Activation of myocardial and renal natriuretic peptides during acute intravascular volume overload in dogs: functional cardiorenal responses to receptor antagonism

1998 ◽  
Vol 95 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Daniel D. BORGESON ◽  
Tracy L. STEVENS ◽  
Denise M. HEUBLEIN ◽  
Yuzuru MATSUDA ◽  
John C. BURNETT

1.A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2.Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10% of body weight over 1 ;h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0±4.2 versus 62±8.0 ;pg/min, P< 0.05). 3.In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6±1.1 to 5.0±1.2 ;pmol/ml, P< 0.05). A significant attenuation of natriuresis (566±91 versus 1241±198 ;μEq/min, P< 0.05) and diuresis (4.8±0.7 versus 10.1±2.0 ;ml/min, P< 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4.These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A A Valentim Goncalves ◽  
T Pereira-Da-Silva ◽  
R Soares ◽  
L De Sousa ◽  
R Ilhao Moreira ◽  
...  

Abstract Introduction Despite being the gold-standard for hemodynamic assessment, right heart catheterization (RHC) was overcome by plasma B-Type Natriuretic Peptide (BNP) levels in daily clinical routine. However, in the first year after heart transplantation (HT), the relationship between BNP and adverse hemodynamics have yielded conflicting results. Purpose The aim of this study was to evaluate whether BNP values can be used to estimate adverse hemodynamics in the first year after HT. Methods Prospective study of consecutive RHC performed in the first year after HT (according to the endomyocardial biopsies program). Plasma BNP levels were measured at the same day. The area under the curve (AUC) was analysed to find the BNP values with higher sensitivity and specificity to detect adverse hemodynamics. Results From 2017 to 2018, 50 RHC were performed. Mean age was 48.7 ± 8.3 years, with mean BNP value of 964.4 ± 1114.7pg/ml. Prediction of adverse hemodynamics by AUC results are represented in the table. BNP values were significantly increased in patients with pulmonary capillary wedge pressure (PCWP) &gt;12mmHg (p &lt; 0.001), cardiac index &lt;2.5L/min/m2 (p = 0.001), mean pulmonary artery pressure (mPAP) ≥25mmHg (p &lt; 0.001), pulmonary vascular resistance &gt; 1,5WU (p = 0.044) and right atrial pressure &gt;5mmHg (p = 0.003). BNP &gt;500pg/ml had a sensitivity of 78.3% and 87.5% and a specificity of 76.0% and 67.7% to detect PCWP &gt;12mmHg and mPAP ≥25mmHg, respectively. Conclusion Significant associations were found between BNP values and adverse hemodynamics in RHC, supporting the clinical utility of BNP in the first year after HT. BNP prediction AUC values SR HEMODYNAMIC PARAMETERS AUC p 95% CI Best BNP value Sensitivity Specificity Pulmonary capillary wedge pressure (PCWP) &gt; 12mmHg 0.798 &lt;0.001 0.671-0.925 &gt; 500pg/ml 78.3% 76.0% Mean pulmonary artery pressure (mPAP) ≥ 25mmHg 0.830 &lt;0.001 0.714-0.946 &gt; 500pg/ml 87.5% 67.7% Cardiac output &lt; 4L/min 0.833 0.002 0.667-1.000 &gt; 1500pg/ml 77.8% 87.5% Cardiac index (CI) &lt; 2.5L/min/m2 0.810 0.001 0.663-0.957 &gt; 1150pg/ml 76.9% 86.1% Pulmonary vascular resistance (PVR) &gt; 1,5WU 0.678 0.044 0.509-0.848 &gt; 200pg/ml 83.3% 47.1% Right atrial pressure (RAP) &gt; 5mmHg 0.744 0.003 0.607-0.880 &gt; 500pg/ml 70.8% 65.4% BNP prediction


1995 ◽  
Vol 88 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Hans Berglund ◽  
Anders Edlund ◽  
Elvar Theodorsson ◽  
Hans Vallin

1. To examine the effects of rate and pressure on release of vasoactive hormones, 10 healthy subjects were examined. 2. A standardized pacing protocol was used to achieve different haemodynamic responses at two predetermined heart rates. Haemodynamic variables, and plasma concentrations of atrial natriuretic peptide, arginine vasopressin, adrenaline and noradrenaline were measured. 3. Right atrioventricular pacing at a rate of 150 impulses/min resulted in disparate responses in right atrial pressure (slight decrease) and pulmonary capillary wedge pressure (increase). Change in arterial plasma concentration of atrial natriuretic peptide correlated to change in pulmonary capillary wedge pressure, and change in arterial plasma concentration of noradrenaline correlated to change in total systemic vascular resistance, whereas concentrations of adrenaline and arginine vasopressin did not alter significantly during the stimulation periods. A significant influence of rate in addition to the pressure related influence on plasma concentration of atrial natriuretic peptide was found. In contrast, an increase in rate in the absence of an increase in atrial pressures did not raise the plasma concentration of atrial natriuretic peptide. There was no significant relationship between change in atrial natriuretic peptide and noradrenaline. 4. These data support the concept of a rate dependence of atrial natriuretic peptide release in man. Increased atrial pressure and thus presumed atrial stretch seems to be a prerequisite for increased plasma concentration of atrial natriuretic peptide. In addition, these results highlight the importance of monitoring both left and right atrial pressure in clinical investigations assessing modulation of atrial natriuretic peptide release.


