Divergent regulation of atrial natriuretic factor receptors in high-output heart failure

1992 ◽  
Vol 263 (6) ◽  
pp. H1790-H1797 ◽  
Author(s):  
R. Garcia ◽  
M. C. Bonhomme ◽  
E. L. Schiffrin
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Heart Weight ◽  
Control Group ◽  
Receptor Density ◽  
Natriuretic Factor ◽  
Shunt Group ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

We have investigated whether binding parameters and subtypes of glomerular, papillary, and vascular atrial natriuretic factor (ANF) receptors differ in rats with moderate high-output heart failure [aortocaval (AC) shunt] from their sham-operated controls. Body weight was lower and relative heart weight was higher in the AC shunt group than in the control group. Plasma renin activity (PRA) was also greater in AC shunt rats. Plasma COOH- and NH2-terminal ANF levels were higher in AC shunt animals than in their control counterparts. Total atrial ANF content was elevated in both the right and left atria of the AC shunt group. Glomerular and papillary ANF receptor density (Bmax) and ANF receptor affinity (Kd) were similar in both AC shunt and control rats. Vascular ANF receptor density and affinity were lower in AC shunt (Bmax = 65 +/- 13 fmol.mg protein; Kd = 467 +/- 52 pM) than in control rats (Bmax = 188 +/- 34 fmol.mg protein; Kd = 278 +/- 11 pM). Irreversible cross-linking of 125I-labeled ANF followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) under reducing conditions and radioautography demonstrated that both high- and low-molecular weight receptors were unchanged in glomerular membranes and downregulated in vascular membranes from AC shunt animals. However, guanosine 3',5'-cyclic monophosphate (cGMP) production by the isolated glomeruli of AC shunt rats was lower than that of controls. We conclude that in the presence of elevated plasma ANF levels, glomerular, papillary, and vascular ANF receptors may be regulated differently.

Atrial natriuretic factor release and natriuresis in rats with high-output heart failure

1990 ◽  
Vol 259 (5) ◽  
pp. H1374-H1379 ◽  
Author(s):  
R. Garcia ◽  
D. Lachance ◽  
G. Thibault
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Left Ventricular ◽  
Heart Weight ◽  
Main Peak ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

We investigated whether rats with high-output heart failure [aortocaval (AC) shunts] release atrial natriuretic factor (ANF) and excrete sodium after moderate volume expansion (VE) as do sham-operated controls. Mean arterial blood pressure was lower (92.5 +/- 4.4 vs. 114.0 +/- 1.3 mmHg) and relative heart weight was higher (545.6 +/- 35.1 vs. 253.8 +/- 9.8 mg/100 g body wt) in animals with AC shunts than in their controls. Central venous pressure (CVP) was elevated (3.61 +/- 0.36 vs. 0.37 +/- 0.94 mmHg) and heart rate decreased (332.5 +/- 8 vs. 370.0 +/- 9.9 beats/min) in AC rats. This group also presented lower basal urinary sodium excretion (UNaV), urinary volume, and hematocrit than their sham-operated controls. Basal plasma COOH- and NH2-terminal ANF levels were greatly elevated in AC shunt animals (165.43 +/- 55.73 and 1,692.98 +/- 305.63 fmol/ml, respectively) when compared with the controls (14.27 +/- 1.49 and 331.67 +/- 29.84 fmol/ml, respectively). VE was performed in conscious rats 3 times at 15-min intervals with human plasma protein fraction. The effect of VE on CVP, left-ventricular end-diastolic pressure, the increases in plasma COOH- and NH2-terminal ANF, and the diuretic and natriuretic responses were similar in both experimental groups. U(NA)V was positively correlated with plasma COOH- (r = 0.50, P less than 0.01) and NH2- (r = 0.60, P less than 0.001) terminal ANF only in the controls. One main peak of immunoreactive ANF corresponding to the elution time of a small peptide such as ANF-(99-126) was detected in the plasma of AC animals after VE. We conclude that ANF release and natriuresis are conserved after moderate VE in a rat model of moderate high-output experimental heart failure.

