Atrial natriuretic factor and right atrial pressure in patients undergoing chronic haemodialysis

1992 ◽  
Vol 29 (3-4) ◽  
pp. 273-277
Author(s):  
G. Tonolo ◽  
V. Scardaccio ◽  
M. La Rocca ◽  
A. Soro ◽  
M. G. Melis ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Chronic Haemodialysis ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial dynamics, atrial natriuretic factor, tachycardia, and blood volume in anesthetized rabbits

1991 ◽  
Vol 261 (1) ◽  
pp. H22-H28 ◽  
Author(s):  
K. A. King ◽  
J. R. Ledsome
Keyword(s):  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Wall Stress ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Atrial Wall ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The effects of tachycardia and a slow (1%/min) 20% reduction and elevation of blood volume (BV) on right atrial pressure (RAP), right atrial dimension (RAD), and plasma immunoreactive atrial natriuretic factor (IR-ANF) were examined in anesthetized rabbits. Plasma IR-ANF was significantly increased during pacing at 6 Hz in the presence of high BV but not at low BV. Mean RAP increased with expansion of BV, but this change was not associated with significant changes in IR-ANF. There were no statistically significant changes in systolic or diastolic RAD with alterations in BV or with tachycardia. Tachycardia had no effect on left atrial dimension. Diastolic right atrial wall stress (DRAS) and minute DRAS increased with a 20% increase in BV, but changes in BV did not affect systolic right atrial wall stress (SRAS) or minute SRAS. Tachycardia decreased DRAS at high BV and significantly increased SRAS and minute SRAS. The increases in SRAS and minute SRAS were greater during tachycardia at high BV, suggesting that an interaction between BV and tachycardia results in potentiation of SRAS and minute SRAS. The results suggest that systolic RAS is a significant factor in ANF release during tachycardia at high BV.

EVIDENCE FOR FENTANYL ALTERATION OF PLASHA ATRIAL NATRIURETIC FACTOR - RIGHT ATRIAL PRESSURE (RELATIONSHIP AFTEH CARDIAC SURGERY

1986 ◽  
Vol 65 (Supplement 3A) ◽  
pp. A511 ◽  
Author(s):  
D. M. PAYEN ◽  
D. LECLERC ◽  
J. J. CARACO ◽  
I. VIOSSAT ◽  
E. CHABRIER ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Atrial Natriuretic Factor ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Dissociation between right atrial pressure and plasma atrial natriuretic factor following prolonged high salt intake

1990 ◽  
Vol 68 (3) ◽  
pp. 408-412
Author(s):  
Jiri Widimsky Jr. ◽  
Otto Kuchel ◽  
Waldemar Debinski ◽  
Gaétan Thibault
Keyword(s):  
Atrial Natriuretic Factor ◽  
Salt Intake ◽  
High Salt ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Salt Loading ◽  
Natriuretic Factor ◽  
High Salt Intake ◽  
Atrial Natriuretic

The influence of prolonged high salt intake on intravascular volume, right atrial pressure, plasma atrial natriuretic factor, and extra-atrial tissue (lung, kidney, and liver) COOH- and NH2-terminal atrial natriuretic factor content was investigated in normotensive rats. Despite prolonged high salt (8% NaCl) intake for 5 weeks, total intravascular volume was not impaired. However, right atrial pressure was increased by 54% (p < 0.01) after salt loading. Although this increment in right atrial pressure should favor atrial natriuretic factor release after NaCl intake, plasma atrial natriuretic factor (COOH-terminal) concentrations markedly decreased from 97.8 ± 27 to 38.9 ± 8 pg/mL. Sodium and circulatory homeostasis was, however, well preserved. The lungs contained the highest levels of COOH- and NH2-terminal atrial natriuretic factor. Salt loading resulted in increased concentrations of low as well as high molecular weight atrial natriuretic factor in the lung but not in the kidney or the liver. Our study indicates a limited role of atrial natriuretic factor in adaptation to prolonged salt consumption in rats. Dissociation between right atrial pressure and plasma atrial natriuretic factor after salt intake implicates other factors regulating circulating peptide levels. Prolonged salt intake increases lung generation of atrial natriuretic factor.Key words: atrial natriuretic factor, volume, atrial pressure, high salt diet.

