Central venous pressure - a physiological stimulus for secretion of atrial natriuretic peptide in humans?

1987 ◽  
Vol 131 (2) ◽  
pp. 265-272 ◽  
Author(s):  
H. J. SCHÜTTEN ◽  
A. C. JOHANNESSEN ◽  
C. TORP-PEDERSEN ◽  
K. SANDER-JENSEN ◽  
P. BIE ◽  
...  
1989 ◽  
Vol 120 (4) ◽  
pp. 519-525 ◽  
Author(s):  
K. Olsson ◽  
B. E. Karlberg ◽  
L. Eriksson

Abstract. Plasma concentrations of atrial natriuretic peptide (ANP) were measured in 6 goats during pregnancy, lactation and a nonpregnant, nonlactating (= control) period before and during a rapid iv load of 0.9% NaCl. The volume of the load was 20% of blood volume. The infusions increased central venous pressure by 7 ± 1 mmHg during pregnancy and 8 ± 1 mmHg during lactation. Before infusions plasma ANP concentrations were 5.7 ± 0.7 pmol/l (control period), 10.8 ± 1.8 pmol/l (pregnancy;P< 0.05),and6.5 ± 1.5 pmol/l (lactation;NS).ANP increased significantly in all periods. Maximal values were 12.5 ± 1.5 (control period), 25.5 ± 2.3 (pregnancy; P< 0.01 vs control period, P<0.05 vs lactation), and 13.0 ± 1.6 (lactation; NS). Renal Na excretion increased similarly during pregnancy and control period, but slightly more during lactation. In 4 of the goats iv infusions of ANP (1 μg/min, 60 min) were given. The infusions caused natriuresis during the control period, but not during pregnancy and lactation, despite more than 10-fold increases of plasma ANP levels. In conclusion, our results indicate that although plasma ANP concentration rose to high levels during acute NaCl loading in pregnant goats, this effect was not important for the natriuresis. Instead, the natriuretic response to ANP appears attenuated during pregnancy, and also during lactation.


1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.


1986 ◽  
Vol 109 (1) ◽  
pp. 9-13 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Christofides ◽  
S. R. Bloom

ABSTRACT The response of plasma atrial natriuretic peptide (ANP) concentration to acute intravascular volume expansion was measured in ten male Wistar rats. An infusion of 3 ml polygelene colloidal solution at 37 °C over 45 s produced peak venous pressure rises of 1·5cm water. A highly significant (P<0·001) rise of immunoreactive plasma ANP from 24·4 ± 2·2 (mean ± s.e.m.) pmol/l to a peak of 70·0±10·5 pmol/l occurred within 2·5 min. Plasma ANP concentrations had virtually returned to basal levels (32·7 ± 2·7 pmol/l) 30 min after this acute volume load. A further infusion of 10 ml polygelene colloidal solution in 2 min produced peak venous pressure rises of 10 cm water and caused a dramatic and significant (P< 0·001) increase of plasma ANP concentration to a peak of 534·8 ± 38·5 pmol/l, occurring 7·5 min after infusion. The plasma ANP concentration had fallen but remained above basal levels 30 min later (137·2 ± 26·4 pmol/l). Similar results were obtained using an identical protocol but with whole rat blood instead of polygelene solution as the volume-expanding agent. Gel column chromatography suggested that the majority of the immunoreactive ANP in rat plasma was of similar molecular size to rat α-ANP(1–28). These results support the hypothesis that blood volume expansion is a potent stimulus for the release of ANP into plasma. J. Endocr. (1986) 109, 9–13


2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Andrew A. House ◽  
Mikko Haapio ◽  
Paolo Lentini ◽  
Ilona Bobek ◽  
Massimo de Cal ◽  
...  

Purpose. Strategies for volume assessment of critically ill patients are limited, yet early goal-directed therapy improves outcomes. Central venous pressure (CVP), Bioimpedance Vectorial Analysis (BIVA), and brain natriuretic peptide (BNP) are potentially useful tools. We studied the utility of these measures, alone and in combination, to predict changing oxygenation.Methods. Thirty-four mechanically ventilated patients, 26 of whom had data beyond the first study day, were studied. Relationships were assessed between CVP, BIVA, BNP, and oxygenation index (O2I) in a cross-sectional (baseline) and longitudinal fashion using both univariate and multivariable modeling.Results. At baseline, CVP and O2I were positively correlated (R=0.39;P=.021), while CVP and BIVA were weakly correlated (R=-0.38;P=.025). The association between slopes of variables over time was negligible, with the exception of BNP, whose slope was correlated with O2I (R=0.40;P=.044). Comparing tertiles of CVP, BIVA, and BNP slopes with the slope of O2I revealed only modest agreement between BNP and O2I (kappa=0.25;P=.067). In a regression model, only BNP was significantly associated with O2I; however, this was strengthened by including CVP in the model.Conclusions. BNP seems to be a valuable noninvasive measure of volume status in critical care and should be assessed in a prospective manner.


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