Mean Plasma Atrial Natriuretic Peptide Research Articles

Acute Supramaximal Exercise-Induced Adiponectin Increase in Healthy Volunteers: Involvement of Natriuretic Peptides

Exercise may modulate lipolysis via leading to natriuretic peptide secretion and beta-adrenergic activation. Adiponectin, an adipose-secreted multifunctional signaling protein, may be the missing link between exercise and lipolytic activity. In this study, we aimed to investigate the effects of supramaximal exercise on plasma levels of adiponectin, atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP) in healthy humans. Thirty-one healthy young adult volunteers (male/female, 15/16; mean age±SD, 20.7±1.7 years) underwent a 30-second Wingate anaerobic exercise test on a cycle ergometer and venous blood sampling before and after the exercise test. Plasma ANP and BNP levels were assayed by radioimmunoassay, whereas adiponectin levels were assayed by enzyme-linked immunosorbent assay. Systolic and diastolic blood pressures, heart rate, hematocrit levels and blood lactate were also measured before and after exercise. The mean plasma adiponectin level significantly increased following a 30-second anaerobic exercise test compared to resting level (17.45±4.70 vs 31.29±5.16 μg/mL, respectively, p<0.001). The mean plasma ANP and BNP levels remained comparable before and after the 30-second anaerobic exercise. A 30-sec supramaximal exercise session enhanced circulating adiponectin levels in both gender groups, whereas ANP and BNP levels exerted non-significant alterations. We suggest that acute anaerobic exercise may affect secretory function of adipose tissue which seems not related with natriuretic peptide secretion.

Plasma atrial natriuretic peptide concentration in warmblood horses with heart valve regurgitations

Objectives This study measured plasma atrial natriuretic peptide (ANP) concentration in horses with heart valve regurgitations (HVR) with and without atrial and ventricular dilatation. Background In humans and small animals, plasma ANP concentration is increased in heart disease and correlates with the severity of clinical signs and heart enlargement. Animals, materials and methods Ten healthy horses (control) and 36 horses with HVR were evaluated by auscultation, electrocardiography, echocardiography, and determination of plasma ANP. Results Control horses demonstrated mean plasma ANP concentration of 21 ± 5.4 pg/mL. Of the 36 horses with HVR, 17 horses possessed normal echocardiographic heart size (group 1), 10 horses had a left atrial dilatation (group 2) and 9 horses had both left atrial and ventricular dilatation (group 3). Mean plasma ANP concentration of groups 1, 2 and 3 was 20.1 ± 5.6 pg/mL, 22.9 ± 11.0 pg/mL and 27.6 ± 17.4 pg/mL, respectively. The plasma ANP concentrations of HVR and control horses were not significantly different. The highest ANP concentrations were observed in horses with atrial and ventricular dilatation. No correlation between left atrial or ventricular size, weight, or sex and the plasma ANP concentration was found. Conclusions No significant differences in plasma ANP concentration was observed between groups. Further study, especially in horses with clinical signs of heart failure is needed.

Effects of sinus rhythm restoration in patients with persistent atrial fibrillation: a clinical, echocardiographic and hormonal study

