Plasma Atrial Natriuretic Peptide Concentrations Research Articles

Clinical implications of measurement of plasma atrial natriuretic peptide concentration in dogs with spontaneous heart disease

To determine whether measurement of plasma atrial natriuretic peptide (ANP) concentration could be used to identify heart disease in dogs and to assess disease severity in affected dogs. Cross-sectional study. 37 healthy dogs and 78 dogs with heart disease. Dogs were divided into 5 groups on the basis of plasma ANP concentration: healthy, ANP-1 (< 50 pg/mL; n = 19), ANP-2 (50 to 100 pg/mL; 24), ANP-3 (101 to 200 pg/mL; 20), and ANP-4 (> 200 pg/mL; 15). All dogs underwent physical examination, echocardiography, thoracic radiography, and blood sampling before treatment. Compared with healthy dogs, dogs with increased plasma ANP concentration had significant concomitant increases in heart rate, cardiothoracic ratio, vertebral heart score, fractional shortening, ratio of left atrial-to-aortic root diameter, and mitral early diastolic flow (E wave) velocity and a significant decrease in relative wall thickness. Use of plasma ANP concentration > 25 pg/mL to identify dogs with heart disease (International Small Animal Cardiac Health Council class > I) had a sensitivity of 91.0% and specificity of 94.7%. Use of plasma ANP concentration > 100 pg/mL to identify dogs with International Small Animal Cardiac Health Council class IIIb heart disease had a sensitivity of 81.0% and specificity of 81.1 %. Results may provide reference values for plasma ANP concentration in dogs and suggest that plasma ANP concentration may help to distinguish dogs with cardiac disease from clinically normal dogs. Measurement of plasma ANP concentration may be a useful marker for predicting the severity of heart disease in dogs.

Plasma atrial natriuretic peptide concentrations in horses with heart disease: A pilot study

Atrial natriuretic peptide (ANP) is a cardiovascular biomarker that might be useful in assessing the severity of cardiac disease in horses. Plasma ANP concentrations (Cp(ANP)) were compared between horses with heart disease but normal chamber size and function (Group A; n=6), horses with heart disease associated with left atrial (LA) enlargement, LA dysfunction, and/or left ventricular (LV) enlargement (Group B; n=5), and horses with no clinically apparent cardiovascular disease (Group C; n=13). The median (min-max) for Cp(ANP) was significantly higher in Group B (53.5 (36.0-70.7) pg/mL), compared to Group A (12.5 (6.3-19.8) pg/mL) and Group C (13.4 (7.2-34.0) pg/mL). Backwards stepwise multiple linear regression showed that Cp(ANP) in horses with heart disease was related to LA dimensions, but not to LV size, LA function, and LV function. The results indicated that Cp(ANP) in horses might be useful in detecting LA enlargement and that Cp(ANP) could be related to the severity of cardiac disease. Larger prospective studies are necessary to confirm these results.

Involvement of the atrial natriuretic peptide in the reduction of arterial pressure induced by swimming but not by running training in hypertensive rats

The aim of this study was to compare, under resting conditions, the influence of chronic training in swimming or running on mean arterial pressure (MAP) and the involvement of the natriuretic peptide system in this response. Two-month-old male spontaneously hypertensive rats (SHR) were divided into three groups—sedentary (SD), swimming (SW) and running (RN)—and were trained for eight weeks under regimens of similar intensities. Atria tissue and plasma atrial natriuretic peptide (ANP) concentrations were measured by radioimmunoassay. ANP mRNA levels in the right and left atria as well as the natriuretic peptide receptors (NPR), NPR-A and NPR-C, mRNA levels in the kidney were determined by real-time PCR. Autoradiography was used to quantify NPR-A and NPR-C in mesenteric adipose tissue. Both training modalities, swimming and running, reduced the mean arterial pressure (MAP) of SHR. Swimming, but not running, training increased plasma levels of ANP compared to the sedentary group (P<0.05). Expression of ANP mRNA in the left atrium was reduced in the RN compared to the SD group (P<0.05). Expression of NPR-A and NPR-C in the kidneys of the SW group decreased significantly (P<0.05) compared to the SD group. Although swimming increased 125I-ANP binding to mesenteric adipose tissue, displacement by c-ANF was reduced, indicating a reduction of NPR-C. These results suggest that the MAP reduction induced by exercise in SHR differs in its mechanisms between the training modalities, as evidenced by the finding that increased levels of ANP were only observed after the swimming regimen.

