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

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.258.1.r232 ◽

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)

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Responsiveness of atrial natriuretic factor to reduction in right atrial pressure in patients with chronic congestive heart failure

Journal of the American College of Cardiology ◽

10.1016/0735-1097(88)90281-1 ◽

1988 ◽

Vol 11 (6) ◽

pp. 1191-1198 ◽

Cited By ~ 27

Author(s):

Mark A. Creager ◽

Alan T. Hirsch ◽

Elizabeth G. Nabel ◽

Sally S. Cutler ◽

Wilson S. Colucci ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Atrial Natriuretic Factor ◽

Atrial Pressure ◽

Right Atrial ◽

Right Atrial Pressure ◽

Chronic Congestive Heart Failure ◽

Natriuretic Factor ◽

Atrial Natriuretic

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.3.h739 ◽

1989 ◽

Vol 257 (3) ◽

pp. H739-H745 ◽

Cited By ~ 4

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)

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.266.5.r1599 ◽

1994 ◽

Vol 266 (5) ◽

pp. R1599-R1604 ◽

Cited By ~ 2

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.1.h22 ◽

1991 ◽

Vol 261 (1) ◽

pp. H22-H28 ◽

Cited By ~ 1

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.

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Captopril enhances renal responsiveness to ANF in dogs with compensated high-output heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.262.3.r509 ◽

1992 ◽

Vol 262 (3) ◽

pp. R509-R516 ◽

Cited By ~ 1

Author(s):

D. Villarreal ◽

R. H. Freeman ◽

R. A. Johnson

Keyword(s):

Heart Failure ◽

Urinary Sodium Excretion ◽

Sodium Balance ◽

Angiotensin Converting Enzyme Inhibition ◽

Systemic Hemodynamic ◽

Av Fistula ◽

High Output Heart Failure ◽

Converting Enzyme Inhibition ◽

Control Infusion ◽

High Output

The systemic hemodynamic, hormonal, and renal effects of chronic angiotensin-converting enzyme inhibition (CEI) with captopril and the responses to synthetic atrial natriuretic factor (ANF) infusions in the presence and absence of captopril were examined in normal dogs (n = 6) and in dogs with an arteriovenous (AV) fistula and compensated high-output heart failure (n = 6). This experimental model is characterized by normalization of the circulating renin-angiotensin-aldosterone system (RAAS) and persistent elevations in central filling pressures and plasma ANF. In both normal and AV-fistula dogs, oral captopril for 1 wk at 35 mg.kg-1.day-1 in three divided doses produced progressive reductions in arterial and atrial pressures (P less than 0.05), plasma ANF (P less than 0.05), and aldosterone (P less than 0.05). After 1-2 days of a modest increase in urinary sodium excretion (UNaV) (P less than 0.05), all of the dogs regained and maintained sodium balance during captopril administration. On the 8th day of the captopril regimen, synthetic ANF was infused at 15 and 30 ng.kg-1.min-1 for 75-min periods each. Control infusion experiments were performed in the same animals before captopril administration. The normal dogs exhibited dose-related elevations in UNaV (P less than 0.05) that were not augmented with captopril (P greater than 0.05). In contrast, in the AV-fistula dogs the observed renal unresponsiveness to synthetic ANF in the control experiments was reversed with chronic CEI, and ANF-induced UNaV achieved levels comparable to those obtained in the normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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