The hemodynamic consequences of atrial fibrillation (AF) may lead to impairment of the left ventricular function and a reduction in exercise capacity. Studies on mechanical and neurohormonal remodelling in patients with AF are becoming increasingly important. The results could possibly enhance treatment strategies of these patients. The aim of this study was to assess changes in exercise capacity, echocardiographic findings and plasma atrial natriuretic peptide (ANP) concentrations in patients with non-rheumatic persistent AF, before and 30 days after successful cardioversion. Methods: We attempted cardioversion in 42 consecutive patients, aged 58±8 years, with persistent non-valvular AF of duration 7.1±7.1 months. They underwent echocardiography examination and submaximal exercise testing 24 h before and 30 days after cardioversion. Exercise capacity was determined during symptom-limited exercise testing, according to a modified Bruce protocol with peak VO 2 analysis. Plasma samples of ANP were obtained at rest: before, the day after, and 30 days after cardioversion therapy, and were prepared by refrigerated centrifugation and stored until radioimmunoassay. The control study group, without AF, comprised of 11 subjects. Results: Cardioversion was successful in 35 patients. However, in six of the 35 patients, AF reappeared within 1 month. There were no statistical differences before cardioversion in exercise tolerance and ejection fraction of left ventricle between the group with successful cardioversion and the group with unsuccessful cardioversion or with recurrence of AF. On the 30th day after cardioversion we recorded a significant increase in exercise tolerance: duration of exercise 13.7±3.2 versus 9.5±3.4 min, ( P<0.05); peak oxygen consumption 32.2±3.6 versus 19.85±3.5 ml/min per kg, ( P<0.05); and ejection fraction of left ventricle 58.6±9.4 versus 52.7±10.2% ( P<0.05); in the sinus rhythm group. There was no significant improvement observed in the AF group. The mean baseline ANP level was 58.5±15.7 pg/ml in the study group and 34.3±10.2 pg/ml in the control group ( P<0.01). The successful therapy reduced significantly the pretreatment mean plasma ANP concentration from 58.5±15.7 to 31.4±15.0 pg/ml, ( P<0.01); the day after cardioversion, in the group of 35 patients. It remained stable for the next 30 days (36.9±15.2 pg/ml) in the group of 29 patients who remained in sinus rhythm, and increased to 53.4±16.4 pg/ml in the group of six patients who had recurrence of AF. Plasma ANP did not change in the group of seven patients with unsuccessful cardioversion. Conclusions: The restoration of sinus rhythm in patients with persistent AF was associated with a significant improvement in cardiac performance and exercise tolerance 1 month after cardioversion. Such improvement was not observed in the group with unsuccessful cardioversion or with AF recurrence. The plasma ANP concentration in patients with AF was significantly reduced after successful cardioversion and remained stable for a period of 30 days.

Atrial natriuretic peptide level after cardioversion of chronic atrial fibrillation

Heart endocrine studies concerning patients with chronic atrial fibrillation (AF) have become increasingly important. Atrial natriuretic peptide (ANP) is released from atrial myocytes. The increased level of ANP in patients with AF is probably caused by the hemodynamic effect of the arrhythmia. The aim of this study was to explore plasma ANP levels in patients with chronic AF and to describe plasma ANP concentration changes following sinus rhythm (SR) restoration. The study group was comprised of 42 patients, aged between 43 and 76 years with chronic AF (more than 1 month) and a relatively controlled ventricular response (85.8±11.3 beats/min). Plasma ANP levels were measured before and 24 h after AF cardioversion. The control group comprised of 11 subjects. All had normal SR without history of AF and were compatible in age, sex and concomitant diseases with the examined group. ANP level values were expressed as mean±standard deviation. The mean plasma ANP level in the AF group was significantly higher than in the control group (59.5±15.6 vs. 34.3±10.2 pg/ml, P<0,001). Electrical or pharmacological cardioversion was performed in 42 patients. SR was successfully restored in 35 patients. Plasma ANP concentrations decreased significantly from baseline values (from 59.4±16.6 to 31.4±15.0 pg/ml, P<0.001) 24 h after cardioversion in the successful group, while they remained unchanged (60.2±10.7 to 59.4±10.4 pg/ml, NS) in patients with an unsuccessful cardioversion. Conclusion: The mean concentration of ANP in patients with chronic AF was nearly two-times higher than in the control group with sinus rhythm. Conversion to SR was associated with a significant decrease and normalization in plasma ANP concentrations.

Increased brain and atrial natriuretic peptides in patients with chronic right ventricular pressure overload: correlation between plasma neurohormones and right ventricular dysfunction