Oestradiol Potentiates Hormone Secretion and Neuronal Activation in Response to Hypertonic Extracellular Volume Expansion in Ovariectomised Rats

Secretion of vasopressin (VP), oxytocin (OT) and atrial natriuretic peptide (ANP) is an essential mechanism for the maintenance of hydromineral homeostasis. Secretion of these hormones is modulated by several circulating factors, including oestradiol. However, it remains unclear how oestradiol exerts this modulation. In the present study we investigated the participation of oestradiol in the secretion of VP, OT and ANP and in activation of vasopressinergic and oxytocinergic neurones of the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus in response to extracellular volume expansion (EVE). For this purpose, ovariectomised (OVX) rats treated for 7 days with vehicle (corn oil, 0.1 ml/rat, OVX+O group) or oestradiol (oestradiol cypionate, 10 μg/kg, OVX+E group) were subjected to either isotonic (0.15 m NaCl, 2 ml/100 g b.w., i.v.) or hypertonic (0.30 m NaCl, 2 ml/100 g b.w., i.v.) EVE. Blood samples were collected for plasma VP, OT and ANP determination. Another group of rats was subjected to cerebral perfusion, and brain sections were processed for c-Fos-VP and c-Fos-OT double-labelling immunohistochemistry. In OVX+O rats, we observed that both isotonic and hypertonic EVE increased plasma OT and ANP concentrations, although no changes were observed in VP secretion. Oestradiol replacement did not alter hormonal secretion in response to isotonic EVE, but it increased VP secretion and potentiated plasma OT and ANP concentrations in response to hypertonic EVE. Immunohistochemical data showed that, in the OVX+O group, hypertonic EVE increased the number of c-Fos-OT and c-Fos-VP double-labelled neurones in the PVN and SON. Oestradiol replacement did not alter neuronal activation in response to isotonic EVE, but it potentiated vasopressinergic and oxytocinergic neuronal activation in the medial magnocellular PVN (PaMM) and SON. Taken together, these results suggest that oestradiol increases the responsiveness of vasopressinergic and oxytocinergic magnocellular neurones in the PVN and SON in response to osmotic stimulation.

The effect of β1-blocker bisoprolol on atrial natriuretic peptide plasma levels in hypertensive patients

The aim of this study was to evaluate the effects of the high selective β1-blocker bisoprolol on atrial natriuretic peptide (ANP) plasma levels in patients with a moderate essential hypertension. The study was divided into two parts: a long-term and a short-term one. In part 1, the long-term effects of the drug, given orally at a daily dose of 10 mg, on plasma ANP concentrations were studied in correlation with the blood pressure and the echocardiographic dimensions of the left heart cavities in the lying position. Plasma ANP levels were raised by 20% despite the drop in blood pressure and the very small, but statistically significant, decrease in left atrial and ventricular diameters. In part 2, the acute effects of a single oral dose of 20 mg bisoprolol in relation to postural changes were studied. Plasma ANP levels in the sitting position were lower than in when lying down, but in both positions they were slightly higher after betablockers. The above findings, taken together with the literature data, favor the theory that the antihypertensive action of beta adrenergic blockers is partially due to the increased secretion of ANP.

Plasma atrial natriuretic peptide in essential hypertension after angiotensin converting enzyme inhibition

The authors have already found that the antihypertensive action of β1-blockers is partially exerted through atrial natriuretic peptide (ANP). On the other hand, the antihypertensive action of angiotensin converting enzyme inhibitors (ACEI) seems to extend to other mechanisms. In this regard we studied the effect of the ACEI Cilazapril (C) on plasma ANP concentration in 21 patients, aged 40–64, with moderate degree essential hypertension. Assessments of the ANP and the other variables [(ECHO cardiac dimensions, blood pressure (BP)] were carried out before and after an 8-week treatment with 2–5 mg daily. ANP was purified by chromatography and assayed by radioimmunoassay (RIA). Systolic and diastolic BP decreased by 18% and 16%, respectively, left ventricular and left atrial diastolic diameters decreased by 6%. ANP increased by 5.7%. All changes were statistically significant. The discordant increase of ANP in relation to BP and cardiac dimensions suggests a direct effect of ACEI mediated either through the sympatholytic or the anti-carvoxypeptidase action. This effect may contribute to BP lowering.

