Content of Atrial Natriuretic Peptide in Cardiomyocytes Granules of Newborn Female Rats with Type 1 Diabetes Mellitus.

Natriuretic peptides and contractile reserve in dilated cardiomyopathy

To compare the concentration of plasma atrial natriuretic peptide in patients with acute myocardial infarction with a healthy population and to determine whether a raised concentration of plasma atrial natriuretic peptide at admission was a predictor of mortality after acute myocardial infarction. Patients with acute myocardial infarction were divided into a group with no congestion (class I) and a group with congestion (class II-IV) according to their highest Killip classification in the first 24 hours after infarction. The concentration of plasma atrial natriuretic peptide was measured at admission. On the basis of the concentration of atrial natriuretic peptide measured in the healthy population, patients were separated into two groups: a group with a high (greater than 200 pg/ml) and a group with a low concentration of atrial natriuretic peptide (less than or equal to 200 pg/ml). The patients were followed for three years. 55 patients admitted to the coronary care unit within 12 hours of the appearance of symptoms of acute myocardial infarction were compared with 51 healthy individuals. Plasma atrial natriuretic peptide, Killip class, mortality. The patients had significantly higher concentrations of atrial natriuretic peptide than the healthy controls. Furthermore, patients with congestion had a significantly higher concentration of atrial natriuretic peptide than the uncongested group of patients. Total mortality was 34.5%. In the group with a low concentration of atrial natriuretic peptide the mortality was only 13.6%, whereas mortality was significantly higher (48.5%) in the group with a high concentration. The measurement of atrial natriuretic peptide separated the patients into low and high risk groups after acute myocardial infarction.

Atrial natriuretic peptide (ANP) concentrations within the reference interval have been reported in patients with alcoholic liver disease, chronic active hepatitis, and hepatocellular carcinoma. Markedly increased ANP concentrations, by contrast, have been found in patients with liver cirrhosis [3]. Exogenously administered ANP has been found to elevate the plasma concentration of its second messenger cyclic guanosine monophosphate (cGMP) in accordance with its physiological effects [4]. Therefore, cGMP increase in plasma can be regarded as a marker for the biological activities of ANP. Because of contradictory reports [2, 3, 5] on ANP in liver cirrhosis we investigated plasma ANP and cGMP concentrations to assess the biological activity of ANP in liver cirrhosis. Plasma ANP concentrations were determined in 124 healthy volunteers (72 males, 52 females) aged 20 64 years (40 _+ 12 years) and plasma cGMP concentrations in 147 healthy blood donors (92 males, 55 females) aged 15-62 years (34+_ 13 years). Plasma ANP and cGMP concentrations were determined in 15 patients with liver cirrhosis (7 males, 8 females) aged 31-69 years (54_+ 14 years). Five patients had ascites. The underlying cause of cirrhosis was cq-antitrypsin deficiency in 4 patients, alcohol abuse in 7, chronic hepatitis in 2, and unknown in 2. Creatinine concentrations in plasma were within the normal range (79.56 -+ 9.547 p.mol/1, range: 66.3-101.66 pmol/1) in all patients. Plasma cGMP concentrations were determined by radioimmunoassay (Amersham International, Amersham, Buckinghamshire, UK), and ANP concentrations in plasma were measured by means of a commercially available radioimmunoassay (Eiken, Tokyo, Japan) without extraction [1]. Results are expressed as mean _+ SD. Groups were compared statistically using Mann-Whitney U test; significance was defined as P<0.05. Plasma cGMP concentrations in patients with liver cirrhosis (4.448_+2.022 nmol/1, range 0.5-8.28 nmot/1, n = 15) did not differ significantly from those in healthy controls (4.637_+ 1.533nmol/1, range, 1.88~.04nmol/1, n=147, P=0.9426; Fig. 1). By contrast, plasma ANP concentrations were significantly higher in patients with cirrhosis (213.867_+83.032 ng/1, range 107-389ng/1, n=15) than in healthy controls (69.5_+ 26.05 ng/1, range 18-151 ng/1, n = 124, P=0.0001; Fig. 1). In the group of patients with liver cirrhosis no significant difference in plasma ANP (206.2_+59.437 versus 217.7-+95.422, P = I ) or plasma cGMP (5.656-+1.804 versus 3.777_+1.897, P=0.142) concentrations were detectable between patients with and patients without ascites. We found increased immunoreactive ANP concentrations without a concomitant increase in plasma cGMP in our patients with liver cirrhosis. In accordance with earlier reports we found no significant difference in plasma concentrations of ANP [3]