OBJECTIVETo evaluate the role of plasma neurohormones in the diagnosis of asymptomatic or minimally symptomatic right ventricular dysfunction.SETTINGTertiary cardiovascular referral centre.METHODSPlasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in 21 asymptomatic or minimally symptomatic patients with chronic right ventricular pressure overload caused by congenital heart disease, and in seven healthy volunteers. Right ventricular ejection fraction was determined using magnetic resonance imaging.RESULTSRight ventricular ejection fraction in the volunteers was higher than in the patients (69.0 (8.2)% v 58.0(12.0)%, respectively; p &lt; 0.006). Left ventricular ejection fraction was 72.3(7.8)% in volunteers and 68.1(11.0)% in patients (NS). There was a significant difference between patients and volunteers in the plasma concentrations of BNP (5.3 (3.5) v 2.3 (1.7) pmol/l, respectively; p &lt; 0.009) and ANP (7.3 (4.5)v 3.6 (1.4) pmol/l; p &lt; 0.05). In both patients and volunteers, mean plasma ANP was higher than mean plasma BNP. Right ventricular ejection fraction was inversely correlated with BNP and ANP (respectively, r = 0.65; p &lt; 0.0002 and r = 0.61; p &lt; 0.002). There was no correlation between left ventricular ejection fraction and BNP (r = 0.2; NS) or ANP (r = 0.52; NS). Similarly, no correlation was shown between the level of right ventricular systolic pressure and either plasma BNP (r = 0.20) or plasma ANP (r = 0.07).CONCLUSIONSThere was a significant inverse correlation between right ventricular ejection fraction and the plasma neurohormones BNP and ANP in asymptomatic or minimally symptomatic patients with right ventricular pressure overload and congenital heart disease. Monitoring changes in BNP and ANP may provide quantitative follow up of right ventricular dysfunction in these patients.

Roles of arginine vasopressin and atrial natriuretic peptide in polydipsia-hyponatremia of schizophrenic patients

Respective contributions of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) to the urinary sodium concentration were evaluated in 23 naturalistic incidents of polydipsia-hyponatremia observed in 11 hospitalized schizophrenics (10 males and 1 female). The sodium concentration of the spontaneously excreted urine was examined before and after the forced water restriction. Before the water restriction, mean (±S.D.) plasma ANP was 52.8±33.9 pg/ml (range=6.9–137). Plasma AVP levels were below 0.3 pg/ml in 15 episodes; relatively high levels (≥0.3) were noted in eight episodes. Means of urinary sodium concentration (mEq/l) were significantly higher in episodes with high AVP (≥0.3) alone (25.0±8.2, n=4), with high ANP (>43) alone (21.3±7.4, n=9), and with high AVP and ANP (26.8±6.4, n=4) as compared to that of the low AVP (<0.3) and ANP (≤43) group (13.5±3.7, n=6). The data indicate that the elevated urinary sodium in polydipsic patients is possibly due to the AVP-induced antidiuresis and/or the ANP-induced natriuresis. In addition, we observed a close relationship between elevated plasma AVP and vomiting, suggesting that vomiting is one of the causal factors responsible for AVP elevations in this syndrome.

Atrial natriuretic peptide in children with idiopathic hypercalciuria

We measured plasma atrial natriuretic peptide (ANP) levels in 30 children with idiopathic hypercalciuria (IH) and 19 normal controls (NC). A calcium (Ca) loading test was performed in all patients to determine the type of IH. Subsequently plasma ANP, cAMP and renin activity (PRA), serum total and ionized Ca, intact parathyroid hormone, aldosterone, and 1,25-dihydroxyvitamin D as well as urine Ca, cAMP, and electrolytes were determined in all subjects. The mean (SD) plasma ANP levels were significantly lower in patients with renal hypercalciuria (RH) [21.4 (4.8) pg/ml] than in those with absorptive hypercalciuria (AH) [26.8 (7.6) pg/ml, P<0.05] and NC [27.6 (6.6) pg/ml, P<0.001]. PRA was significantly lower in AH [2.9 (1.3) ng/ml per hour] than in RH patients [7.8 (6.8) ng/ml per hour, P<0.01] and in NC [6.8 (4.6) ng/ml per hour, P<0.005]. Serum aldosterone values were significantly lower in AH [14.5 (11.4) ng/dl] than in RH patients [25.4 (14.1) ng/dl, P<0.05] and in NC [32.6 (20.5), P<0.001]. The lower plasma ANP levels in RH than in AH patients and in NC may be due to Ca depletion. The lower PRA and serum aldosterone levels in AH than in RH patients and in NC may be attributed to Ca excess.