Myocardial injury-related changes in plasma NT-proBNP and ANP concentrations in a canine model of ischemic myocardial injury

Serial changes in plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and atrial natriuretic peptide (ANP) concentrations are unknown in dogs with myocardial injury. The time-course secretory responses between NT-proBNP and ANP or cardiac troponin-T (cTnT) related to myocardial infarction (MI) were investigated in this study. Six dogs were anaesthetised and the left anterior descending artery was ligated. A transient decrease in cardiac function was detected 1h after MI but returned to baseline levels within 7 days and remained so for 6 months. Echocardiographic examination revealed focal ventricular dyskinesis throughout the study. Six months following MI, the left atrium to aorta ratio increased significantly although the relative wall thickness decreased significantly from baseline. Significantly elevated plasma NT-proBNP and cTnT concentrations were detected 1 day after MI and these gradually decreased over 28 days to baseline levels without left ventricular pressure elevation. Plasma ANP was elevated significantly 6 months after MI. The NT-proBNP assay is a helpful diagnostic indicator for identifying asymptomatic acute and subacute myocardial injury whereas plasma ANP concentration mainly reflects atrial dilation.

Current biochemistry, molecular biology, and clinical relevance of natriuretic peptides

The mammalian natriuretic peptide family consists of atrial (ANP), brain [B-type; BNP] and C-type natriuretic peptide (CNP) and three receptors, natriuretic receptors-A (NPR-A), -B (NPR-B) and -C (NPR-C). Both ANP and BNP are abundantly expressed in the heart and are secreted mainly from the atria and ventricles, respectively. By contrast, CNP is mainly expressed in the central nervous system, bone and vasculature. Plasma concentrations of both ANP and BNP are elevated in patients with cardiovascular disease, though the magnitude of the increase in BNP is usually greater than the increase in ANP. This makes BNP is a clinically useful diagnostic marker for several pathophysiological conditions, including heart failure, ventricular remodeling and pulmonary hypertension, among others. Recent studies have shown that in addition to BNP-32, proBNP-108 also circulates in human plasma and that levels of both forms are increased in heart failure. Furthermore, proBNP-108 is O-glycosylated and circulates at higher levels in patients with severe heart failure. In this review we discuss recent progress in our understanding of the biochemistry, molecular biology and clinical relevance of the natriuretic peptide system.

Plasma ANP and BNP during exercise in patients with major depressive disorder and in healthy controls

Background Increased levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have been shown to reduce the hormones in the HPA axis. In this study we addressed the question whether patients with unmedicated major depressive disorder (MDD) might have altered baseline levels of these natriuretic peptides and an altered response to acute exercise. Methods An incremental exercise test was performed in 18 patients with MDD and in 18 healthy controls. Plasma concentrations of ANP and BNP were determined at rest, during the exercise test and 30 min post exercise using immunoradiometric assays. Results During the exercise test the concentrations of ANP and BNP increased significantly in both groups. The MDD group showed significantly lower levels of ANP than the controls at rest, at maximal work rate and post exercise and of BNP at rest and at maximal work rate. The dynamic changes of both ANP and BNP, respectively, from baseline to maximal work rate were significantly lower in the MDD group. A slightly lower (non-significant) maximal work rate was observed in the MDD group compared with the controls. Limitations Group sizes are relatively limited. Conclusion Lower concentrations of ANP and BNP during rest and exercise were observed in the MDD patients together with a decreased dynamic response to maximal exercise. Hypothetically, the reduced ANP and BNP concentration contributes to the high hormone levels in the HPA system seen in depressive disorders. Of interest for future research is whether physical training might increase the levels of ANP and BNP and thereby diminish depressive symptoms.

