± 9.4 pg/ml in patients with elevated LVEDP. These data demonstrate that BNP and ANP levels are strongly elevated in patients with dialysis-dependent chronic renal failure compared to patients with normal LVEDP (BNP 15.6-fold, ANP 2.2-fold, after hemodialysis; P < 0.001 or elevated LVEDP (BNP 6.1-fold, ANP 2.0-fold, before hemodialysis; P < 0.001), and that the elevation in BNP concentrations was more pronounced than that in ANP plasma concentrations. The present results provide support that other factors than volume overload, for example, decreased renal clearance, are also involved in the elevationin BNP and ANP plasma levels in chronic renal failure. The stronger elevation in BNP concentrations in patients with chronic renal failure and in patients with elevated LVEDP and the less pronounced decrease during hemodialysis suggest a different regulation of BNP and ANP plasma concentrations.[/ p]Abbreviations ANP atrial natriuretic peptide - BNP brain natriuretic peptide - LVEDP left ventricular end-diastolic pressure Correspondence to: C. Haug