An Experimental Study of Atrial Natriuretic Peptide Levels and the Effect of Inhaled Nitric Oxide After Pneumonectomy

The aim of this study was to investigate the changes in atrial natriuretic peptide (ANP) levels and lung cyclic guanosine 3',5'-monophosphate (cGMP) concentrations caused by pneumonectomy (Pn), and the effect of inhaled nitric oxide (NO) after Pn in a canine model. The mean pulmonary arterial pressure (PAP) and plasma ANP levels were measured over 180 min in two groups of dogs, one subjected to 60 min of 5 ppm NO inhalation (Pn + NO group, n = 5) and one subjected to 180 min without NO inhalation (Pn group, n = 5). The ANP and cGMP levels in the lung were also measured before and after Pn. Both the PAP and ANP levels increased significantly. Inhaled NO rapidly reduced the PAP and plasma ANP to levels similar to those before Pn. The lung ANP level was significantly increased after Pn, but inhaled NO reduced it to a level similar to that before Pn. The lung cGMP level, which was significantly decreased after Pn, was significantly increased by NO inhalation. These results indicate that NO administration may be effective for preventing post-Pn pulmonary hypertension, although an elevation in ANP does not reduce the PAP.

Plasma Concentration of Atrial and Brain Natriuretic Peptides in the Patients with Essential Hypertension

Background:Left ventricular hypertrophy (LVH is one of the complications of hypertension and has been known as an independent risk factor of cardiovascular complications. Recently, it has been reported that hypertensive patients with LVH had the most advanced extracardiac target-organ damage compared with other groups. Previous reports have shown that mean plasma atrial natriuretic peptide (ANP and brain natriuretic peptide (BNP levels in hypertensive patients are higher than in normotensive subjects. Therefore, in this study, we investigated the relationships between the plasma ANP and BNP levels and the degree of LVH in hypertensive patients and in normotensive subjects and also investigated the clinical significance of measurement of plasma ANP and BNP levels. Methods:In all study subjects, left ventricle mass index (LVMI and left ventricle geometry were measured by M-mode echocardiography. Measurements were made by the recommend- ations of the American Society of Echocardiography. Plasma ANP and BNP levels were measured by radioim- munoassay method. Results:1 57% of the hypertensive patients had eccentric hypertrophy and 6% had concentric hypertrophy. 2 LV mass and LVMI of normotensive subjects and hypertensive patients were 169± 53 g, 229±64 g and 99±27.3 g/m 2 , 142±37.7 g/m 2 , respectively (p<0.05. 3 There were statistically signifi- cant correlations between blood pressure and LVMI in all subjects (r=0.43, p<0.05. 4 Plasma ANP levels were significantly increased in hypertensive patients than normotensive subjects (28.2±14.3 pg/mL and 42.8±26 pg/mL, respectively;p<0.05. 5 Plasma BNP levels were significantly increased in hypertensive patients than normotensive subjects (18.4±5.4 pg/mL and 36.5±26 pg/mL;respectively, p<0.05. 6 Plasma BNP levels were significantly increased in 63% of the hypertensive patients with LVH (p<0.05. 7 There were statistically significant correlations between blood pressure and plasma ANP and BNP levels (ANP:r=0.39, p<0.05, BNP:r=0.31, p<0.05. Conclusions:Plasma ANP and BNP levels were increased in the hyperten- sive patients but only plasma BNP levels were significantly increased in the hypertensive patients with LVH. Measurement of plasma BNP levels may be useful for early detection of LVH, an independent risk factor of cardiovascular complications. Therefore intensive blood pressure control in these patients may reduce cardio-