The effect of different exercise-testing protocols on atrial natriuretic peptide

The aim of this study was to examine and to compare alterations in the secretion of atrial natriuretic peptide (ANP) during different exercise-testing protocols in moderately trained men. Fifteen healthy male physical education students were studied (mean age 22·3 ± 2·5 years, training experience 12·3 ± 2·5 years, height 1·80 ± 0·06 m, weight 77·4 ± 8·2 kg). Participants performed an initial graded maximal exercise testing on a treadmill for the determination of VO(2max) (duration 7·45-9·3 min and VO(2max) 55·05 ± 3·13 ml kg(-1) min(-1) ) and were examined with active recovery (AR), passive recovery (PR) and continuous running (CR) in random order. Blood samples for plasma ANP concentration were taken at rest (baseline measurement), immediately after the end of exercise as well as after 30 min in passive recovery time (PRT). The plasma ANP concentration was determined by radioimmunoassay (RIA). The results showed that ANP plasma values increased significantly from the rest period to maximal values. In the short-term graded maximal exercise testing the ANP plasma values increased by 56·2% (44·8 ± 10·4 pg ml(-1) versus 102·3 ± 31·3 pg ml(-1) , P<0.001) and in the CR testing the ANP levels increased by 29·2% (44·8 ± 10·4 pg ml(-1) versus 63·3 ± 19·8 pg ml(-1) , P<0.001) compared to the baseline measurement. Moreover, the values of ANP decreased significantly (range 46·4-51·2%, P<0.001) in PRT after the end of the four different exercise modes. However, no significant difference was evident when ANP values at rest and after AR and PR were compared. It is concluded that the exercise testing protocol may affect the plasma ANP concentrations. Particularly, short-term maximal exercise significantly increases ANP values, while the intermittent exercise form of active and passive recovery decreases ANP concentrations.

Central Administration of Kisspeptin-10 Inhibits Water and Sodium Excretion of Anesthetized Male Rats and the Involvement of Arginine Vasopressin

Aim. To investigate the effect of hypothalamus kisspeptin on water and sodium excretion and the possible mechanism. Method. The intracerebroventricular (icv) administration and radioimmunoassay were used to observe the effect of kisspeptin-10 on urine flow, sodium and potassium excretion, plasma arginine vasopressin (AVP), and atrial natriuretic peptide (ANP) concentrations in anesthetized male rats. The mediation of renal sympathetic nerve was also investigated by studies conducted on rats with bilateral renal sympathetic denervation. Results. The urine flow, sodium excretion, and free water clearance decreased significantly by icv injection of 5 nmol kisspeptin-10 (p < 0.05) from 30 to 60 min post-injection. Meanwhile, plasma AVP concentrations increased significantly 30 min after the icv injection of 5 nmol kisspeptin-10 (p < 0.05), whereas the equal dose of kisspeptin-10 did not significantly change plasma ANP concentrations. The mean arterial blood pressure, heart rate, and potassium excretion did not significantly change during the experiment. Furthermore, pretreatment with 5 nmol kisspeptin-10 could still significantly decrease urine flow and sodium excretion in renal sympathetic denervated rats. Conclusion. Central administration of kisspeptin-10 could inhibit sodium excretion and urine flow in anesthetized male rats, which is probably mediated by increasing the plasma AVP concentration and is independent of plasma ANP concentration and renal sympathetic nerve activity.