A long-term effect of pentobarbital treatment on the storage and release of atrial natriuretic peptide (ANP) was investigated in rats. The experimental group was treated with pentobarbital (50 mg/kg, ip), and the control group was injected with the vehicle only. They were used one week after the treatment. Male and female rats were used separately to see if there exists a sex difference in the response to pentobarbital. In male rats, the plasma ANP measured in a conscious state was significantly higher in the experimental group than in the control. The ANP content as well as the number of specific granules in the atrial tissue was significantly lower in the experimental group. In response to extracellular volume expansion (VE), amounting up to 5% of the body weight over 30 min, while the plasma ANP increased in the control, it did not significantly change in the experimental group. Urinary responses to the exogenous infusion of ANP did not differ in magnitude between the two groups. In female rats, neither the plasma level nor the atrial content of ANP (or the atrial granularity) was different between the experimental and control groups. Nor did the increase of plasma ANP in response to VE differ in magnitude between the two groups in female rats. These results indicate that pentobarbital may have a long-term effect on the storage and release of ANP.

The influence of physiological cardiac hypertrophy on the concentration of plasma atrial natriuretic peptide was studied in six male athletes and six normally active, matched control men. They were examined by echocardiography during a graded exercise test on a bicycle ergometer. Plasma atrial natriuretic peptide was measured at rest, at each workload until exhaustion, and 15 and 30 minutes after the exercise test. Echocardiography showed that the athletes had a significantly larger left atrium, left ventricular end diastolic diameter, left ventricular posterior wall, interventricular septum, left ventricular ejection fraction, and left ventricular mass than the controls. The athletes performed significantly more work than the control group--325 W v 277 W. The plasma concentration of atrial natriuretic peptide rose by a mean factor of 2.76 (range 1.78-4.28) in all men from rest to maximum exercise. There were no differences between the athletes and the controls in the concentrations of plasma atrial natriuretic peptide at rest, at any workload, or at maximum workload. Neither was there any difference in the increase in plasma atrial natriuretic peptide between the groups. There was no correlation between the plasma concentrations of atrial natriuretic peptide and any of the variables measured by echocardiography. In healthy young men plasma atrial natriuretic peptide rises by a factor of about 2.8 during maximum exercise and the size of the chambers on the left side of the heart or left ventricular hypertrophy does not seem to influence the concentration of plasma atrial natriuretic peptide at rest or during exercise.

To quantify the renal excretion of atrial natriuretic peptide (ANP) in birds, synthetic ANP was infused intravenously into conscious Pekin ducks at rates of 10, 30 and 90 ng/kg per min for 30 min and the relationships between plasma and urine ANP concentrations were monitored by RIA. The infusions of ANP produced dose-dependent elevations in the plasma concentrations of the hormone; however, urinary concentrations and excretion rates did not change significantly from the basal values of 142.2 +/- 21.5 pg/ml and 26.4 +/- 4.5 pg/min per kg respectively. The metabolic clearance rate of ANP remained constant at each infusion dose (approximately 200 ml/min per kg). The urinary clearance rates (< 0.3 ml/min per kg) indicated that the fraction of ANP cleared from the blood via the urine was less than 0.2%. Clearly, excretion of intact ANP via this route is not a quantitatively important means of elimination for this hormone in birds.