Atrial Natriuretic Peptide and Blood Pressure in a Population-Based Sample

To assess the relationship of plasma atrial natriuretic peptide (ANP) levels with blood pressure levels and the occurrence of hypertension in a large population-based sample. We performed a cross-sectional study of the relationship between ANP levels and blood pressure levels, diagnosis of hypertension, and family history of hypertension in Caucasians from Rochester, Minnesota. Plasma ANP and blood pressure levels were measured in 1,338 Caucasian subjects who were members of 301 three-generation families from the population of Rochester. Hypertension was defined as systolic blood pressure of 140 mm Hg or more or diastolic blood pressure of 90 mm Hg or more. Each subject in the parental generation was categorized as having zero, one, or two parents with hypertension. Analyses were done separately for each generation and gender stratum. Within gender and generation strata, we noted no consistent pattern of positive or negative correlation of plasma ANP levels with systolic blood pressure, diastolic blood pressure, or heart rate. Within the grandparental generation, mean plasma ANP levels did not differ between those with normal blood pressure and those with hypertension. In the parental generation, mean plasma ANP levels did not differ between subjects with zero, one, or two parents with hypertension. In Caucasians, interindividual differences in plasma ANP levels are not associated with interindividual differences in blood pressure levels, the diagnosis of hypertension, or family history of hypertension.

Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats.

To examine the role of vasopressin (AVP) receptors in the regulation of the hemodynamics and release of atrial natriuretic peptide (ANP), and the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrectomized rats with non-peptide, selective antagonists for the V1-receptor or V2-receptor of AVP. In the control group, HS alone increased mean arterial pressure, plasma ANP and AVP, plasma volume and plasma osmolality, and decreased the heart rate. In the V1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in heart rate were completely abolished and an increase in plasma ANP was attenuated. In the V2-receptor antagonist group, increases in mean arterial pressure and plasma ANP and a decrease in heart rate were attenuated. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V2-receptor antagonist group is significantly higher than that in the control group. In both experimental groups, increases in plasma AVP, plasma volume and plasma osmolality were not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by the pressor effect of AVP, mainly through V1-receptors, and that the depressor effect of AVP through V2-receptors may not influence tonically HS-induced hypertension. Moreover, HS-induced increase in plasma ANP is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmotic AVP release.

Participation of endogenous atrial natriuretic peptide in the regulation of urinary protein excretion in experimental diabetic rats.

1. In order to determine whether atrial natriuretic peptide might play a role in the development of glomerular hyperfiltration in diabetes mellitus, we examined the effects of administration of glucose, albumin, atrial natriuretic peptide and an atrial natriuretic peptide receptor antagonist on renal function in rats with streptozotocin-induced diabetes mellitus and vehicle-treated control rats. 2. Four weeks after treatment, rats with diabetes mellitus had a higher mean plasma atrial natriuretic peptide concentration than controls [152 +/- 5 (SE) versus 115 +/- 6 pg/ml, P < 0.01] and a higher glomerular filtration rate (3.3 +/- 0.1 versus 2.7 +/- 0.2 ml min-1 kg-1, P < 0.05). 3. Infusion of albumin or glucose caused significant increases in atrial pressure, plasma atrial natriuretic peptide concentration and urinary excretion of sodium and protein in both groups of rats. 4. Increasing plasma atrial natriuretic peptide concentration by 60% via atrial natriuretic peptide infusion increased urinary excretion of sodium and protein in both control rats and rats with diabetic mellitus. 5. Administration of the atrial natriuretic peptide receptor antagonist HS-142-1 to diabetic rats resulted in diminished urinary excretion of both sodium (-61 +/- 14%, P < 0.02) and protein (-51 +/- 17%, P < 0.05). These changes were associated with a significant reduction in glomerular filtration rate (-32 +/- 11%, P < 0.05) and urinary cGMP excretion (-40 +/- 14%, P < 0.05). No significant effects of HS-42-1 on renal function were observed in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effects of Posture Change and Continuous Positive Airway Pressure on Cardiac Natriuretic Peptides in Congestive Heart Failure