Effects of urotensin II on hypoxia‐induced ANP secretion in rats

Urotensin II (UII) is a vasoactive peptide with many potent effects in the cardiovascular system through a G‐protein‐coupled receptor termed UT. The synthesis and secretion of atrial natriuretic peptide (ANP) are increased during hypoxic condition and plays an important role in adaptation to hypoxia and in the pathogenesis of cardiopulmonary diseases. The present study was to investigate the effects of human UII (hUII) on ANP secretion in hypoxia condition in vitro and in vivo experiments. Hypoxia caused an increase in ANP secretion compared to normoxia in isolated perfused beating rat atria. hUII (10‐10 M) decreased hypoxia‐induced ANP secretion whereas hUII receptor antagonist, urantide (10‐6 M), increased it. However, there were no significant changes in atrial contractility, stroke volume, and extracellular fluid (ECF) translocation by hUII in hypoxia condition. The pretreatment with urantide attenuated the effect of hUII on hypoxia‐induced ANP secretion. Monocrotaline‐treated (MCT, 60mg/kg, sc., 4weeks) rats increased UII level in plasma. In vivo experiment, hUII (5*10‐6 M injection plus 2.5*10‐6 M infusion for 15 min) was infused into MCT‐treated and control rats anesthetized with ketamine. hUII increased blood pressure and heart rate in both groups without significant difference. Interestingly, intravenous infusion of hUII decreased plasma concentration of ANP in MCT‐treated rats whereas hUII increased plasma concentration of ANP in control rats. The ANP generation may protect against the hypoxia and pulmonary hypertension. These results suggest that hUII may play a pathophysiological role in the regulation of ANP secretion in hypoxic condition. Supported by the KOSEF (R13‐2008‐005‐00000‐0).

Angiotensin‐(1‐7) stimulates high atrial pacing‐induced ANP secretion

Angiotensin‐(1‐7) [Ang‐(1‐7)] has many beneficial roles in cardiovascular physiology, counterbalancing Angiotensin II functions. It is considered as one of the theurapeutic agent for cardiovascular diseases in the future. The aim of the present study is to elucidate the modulatory role of Ang‐(1‐7) in atrial natriuretic peptide (ANP) secretion using isolated perfused beating rat atria and cardiac hypertrophied rat model. Ang‐(1‐7) (10−8, 10−7, and 10−6M) increased the ANP secretion and ANP concentration in a dose‐dependent manner at high atrial pacing (6.0 Hz) with an increased cGMP amount. However, Ang‐(1‐7) did not cause any changes in atrial parameters at low atrial pacing (1.2 Hz). An antagonist of Mas receptor or inhibitors of phosphoinositide 3‐kinase (PI3K), protein kinase B (Akt), or nitric oxide synthase pretreatment blocked the increase of high atrial pacing‐induced ANP secretion by Ang‐(1‐7). The inhibition of Na+/H+ exchanger‐1 (NHE‐1) and calcium/calmodulin‐dependent kinase II (CaMKII) showed the similar result. Ang‐(1‐7) did not show any changes in intracellular calcium concentration in quiescent atrial myocytes. However, Ang‐(1‐7) attenuated an increase of intracellular calcium concentration induced by angiotensin II. Intravenous infusion of Ang‐(1‐7) increased the plasma concentration of ANP by 2‐fold without changes in blood pressure and heart rate in isoproterenol‐treated rats but not in control rats. Ang‐(1‐7) attenuated cardiac hypertrophy induced by isoproterenol. These results suggest that Ang‐(1‐7) increased the ANP secretion at high atrial pacing via Mas/PI3K/Akt pathway and the activation of NHE‐1 and CaMKII.Supported by the KOSEF (R13‐2008‐005‐00000‐0).

Angiotensin-(1–7) stimulates high atrial pacing-induced ANP secretion via Mas/PI3-kinase/Akt axis and Na+/H+ exchanger

Angiotensin-(1-7) [ANG-(1-7)], one of the bioactive peptides produced in the renin-angiotensin system, plays a pivotal role in cardiovascular physiology by providing a counterbalance to the function of ANG II. Recently, it has been considered as a potential candidate for therapeutic use in the treatment of various types of cardiovascular diseases. The aim of the present study is to explain the modulatory role of ANG-(1-7) in atrial natriuretic peptide (ANP) secretion and investigate the functional relationship between two peptides to induce cardiovascular effects using isolated perfused beating rat atria and a cardiac hypertrophied rat model. ANG-(1-7) (0.01, 0.1, and 1 muM) increased ANP secretion and ANP concentration in a dose-dependent manner at high atrial pacing (6.0 Hz) with increased cGMP production. However, at low atrial pacing (1.2 Hz), ANG-(1-7) did not cause changes in atrial parameters. Pretreatment with an antagonist of the Mas receptor or with inhibitors of phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), or nitric oxide synthase blocked the augmentation of high atrial pacing-induced ANP secretion by ANG-(1-7). A similar result was observed with the inhibition of the Na(+)/H(+) exchanger-1 and Ca(2+)/calmodulin-dependent kinase II (CaMKII). ANG-(1-7) did not show basal intracellular Ca(2+) signaling in quiescent atrial myocytes. In an in vivo study using an isoproterenol-induced cardiac hypertrophy animal model, an acute infusion of ANG-(1-7) increased the plasma concentration of ANP by twofold without changes in blood pressure and heart rate. A chronic administration of ANG-(1-7) increased the plasma ANP level and attenuated isoproterenol-induced cardiac hypertrophy. The antihypertrophic effect was abrogated by a cotreatment with the natriuretic peptide receptor-A antagonist. These results suggest that 1) ANG-(1-7) increased ANP secretion at high atrial pacing via the Mas/PI3K/Akt pathway and the activation of Na(+)/H(+) exchanger-1 and CaMKII and 2) ANG-(1-7) decreased cardiac hypertrophy which might be mediated by ANP.