ANF and postprandial control of sodium excretion in dogs with compensated heart failure

1990 ◽  
Vol 258 (1) ◽  
pp. R232-R239
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
M. W. Brands
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Right Atrial ◽  
Av Fistula ◽  
Feeding Experiments ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
Series Of Experiments ◽  
High Output ◽  
Atrial Natriuretic

The changes in plasma immunoreactive atrial natriuretic factor (iANF) and urinary Na excretion that occur in response to an oral load of Na and to infusion of synthetic atrial natriuretic factor (ANF) were examined in conscious dogs with an arteriovenous (AV) fistula and chronic compensated high-output heart failure. After ingestion of a meal containing 125 meq Na, plasma iANF and right atrial pressure increased from high basal levels of 506 +/- 46 pg/ml and 96 +/- 5 mmH2O to peak responses of 728 +/- 43 pg/ml (P less than 0.05) and 104 +/- 6 mmH2O (P less than 0.05). These increases were associated with a brisk postprandial natriuresis and diuresis of a magnitude previously observed in normal dogs. Synthetic ANF infusions that achieved plasma iANF levels of similar and higher magnitude to those observed during the feeding experiments did not produce a significant natriuresis in these AV fistula dogs. In separate series of experiments, chronic effects of normal and low-Na diets on daily Na excretion and postabsorptive plasma iANF, renin, and aldosterone were studied in normal and AV fistula dogs. During the normal Na diet of 40 meq/day, both groups had normal levels of renin and aldosterone, but Na balance was achieved in AV fistula animals in the presence of a fourfold elevation in plasma iANF compared with normal dogs (P less than 0.05). During 2 wk of Na restriction, cumulative negative Na balance and marked stimulation of renin and aldosterone were similar in normal and AV fistula animals, but plasma iANF did not change significantly in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

DOCA administration and atrial natriuretic factor in dogs with chronic heart failure

1989 ◽  
Vol 257 (3) ◽  
pp. H739-H745 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
M. W. Brands
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Base Line ◽  
Cardiac Reserve ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

The chronic reserve for the secretion of atrial natriuretic factor (ANF) was studied in conscious dogs with an arteriovenous (a-v) fistula, a model of high-output heart failure. After the first 7 days of marked sodium retention after creation of the a-v fistula, the animals regained sodium balance for the subsequent 3 wk. This compensatory natriuresis occurred in the presence of significant increases in right atrial pressure and was associated with marked and sustained elevations in plasma ANF and with the return of plasma renin and aldosterone to base-line values. The cardiac reserve for ANF secretion was further evaluated in these dogs with compensated high-output heart failure during additional progressive elevations in cardiac filling pressures induced by 3 wk of deoxycorticosterone acetate (DOCA) administration. During the DOCA regimen, plasma ANF increased an additional twofold from its high base line. Arterial blood pressure increased by 6–12 mmHg, and plasma renin activity was suppressed. However, the animals consistently retained sodium, and the high plasma levels of ANF were unable to counterbalance the sodium-retaining actions of DOCA. After termination of DOCA, the dogs exhibited a marked natriuresis, and all the hemodynamic and hormonal parameters returned to pre-DOCA control levels. This longitudinal study demonstrates that the cardiac reserve for chronic ANF secretion is well maintained in dogs with an a-v fistula during progressive cardiac volume overload. The present results suggest that the ANF endocrine system may represent one chronic compensatory mechanism to achieve sodium balance in heart failure when there is concomitant normalization of the renin-aldosterone system.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of atrial natriuretic factor in rats with experimental high-output heart failure

1988 ◽  
Vol 33 (3) ◽  
pp. 656-661 ◽  
Author(s):  
Aaron Hoffman ◽  
John C. Burnett ◽  
Aviad Haramati ◽  
Joseph Winaver
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

Effects of renal denervation on postprandial sodium excretion in experimental heart failure

1994 ◽  
Vol 266 (5) ◽  
pp. R1599-R1604 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson ◽  
J. C. Simmons
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
High Salt ◽  
Renal Nerves ◽  
Av Fistula ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
Filtered Load ◽  
High Output

The hormonal, hemodynamic and renal excretory changes after an oral load of sodium were examined in renal-denervated dogs with an arteriovenous (AV) fistula and the syndrome of compensated high-output heart failure. After ingestion of a meal containing 125 meq of sodium, the total postprandial urinary sodium excretion and fractional sodium excretion were approximately twofold higher in the renal-denervated AV fistula dogs, compared with a control group with intact renal nerves (P < 0.05). The postprandial elevations in right atrial pressure, plasma atrial natriuretic factor, and filtered load of sodium were similar in the two groups (P > 0.05). Mean arterial pressure and plasma renin activity remained unchanged from baseline in the two subsets of animals (P > 0.05). In the renal-denervated AV fistula dogs, ingestion of a low-salt meal containing 2-3 meq of sodium produced elevations in creatinine clearance and filtered load of sodium of similar magnitude to the high-salt meal. However, the increases in sodium excretion and plasma atrial natriuretic factor were modest and inconsistent. These results demonstrate that the renal nerves play an important modulatory role for postprandial sodium metabolism after a high-salt meal in experimental compensated high-output heart failure. It is suggested that the renal nerves attenuate the expression of postprandial natriuretic mechanisms via a direct tubular mechanism of action.

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.

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