目的 探讨血浆脑钠素(BNP)、心钠素(ANP)浓度变化对心力衰竭的诊断价值.方法 分别采用酶联免疫法和放射免疫法检测75例心力衰竭患者(NYHAⅡ～Ⅳ级)和25名健康对照者的血浆BNP和ANP浓度,同时采用纽约心脏病学会(NYHA)标准对心功能分级和用超声心动图检查评定患者心功能.结果 心力衰竭组血浆BNP浓度为(1 794.1±724.5) ng/L、ANP浓度为(948.5 ± 520.7) ng/L,与正常对照组BNP(90.5±55.8) ng/L、ANP(121.7±71.1 ) ng/L比较差异有统计学意义(P＜0.01).BNP浓度心功能Ⅱ级为(552.9 ±339.6) ng/L、Ⅲ级(1 303.9±566.4 ) ng/L、Ⅳ级(3 625.5±1 069.2) ng/L,两两比较差异有统计学意义(P＜0.05);ANP浓度Ⅱ级为(518.8±376.3) ng/L、Ⅲ级(1 061.9±521.3) ng/L、ⅣV级(1 264.7±798.1) ng/L,Ⅱ级与Ⅲ级、Ⅳ级比较差异有统计学意义(P＜0.05),而Ⅲ级和Ⅳ级比较差异无统计学意义(P＞0.05).左心室射血分数LVEF＞40%的患者BNP为(1 096.7±656.6) ng/L、ANP为(931.6±320.9 ) ng/L,LVEF＜40%的患者BNP(2 659.4±743.5 ) ng/L、ANP(974.3±555.6 ) ng/L,两组患者血浆BNP浓度差异有统计学意义(P＜0.05);而ANP差异无统计学意义(P＞0.05).BNP和ANP在受试者工作特征(ROC)曲线下的面积分别为0.97和 0.85,两者曲线下面积差异有统计学意义(P＜0.01).结论 血浆BNP比ANP对心力衰竭患者的诊断具有更高的准确性,BNP与超声心动图反映的血流动力学状况指标LVEF及NYHA分级具有较好的相关性,可以作为心力衰竭分级的一个良好的诊断指标。

The existence of low concentrations of atrial natriuretic peptide (ANP) in canine cerebrospinal fluid which does not correlate with plasma ANP levels.

Atrial natriuretic peptide in the dog with mitral regurgitation

Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase.

Atrial Natriuretic Peptide Reduces Vascular Leakage and Choroidal Neovascularization

ObjectivesTo study the protective effects of Atrial Natriuretic Peptide (ANP) Injection on the cultured human umbilial vein endothelial cells injured by hypoxia-reoxygenationMethodshypoxia-reoxygenation group (n = 6): cells were cultured in...

ObjectiveTo study the protective effects of Atrial Natriuretic Peptide (ANP) Injection on the cultured human umbilical vein endothelial cells injured by hypoxia-reoxygenation.MethodsHypoxia-reoxygenation group (n=6): cells were cultured in the hypoxia...

The present study describes the concentration and molecular form of atrial natriuretic peptide (ANP) in Holstein dairy cattle with mild (bacterial endocarditis; BEC) or severe (dilated cardiomyopathy; DCM) heart failure. Significant increases in plasma concentration of ANP were observed in cattle with DCM (73.3 +/- 16.02 pmol/l, n = 4, P less than 0.01) and BEC (20.6 +/- 3.45 pmol/l, n = 7, P less than 0.05), when compared with those in control cattle (14.5 +/- 1.84 pmol/l, n = 12). The concentration of ANP in cattle with DCM was significantly (P less than 0.01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r = 0.95, P less than 0.01) and left ventricular end-diastolic pressure (r = 0.84, P less than 0.01). Gel-permeation chromatography of ANP in plasma and the right atrium from control and cattle with BEC revealed a single peak corresponding to the elution position of authentic human ANP(99-126) in plasma, and two peaks corresponding to those of authentic human ANP(99-126) and pro-ANP in the atrial extract. In cattle with DCM, however, peaks corresponding to the elution positions of authentic human beta-ANP and/or pro-ANP were detected in addition to the peak corresponding to ANP(99-126). The content of ANP in the right atrium of cattle with DCM was significantly (P less than 0.05) increased compared with that in control cattle and those with BEC. The present study therefore suggests that the synthesis and secretion of ANP might be stimulated by atrial distention induced by increased atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension induced by nitric oxide synthase inhibition activates the atrial natriuretic peptide (ANP) system