Atrial natriuretic peptide and plasma renin activity in patients with stable chronic obstructive pulmonary disease

The relationship between plasma atrial natriuretic peptide (ANP) and plasma renin activity (PRA) was examined in patients with stable chronic obstructive pulmonary disease (COPD, n = 17). The plasma ANP level in patients was approximately twice that in normal subjects. A reciprocal relationship between ANP and PRA was shown in normal subjects; however, this relationship was not observed in COPD. Plasma ANP levels inversely correlated with PaO2, and tended to inversely correlate with angiotensin converting enzyme activity in serum. These results demonstrate that patients with COPD have higher plasma ANP concentration, and that ANP and PRA are not reciprocally related in stable COPD.

Leptin reduces plasma ANP level via nitric oxide-dependent mechanism

Leptin is a circulating adipocyte-derived hormone that influences blood pressure (BP) and metabolism. This study was designed to define the possible role of leptin in regulation of the atrial natriuretic peptide (ANP) system using acute and chronic experiments. Intravenous infusion of rat leptin (250 microg/kg injection plus 2 microg.kg(-1).min(-1) for 20 min) into Sprague-Dawley rats increased BP by 25 mmHg and decreased plasma level of ANP from 80.3 +/- 3.45 to 51.8 +/- 3.3 pg/ml. Reserpinization attenuated the rise in BP, but not the reduction of plasma ANP during leptin infusion. N(omega)-nitro-l-arginine methyl ester prevented the effects of leptin on the reduction of ANP level. In hyperleptinemic rats that received adenovirus containing rat leptin cDNA (AdCMV-leptin), BP increased during first 2 days and then recovered to control value. Plasma concentration of ANP and expression of ANP mRNA, but not of atrial ANP, in hyperleptinemic rats were lower than in the control groups on the first and second week after administration of AdCMV-leptin. These effects were not observed by the pretreatment with N(omega)-nitro-l-arginine methyl ester. No differences in renal function and ANP receptor density in the kidney were found between hyperleptinemic and control rats. Basal ANP secretion and isoproterenol-induced suppression of ANP secretion from isolated, perfused atria of hyperleptinemic rats were not different from those of other control groups. These data suggest that leptin inhibits ANP secretion indirectly through nitric oxide without changing basal or isoproterenol-induced ANP secretion.

Effects of three different methods of anesthesia on the release of brain natriuretic peptid in patients with cardiac risk undergoing lower extremity surgery