We studied changes in the peripheral plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in seven patients with congestive heart failure (CHF) during four 1-h protocols during which patients maintained either an upright or a supine posture with or without nasal continuous positive airway pressure therapy (N-CPAP) at a pressure of 10 cm H2O (FIO2 = 0.21). The mean plasma ANP concentration of patients increased significantly from baseline at the end of 1 h of recumbency (65.9 +/- 5.8 to 82.6 +/- 8.3 pg/mL (mean +/- standard error); p < 0.05). This increase was prevented by concomitant N-CPAP therapy (72.1 +/- 8.0 to 61.0 +/- 8.8 pg/mL; p = NS). The mean level of ANP decreased significantly (71.9 +/- 9.0 to 62.5 +/- 8.0 pg/mL; p < 0.05) while patients simply maintained an upright posture. A significant reduction was also observed when patients remained upright with accompanying N-CPAP (72.6 +/- 10.9 to 54.6 +/- 4.3 pg/mL; p < 0.05). There were no significant changes observed in the mean level of BNP for any of the protocols undertaken. We conclude that in patients with chronic CHF, (1) an increase in ANP concentration occurs with recumbency, and this can be prevented by N-CPAP therapy; (2) a decrease in ANP occurs with maintenance of an upright posture, and that this reduction may be augmented by N-CPAP; and (3) no net change in BNP concentration occurs with either posture change or N-CPAP.

Elevated Plasma Atrial Natriuretic Peptide Concentrations in Hypertensive Patients with Acute Myocardial Infarction

Atrial natriuretic peptide (ANP) has been extensively studied in cardiovascular disorders in recent years. Particular attention has been paid to the role of ANP in the pathogenesis of hypertension and congestive heart failure and in the neurohormonal response to myocardial infarction. However, no published data are available on the significance of ANP in hypertensive patients with acute myocardial infarction. We studied the relationship between plasma ANP concentration and systolic blood pressure, diastolic blood pressure, left atrial dimension, left ventricular diastolic dimension and left ventricular mass index in patients with essential hypertension in the acute phase of myocardial infarction. Plasma ANP concentrations were determined at 0, 4, 8, 16, 24, 48 and 72 h after admission in 40 patients with a first myocardial infarction (18 hypertensive patients, group 1; 22 normotensive patients, group 2). Left atrial dimension and left ventricular diastolic dimension were assessed echocardiographically within the first 48 h of acute myocardial infarction. Maximum and mean plasma ANP values at 0, 4, 8, 16, 24, 48, and 72 h as well as mean ANP concentrations within the 72 h period were higher in group 1 than in group 2 (P < 0.001). Plasma ANP concentration, left atrial dimension (r = 0.59) and left ventricular diastolic dimension (r = 0.56) were positively correlated in both groups. Acute myocardial infarction is characterized by a more pronounced rise in plasma ANP concentration in hypertensive patients than in those without a history of hypertension. Plasma ANP concentration correlates with left heart chamber sizes.

Plasma levels of atrial natriuretic peptide in normal and hyprtensive pregnancies: A meta-analysis

Our goals were (1) to use meta-analysis to determine whether pregnancy and the puerperium are accompanied by alterations in plasma atrial natriuretic peptide levels when compared with the nonpregnant state and (2) to evaluate the additional effects of hypertensive disease during pregnancy on plasma atrial natriuretic peptide levels. Articles measuring atrial natriuretic peptide levels during pregnancy were reviewed. Data from articles meeting inclusion criteria were abstracted, and a meta-analysis was performed with the use of the maximum likelihood methods of Jennrich and Schluchter (Biometrics 1986;42:805-20). The mean atrial natriuretic peptide level in nonpregnant control subjects was 28.7 pg/ml (95% confidence interval 22.5 to 36.7). The mean plasma atrial natriuretic peptide level rose 41% to 40.5 pg/ml (95% confidence interval 31.7 to 51.8) in the third trimester (p < 0.0001). It was 71.1 pg/ml (95% confidence interval 51.2 to 98.7) or 148% greater than the mean nonpregnant level during the first week post partum (p < 0.0001). Compared with levels in pregnant control subjects, plasma atrial natriuretic peptide levels increased 52% to 52.1 pg/ml (95% confidence interval 32.9 to 82.5) in women with gestational hypertension (p < 0.005) and 130% to 78.8 pg/ml (95% confidence interval 52.3 to 118.8) in women with preeclampsia (p < 0.0001). Chronic hypertension did not significantly alter atrial natriuretic peptide levels. The 41% increase in atrial natriuretic peptide levels in the third trimester suggests that atrial stretch receptors sense the expanded blood volume as normal to moderately increased. The rise in atrial natriuretic peptide during the first week post partum is consistent with known hemodynamic changes and suggests that atrial natriuretic peptide may be involved in the postpartum diuresis. The marked increase in plasma atrial natriuretic peptide levels observed in preeclampsia is not likely to result from elevated arterial pressures alone but may reflect underlying factors unique to this disease process.