Effects of repeated increments in right atrial pressure on secretion of atrial natriuretic factor

1988 ◽  
Vol 61 (11) ◽  
pp. 932-934 ◽  
Author(s):  
Mathias C. Haufe ◽  
Jochen Weil ◽  
Rupert Gerzer ◽  
Johanna E. Ernst ◽  
Karl Theisen
Keyword(s):  
Atrial Natriuretic Factor ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Control of atrial natriuretic factor by right and left atrial distension in pregnant sheep

1995 ◽  
Vol 268 (6) ◽  
pp. R1411-R1417
Author(s):  
D. Javeshghani ◽  
S. Mukaddam-Daher ◽  
L. Fan ◽  
Z. Guan ◽  
J. Gutkowska ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Natriuretic Factor ◽  
Pregnant Sheep ◽  
Vascular Catheters ◽  
The Right ◽  
Left Atrial Distension ◽  
Atrial Natriuretic

Previous studies of the atrial stretch-atrial natriuretic factor (ANF) relationship during pregnancy have employed volume expansion and measured only right atrial pressure (RAP). Consequently, we studied nonpregnant (n = 7) and 115- to 125-day pregnant (n = 7) sheep and assessed the ANF response to changes of RAP and left atrial pressure (LAP) induced by graded balloon inflation. Ewes prepared with vascular catheters and atrial balloons were studied after recovery from preparatory surgical procedures. The basal levels of mean arterial pressure (MAP, 83 +/- 3 mmHg), RAP (2.1 +/- 0.7 mmHg), LAP (4.7 +/- 0.9 mmHg), and heart rate (HR, 102 +/- 6 beats/min) were similar in nonpregnant and pregnant sheep. Pregnancy also resulted in elevation of ANF concentration from 25 +/- 6 to 57 +/- 4 fmol/ml. With right atrial distension, the RAP-ANF relationships were similar in both nonpregnant and pregnant sheep, with a 10-mmHg increase in RAP increasing ANF by an average of 95 +/- 9 fmol/ml. In nonpregnant sheep, the LAP-ANF relationship was more responsive than RAP-ANF because a 10-mmHg increase in LAP resulted in a 193 +/- 10 fmol/ml increase in ANF. Moreover, during pregnancy, the LAP-ANF relationship was significantly more sensitive because a 10-mmHg increase in LAP resulted in a 433 +/- 15 fmol/ml elevation of ANF. These data demonstrate that plasma ANF levels are more responsive to distension of the left atria than to the right. More importantly, the ANF response to left, but not right, atrial distension is enhanced by pregnancy.

Release of atrial natriuretic factor from heart-lung preparations of inbred Dahl rats

1987 ◽  
Vol 253 (5) ◽  
pp. H1044-H1052 ◽  
Author(s):  
M. O. Onwochei ◽  
R. M. Snajdar ◽  
J. P. Rapp
Keyword(s):  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Isolated Heart ◽  
Strain Difference ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Bicarbonate Buffer ◽  
Natriuretic Factor ◽  
Salt Hypertension ◽  
Atrial Natriuretic