1987 ◽  
Vol 252 (2) ◽  
pp. R336-R340 ◽  
Author(s):  
R. S. Zimmerman ◽  
B. S. Edwards ◽  
T. R. Schwab ◽  
D. M. Heublein ◽  
J. C. Burnett

The relationship between atrial pressure, atrial natriuretic peptide (ANP), the renin-angiotensin-aldosterone system, and renal hemodynamic and excretory function was examined during and following acute 10% body weight saline volume expansion and measurements were made at 3.3, 6.6, and 10% body weight volume expansion in pentobarbital anesthetized dogs (n = 10). Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), fractional excretion of Na (FENa), and ANP all increased in parallel during volume expansion. Plasma renin activity (PRA) and aldosterone decreased in parallel during 10% volume expansion. Following 10% volume expansion, saline was infused at the peak urine flow rate to maintain peak volume expansion. Despite continued saline infusion, RAP, PCWP, and ANP decreased in parallel. In contrast, FENa remained increased, and aldosterone and PRA remained depressed. These studies demonstrate that atrial pressures, ANP, and FENa increase in parallel during volume expansion; this suggests a role for ANP in modulating acute atrial volume overload. During stable volume expansion periods, however, despite a decrease in ANP levels, Na excretion remains elevated, suggesting that non-ANP mechanisms may be important in maintaining natriuresis during stable volume expansion.


2014 ◽  
Vol 167 (6) ◽  
pp. 876-883 ◽  
Author(s):  
Anikó I. Nagy ◽  
Ashwin Venkateshvaran ◽  
Pravat Kumar Dash ◽  
Banajit Barooah ◽  
Béla Merkely ◽  
...  

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
P Hartmund Frederiksen ◽  
N L Christensen ◽  
R Bakkestroem ◽  
R C Storch ◽  
A Banke ◽  
...  

Abstract Funding Acknowledgements Supported by the Danish Heart Foundation Background Two dimensional speckle tracking provide reproducible regional and global assessment of left ventricular (LV) function. Valvular heart disease imposes both pressure overload (aortic stenosis (AS) and volume overload (mitral regurgitation (MR) on the LV. Despite high prevalence of valvular heart disease, little is known about the relationship between longitudinal strain (LS) measures and exercise hemodynamics in the pressure over loaded LV AS and the volume over loaded LV in MR. Purpose To describe the relationship between segmental LS in AS and MR according to normal or increased pulmonary capillary wedge pressure with exercise. Methods In a cross-sectional study patients with asymptomatic AS (aortic valve area &lt;1 cm2 and peak velocity &gt;3.5 m/s) and patients with primary MR (effective regurgitant orifice &gt; 0.30 cm2) underwent echocardiography and stress test in semi-supine position with invasive hemodynamic assessment using a Swan-Ganz catheter. Echocardiograms were performed at rest on a Vivid 9 (GE, Horten, Norway) and stored for offline analysis. Semi-automatic software (Echopac version 202, GE) was used for LS analysis and recorded using an 18-segment model of the LV followed by segmentation into basal (BAS), midventricular (MID) and apical (API) segments. Semi-supine stress test was performed with increase in workload every third minute until exhaustion; at maximum exercise, pulmonary capillary wedge pressure was measured (maxPCWP). Patients were grouped according to maxPCWP &gt; 28 mmHg (group 1) or ≤ 28 mmHg (group 2). Results are shown as mean ± SD, student’s t-test was used for continues data and pearsons chi-squared test was used for categorical data. Results Thirty-five patients with AS (age 73 ± 7.0 years, 74% men), and in 44 patients with MR (age 64 ± 8.8 years, 77% men) were studied. Patients with AS had a global LS of -18.8 ± 3.3% vs. -21.5 ± 3.3% in MR patients (p = 0.001). Basal, midventricular and apical LS was -14.5%±2.2%, -18.4 ± 2.9% and -26.3 ± 5.5% in AS patients and -18.4 ± 2.6%, -21.9 ± 2.9% and -26.7 ± 5.1% in MR patients (p &lt; 0.001, p &lt; 0.001 and 0.442, respectively). The proportion of AS patients that were in group 1(n = 23) were higher than the proportion of MI patients that were in group 1 (n = 19, 66 % vs 42%, p = 0.046). Patients in group 1 had lower LS in all segments (BAS: -15.7 ± 2.8% vs -17.7 ± 3.1%, MID: -19.3 ± 2.9% vs. -21.6 ± 3.4%, API: -26.0 ± 5.0% vs -27.8 ± 5.4%) but only BAS and MID segments were statistically significant(p = 0.005 and p = 0.002, respectively). In both AS and MR, patients in group 1 had lower segmental LS, but only MID LS in MR patients was statistically significant (-20.9%±2.5% vs -22.7 ± 2.9%, p = 0.030). Conclusion In patients with AS or MR PCWP above 28 mmHg with exercise was associated with lower LS in BAS and MID segments. This implies that in both pressure and volume overload resting LV function is depressed when patients have abnormally elevated filling pressure with exercise. Abstract P1384 Figure. Longitudinal strain


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