Effect of acute lung injury and coexisting disorders on plasma concentrations of atrial natriuretic peptide

To clarify how plasma atrial natriuretic peptide concentrations vary with the severity of acute lung injury. The influence of coexisting diseases which trigger acute lung injury was also examined. Prospective study. Intensive care unit of a university hospital. Fifty patients who had standard risk factors for acute lung injury including sepsis syndrome, major surgery, prolonged hypotension, aspiration of gastric contents, and burns. Twenty-five of these patients had acute lung injury (group 3) caused by these disorders; the remaining 25 patients had risk factors only (group 2). Ten age-matched normal volunteers were selected as controls (group 1). None. Plasma atrial natriuretic peptide concentration was measured in these patients and compared with the severity of acute lung injury. In group 3, a significant increase in the mean plasma atrial natriuretic peptide concentration was observed (188 +/- 78 pg/mL, p < .01) compared with group 2 (54 +/- 28 pg/mL) and the age-matched control group (30 +/- 8 pg/mL). This increase was related to the onset of acute lung injury and returned to control concentrations after recovery. Plasma atrial natriuretic peptide concentrations in group 3 correlated highly with a lung injury score representing the severity of acute lung injury (r2 = .45, p < .01), but did not correlate with other cardiopulmonary variables. The results suggest that severity of lung injury, but not other predisposing disorders, may be the key factor leading to the increase in plasma atrial natriuretic peptide concentrations observed in these patients.

Effect of acute lung injury and coexisting disorders on plasma concentrations of atrial natriuretic peptide

Objective: To clarify how plasma atrial natriuretic peptide concentrations vary with the severity of acute lung injury. The influence of coexisting diseases which trigger acute lung injury was also examined. Design: Prospective study. Setting: Intensive care unit of a university hospital. Patients: Fifty patients who had standard risk factors for acute lung injury including sepsis syndrome, major surgery, prolonged hypotension, aspiration of gastric contents, and burns. Twenty-five of these patients had acute lung injury (group 3) caused by these disorders; the remaining 25 patients had risk factors only (group 2). Ten age-matched normal volunteers were selected as controls (group 1). Intervention: None. Measurements and Main Results: Plasma atrial natriuretic peptide concentration was measured in these patients and compared with the severity of acute lung injury. In group 3, a significant increase in the mean plasma atrial natriuretic peptide concentration was observed (188 ± 78 pg/mL,p< .01) compared with group 2 (54 ± 28 pg/mL) and the age-matched control group (30 ± 8 pg/mL). This increase was related to the onset of acute lung injury and returned to control concentrations after recovery. Plasma atrial natriuretic peptide concentrations in group 3 correlated highly with a lung injury score representing the severity of acute lung injury (r2 = .45,p< .01), but did not correlate with other cardiopulmonary variables. Conclusion: The results suggest that severity of lung injury, but not other predisposing disorders, may be the key factor leading to the increase in plasma atrial natriuretic peptide concentrations observed in these patients. (Crit Care Med 1994; 22:1762–1768)

Plasma atrial natriuretic peptide levels in elderly hypertensives: effects of blood pressure reduction with amlodipine