Isolated heart-lung preparations from hypertensive inbred Dahl salt-hypertension sensitive (S) and normotensive inbred Dahl salt-hypertension resistant (R) rats were perfused using 15% washed rat red blood cells in Krebs-Ringer bicarbonate buffer. Atrial pressures were increased by increasing venous return (preload) or by increasing the arterial resistance (afterload). Increases in preload at a constant afterload produced increases in the right and left atrial pressures equivalent between S and R strains. Atrial natriuretic factor (ANF) release was linearly related to right atrial pressure (RAP) or left atrial pressure (LAP) in either strain, but S released more ANF at each level of preload, and the slope of the line relating ANF release to RAP was significantly greater in S than R. When the heart-lung preparations were subjected to changes in afterload at a constant preload, LAP was significantly increased in R but not in S rats, and concomitantly ANF increased in R but not in S. In the afterload experiments, as in the preload studies, S released more ANF than R for comparable LAP. It is concluded that 1) at any atrial pressure, hearts of hypertensive S rats release more ANF than hearts of normotensive R rats, 2) this strain difference is probably a consequence of hypertension, and 3) the observed relationships between ANF release and atrial pressures support the contention that atrial distention stimulates the release of ANF.

Atrial natriuretic factor secretion in dogs with experimental high-output heart failure

1987 ◽  
Vol 252 (4) ◽  
pp. H692-H696 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
K. M. Verburg ◽  
R. C. Vari
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Sodium Balance ◽  
Av Fistula ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output

The temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (iANF) were studied in six conscious dogs with an arteriovenous (AV) fistula, a model of chronic high-output heart failure. Following the creation of the AV fistula, the dogs retained sodium avidly for 5 days, and plasma renin activity, plasma aldosterone concentration, and right atrial pressure increased significantly from controls. During this initial stage, iANF increased only modestly. From day 6 to 14, the dogs increased their daily sodium excretion and approached sodium balance. This natriuretic response was associated with a significant rise in iANF, with the return of renin and aldosterone levels to base line, and with a progressive significant elevation in right atrial pressure. Thus, in dogs with an AV fistula and cardiac volume overload, chronic increases in atrial pressure appear to be a sustained stimulus for the release of ANF. It is suggested that following the initial period of sodium retention in this experimental mental model of heart failure, chronic endocrine adjustments for the reestablishment of sodium balance involve an increase in ANF which subsequently can exert a tonic inhibitory action on the renin-aldosterone axis. It is concluded that the ANF endocrine system might function as an effective chronic compensatory mechanism to help promote sodium and water excretion in dogs with an AV fistula through the suppression of the renin-aldosterone system and possibly through its direct renal actions.

Release of atrial natriuretic factor during infusion of isoproterenol and angiotensin II

1989 ◽  
Vol 257 (4) ◽  
pp. R896-R900
Author(s):  
G. Christensen ◽  
A. Ilebekk ◽  
F. Kiil
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Adrenergic Stimulation ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Release of atrial natriuretic factor (ANF) is related to atrial pressure and heart rate and may be influenced by beta-adrenergic stimulation and angiotensin II. Experiments in five closed-chest dogs showed lower plasma immunoreactive (ir) ANF during intravenous (iv) isoproterenol (0.2-0.3 micrograms.kg-1.min-1) and higher plasma ir-ANF during iv angiotensin II (0.2-0.3 micrograms.kg-1.min-1) than during blood volume expansion measured at equal mean right atrial pressure (RAP) and heart rate. This indicated that the agents may affect ANF release differently, possibly through their effects on left atrial pressure (LAP). In five open-chest dogs with right atrial pacing at 216 +/- 1 beats/min, blood volume was expanded until mean RAP was 9 mmHg. Mean LAP rose to 16.8 +/- 2.0 mmHg, and plasma ir-ANF rose from 57 +/- 6 to 219 +/- 39 pg/ml. At a constant mean RAP of 9 mmHg, iv isoproterenol infusion reduced mean LAP to 12.6 +/- 1.4 mmHg and reduced plasma ir-ANF by 115 +/- 31 to 105 +/- 13 pg/ml. During iv angiotensin II infusion at a mean RAP of 9 mmHg, mean LAP rose to 23.2 +/- 2.2 mmHg and plasma ir-ANF averaged 281 +/- 77 pg/ml. The correlation between plasma ir-ANF and LAP (r = 0.83) indicates that the different effects of isoproterenol and angiotensin II on ANF release can be accounted for by the effects on LAP.

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