To investigate if intra and postoperative thoracal epidural analgesia could decrease plasma concentrations of brain natriuretic peptide (BNP) in patients who were at risk for, or had, coronary artery disease (CAD) and undergoing lower extremity operations. Materials and methods: Sixty patients with risk of CAD scheduled to undergo lower extremity surgery were divided into 3 groups. Group G was administered general anesthesia followed by intravenous patient-controlled analgesia (I.V PCA) (n = 20). Group L was administered lumbar epidural anesthesia followed by lumbar epidural analgesia (n = 20). Group T was administered general anesthesia combined with intra and postoperative thoracal epidural analgesia as well as I.V PCA (n = 20). Visual analog scale pain scores, hemodynamics, plasma catecholamines, cardiac troponin I (cTnI), atrial natriuretic peptide (ANP), and BNP were measured preoperatively and measurements were extended to 90 min after skin incision, towards the end of surgery, and in the morning of day 1, 2, and 3 postoperation. The data were statistically compared using multiple comparison tests. Results: Baseline ANP and BNP concentrations were similar in all groups (G: 25.8 ± 4.51 and 25.9 ± 8.52 pg/mL; L: 23.9 ± 3.67 and 20.8 ± 9.8 pg/mL; T: 24.7 ± 4.27 and 23.0 ± 5.98 pg/mL, respectively). The postoperative plasma BNP concentrations of group T were lower than those of groups L and G. and similarly group L was lower compared to group G in terms of postoperative plasma BNP concentrations (P < 0.05). Peak plasma concentrations of BNP were 162.4 ± 29.4, 110.6 ± 12.2, and 69.0 ± 6.9 for groups G, L, and T, respectively (P < 0.05). However, there was no group difference in peak plasma ANP concentrations. Baseline epinephrine and norepinephrine concentrations were also similar across the groups. Peak plasma epinephrine concentrations of group T were lower than those of groups G and L (P < 0.05). Plasma cTnI concentrations were within normal limits (

Central administration of kisspeptin-10 inhibits natriuresis and diuresis induced by blood volume expansion in anesthetized male rats

To investigate the possible role of hypothalamic kisspeptin in the regulation of body fluid metabolism and maintenance of internal homeostasis. Natriuresis and diuresis were induced by blood volume expansion (VE) in anesthetized male rats and kisspeptin-10 was intracerebroventricularly (icv) administered. Radioimmunoassay (RIA) was used to measure the plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations during the VE. The mediation of the renal sympathetic nerve was also investigated in rats with bilateral renal sympathetic denervation. The increased urine flow and sodium excretion induced by VE were significantly inhibited by icv injection of 5 nmol kisspeptin-10 (P<0.05), which peaked 20 min after the decrease in VE. The mean arterial blood pressure and heart rate did not change during the experiment. Plasma AVP concentrations were significantly increased 20 min after icv injection of 5 nmol kisspeptin-10 during VE (P<0.05), while pretreatment with 5 nmol kisspeptin-10 did not significantly change plasma ANP concentrations. Furthermore, pretreatment with 5 nmol kisspeptin-10 could significantly inhibit VE-induced natriuresis and diuresis in renal sympathetic denervated rats (P<0.05). Central administration of kisspeptin-10 inhibited VE-induced natriuresis and diuresis. This effect was likely mediated by increasing AVP release independent of plasma ANP concentration and renal sympathetic nerve activity.

Protective effects of vasonatrin peptide against hypobaric hypoxia‐induced pulmonary hypertension in rats

1. The aim of the present study was to investigate the in vivo effects of vasonatrin peptide (VNP) on hypoxia-induced pulmonary hypertension (HPH). 2. The HPH model was developed by subjecting rats to hypobaric hypoxia. The HPH rats were then treated with either VNP (50 microg/kg per day, i.p.) or saline (0.5 mL, i.p.) every day for 7 days. Haemodynamic indices, right ventricular hypertrophy (RVH) and remodelling of the pulmonary arteries were evaluated. In addition, plasma levels of atrial natriuretic peptide (ANP), endothelin (ET)-1 and angiotensin II (AngII) were determined, as was natriuretic peptide receptor-C (NPR-C) mRNA expression in the right ventricle. 3. Hypobaric hypoxia induced severe HPH compared with the normoxic control group. Treatment of HPH rats with VNP for 1 week significantly reduced mean pulmonary arterial pressure, pulmonary vascular resistance, RVH and muscularization of the pulmonary arteries, although pulmonary blood flow was increased in this group. In addition, significantly lower levels of plasma ET-1 and AngII and cardiac NPR-C mRNA expression were observed in VNP-treated compared with saline-treated HPH rats, whereas higher plasma concentrations of ANP were found in the former group. Acute intravenous administration of 50 microg/kg VNP significantly ameliorated pulmonary haemodynamics in HPH rats. 4. Taken together, the date indicate that VNP has certain preventative and therapeutic effects against HPH.

Mupirocin for preventing exit-site infection and peritonitis in patients undergoing peritoneal dialysis. Was it effective?

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