Atrial natriuretic peptide (ANP) is a hormone of relatively recent discovery concerned with sodium homeostasis. Increased levels of ANP are found in the elderly and in hypertensives, but the mechanisms for this are unclear. This study determined the effect of amlodipine, a calcium antagonist, which is the only class of antihypertensive agent that has little or no influence on the renin-angiotensin system (Bauer and Reams, 1988) on plasma ANP in a group of 18 elderly hypertensives and a placebo (vit B complex) on a further group of 6 elderly hypertensives. The mean pre-treatment plasma ANP was 62.7 pg/ml (range 18–148.7 pg/ml) and 52.0 pg/ml (range 15.0–148.4 pg/ml) after treatment with amlodipine (not statistically significant). However, systolic blood pressure fell from a mean of 181.6 mmHg to 151.1 mmHg and diastolic blood pressure fell from a mean of 101.6 mmHg to 83.6 mmHg after treatment with amlodipine (statistically significant, P < 0.001). In the group treated with vit B complex, the mean plasma ANP level was 68.4 pg/ml (range 31.4–119.5 pg/ml) before treatment and 63.6 pg/ml (range 29.2–127.3 pg/ml) after treatment. This was not statistically significant and there was no significant change in blood pressure. These findings reinforce the theory that raised plasma ANP levels found in elderly hypertensives are a function of the aging process itself or of age-related physiological changes rather than the result of hypertension.

Association of a nocturnal rise in plasma alpha-atrial natriuretic peptide and reversed diurnal blood pressure rhythm in hospitalized normotensive subjects with non-insulin dependent diabetes mellitus.

Diurnal changes in plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and plasma aldosterone as related to those in blood pressure (BP) were studied under hospital conditions in 18 diabetic subjects without proteinuria and 8 age-matched control subjects. Of 18 diabetic subjects, 10 had a normal diurnal BP rhythm with the peak value in the afternoon (group 1) and 8 had a reversed BP rhythm with the peak value during the night (group 2). Autonomic dysfunction estimated by measuring orthostatic BP and heart-rate changes and beat-to-beat heart-rate variations was more pronounced in group 2 than in group 1. Fasting plasma glucose and HbA1c were similarly high in both diabetic groups. Group 1 showed modestly elevated mean 24-h MBP and plasma ANP levels, modestly low mean 24-h PRA and plasma aldosterone levels, and a lack of diurnal ANP changes similar to that in controls. Group 2 showed markedly elevated mean 24-h BP and plasma ANP levels, markedly low mean 24-h PRA and plasma aldosterone levels, and nocturnal rises in plasma ANP and BP. PRA and plasma aldosterone exhibited circadian rhythms with their peak values found in the early morning in all three groups. The daytime/overnight excretion ratios of sodium and water were normal in group 1 and low in group 2. These results indicate that diurnal changes in plasma ANP, PRA and plasma aldosterone are altered in diabetic subjects with normal and reversed diurnal BP rhythms, predominantly in the latter.

Water-balance hormones during long-term follow-up of oral dDAVP treatment in diabetes insipidus.

The aim of the present study was to investigate the hormonal control of water-balance in children with diabetes insipidus and to assess safety and efficacy of long-term treatment with oral dDAVP. Plasma atrial natriuretic peptide, plasma renin activity, aldosterone, plasma and urinary cyclic 3'5'-guanosine monophosphate and urinary prostaglandin E2 were measured in eight patients (aged 3-21 y) with central diabetes insipidus. At baseline, 12 h after the last dDAVP dose, patients had hypotonic polyuria but normal plasma sodium concentrations and plasma osmolality relative to a control group. The mean plasma atrial natriuretic peptide concentration in patients (26.2 +/- 2.6 pg/ml) tended to be lower than in controls (36.5 +/- 8.2 pg/ml, mean +/- SEM), although the difference was not significant. Plasma cyclic 3'5' guanosine monophosphate was higher in controls (6.0 +/- 0.6 pmol/ml, mean +/- SEM) than in patients (3.8 +/- 0.3 pmol/ml). Aldosterone, plasma renin activity, urinary cyclic guanosine monophosphate and urinary prostaglandin E2 were similar in the two groups. During 3 h following dDAVP administration, atrial natriuretic peptide levels did not change in patients but decreased significantly in controls to 23.0 +/- 4.0 pg/ml. No adverse reactions, or circulating antibodies against dDAVP, were observed after 3.5 years of oral dDAVP treatment. The average oral dDAVP dosage was similar after 1 and 3.5 years of treatment (906 +/- 406 micrograms/24 h, mean +/- SD). Water-balance is not detectably different from normal in correctly treated diabetes insipidus patients in terms of plasma atrial natriuretic peptide, plasma renin activity and aldosterone levels. Long-term oral dDAVP treatment is safe and efficacious.