Effect of Cardiac Tamponade on Atrial Natriuretic Peptide Concentrations: Influence of Stretch and Pressure

1990 ◽  
Vol 79 (4) ◽  
pp. 377-380 ◽  
Author(s):  
J. Au ◽  
J. E. Brown ◽  
M. R. Lee ◽  
N. A. Boon

1. In order to study the role of atrial pressure and atrial stretch on the release of atrial natriuretic peptide we have measured plasma atrial natriuretic peptide concentration, urine output and haemodynamic variables in eight patients during and 30 min after the relief of cardiac tamponade. This condition is characterized by high atrial pressure with little or no atrial stretch. 2. Relief of tamponade was associated with a rise in urine output (53 ± 27.9 to 101 ± 24.5 ml/h, mean ± sem; P = 0.09), systolic blood pressure (95 ± 9.6 to 126 ± 7.0 mmHg, P < 0.0001), and plasma atrial natriuretic peptide concentration (369.5 ± 70.9 to 490.3 ± 94.7 pg/ml, P < 0.05) despite a large fall in right atrial pressure (18.6 ± 1.6 to 9.5 ± 1.3 mmHg, P < 0.001). 3. These results suggest, therefore, that an increase in atrial stretch, rather than in atrial pressure, stimulates the release of atrial natriuretic peptide.

1992 ◽  
Vol 6 (6) ◽  
pp. 686-691 ◽  
Author(s):  
Tetsuhiro Sakai ◽  
Terry W. Latson ◽  
Charles W. Whitten ◽  
David N. O'Flaherty ◽  
Dac Vu ◽  
...  

1991 ◽  
Vol 81 (s25) ◽  
pp. 509-514 ◽  
Author(s):  
J. Duggan ◽  
S. Kilfeather ◽  
S. L. Lightman ◽  
E. O'Brien ◽  
K. O'Malley

1. Ageing and hypertension are associated with changes in the way in which the body handles sodium. This may involve changes in plasma atrial natriuretic peptide concentration, since atrial natriuretic peptide is a regulator of sodium handling by the kidney and the plasma atrial natriuretic peptide concentration is increased in both ageing and hypertension. An increase in the plasma atrial natriuretic peptide concentration could also be associated with a change in atrial natriuretic peptide receptor density, possibly involving down-regulation. 2. To investigate these possibilities plasma atrial natriuretic peptide concentration and platelet atrial natriuretic peptide binding site density were measured in 18 young, 11 middle-aged and 12 elderly healthy subjects and in 23 patients with mild to moderate essential hypertension. 3. In normotensive subjects, the plasma atrial natriuretic peptide concentration increased with age (r = 0.49, P < 0.01) and was significantly higher in elderly than young subjects (mean ± sem, 31.9 ± 4.5 versus 18.3 ± 2.0 pmol/l, P < 0.05). The plasma atrial natriuretic peptide concentration increased with the mean arterial pressure in normotensive subjects (r = 0.47, P < 0.01). Multiple regression analysis did not show independent relationships between the plasma atrial natriuretic peptide concentration and either age or mean arterial pressure in normotensive subjects alone. However, when normotensive subjects and hypertensive patients were considered together, multiple regression revealed both age and mean arterial pressure as independent predictors of the plasma atrial natriuretic peptide concentration (P < 0.05, P < 0.01, respectively). In normotensive subjects, the platelet atrial natriuretic peptide binding site density did not change with age (r = 0.19, P = 0.27). 4. The plasma atrial natriuretic peptide concentration was elevated in hypertensive patients (37.6 ± 2.5 versus 30.4 ± 3.1 pmol/l, P < 0.05). There was no significant difference in the platelet atrial natriuretic peptide binding site density between hypertensive patients and normotensive subjects. 5. It is concluded that the plasma atrial natriuretic peptide concentration increases with age. The exact mechanism is uncertain, but it may play a role in the altered renal sodium handling seen with age. The elevation in the plasma atrial natriuretic peptide concentration with age is insufficient to induce a secondary reduction in atrial natriuretic peptide binding site density. Similarly, the elevation of the plasma atrial natriuretic peptide concentration in patients with mild to moderate hypertension does not lead to down-regulation of platelet atrial natriuretic peptide binding site density. It appears that increases in circulating atrial natriuretic peptide, greater than those observed in ageing and moderate hypertension, are required to induce down-regulation of platelet atrial natriuretic peptide binding site density.


1990 ◽  
Vol 124 (3) ◽  
pp. 463-467 ◽  
Author(s):  
N. Takemura ◽  
H. Koyama ◽  
T. Sako ◽  
K. Ando ◽  
S. Motoyoshi ◽  
...  

ABSTRACT 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<0·01) and BEC (20·6± 3·45 pmol/l, n=7, P<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<0·01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r =0·95, P<0·01) and left ventricular end-diastolic pressure (r= 0·84, P<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 β-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<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. This suggestion is supported by the fact that the middle molecular weight form of ANP, possibly corresponding to human β-ANP, was detected in both the plasma and atria of the cattle with severe heart failure. Journal of Endocrinology (1990) 124, 463–467


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