TY - JOUR
T1 - ANF and postprandial control of sodium excretion in dogs with compensated heart failure
AU - Villarreal, D.
AU - Freeman, R. H.
AU - Brands, M. W.
PY - 1990
Y1 - 1990
N2 - 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 < 0.05) and 104 ± 6 mmH2O (P < 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 < 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. The results of this study suggest that the ANF endocrine system is involved in postprandial regulation of Na excretion when the postprandial intravascular volume expansion facilitates the release and natriuretic actions of the cardiac hormone. In the postabsorptive state, however, the activity of the renin-angiotensin-aldosterone system is closely related to dietary Na intake and appears to function independently of the ANF system for the prevention of Na loss.
AB - 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 < 0.05) and 104 ± 6 mmH2O (P < 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 < 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. The results of this study suggest that the ANF endocrine system is involved in postprandial regulation of Na excretion when the postprandial intravascular volume expansion facilitates the release and natriuretic actions of the cardiac hormone. In the postabsorptive state, however, the activity of the renin-angiotensin-aldosterone system is closely related to dietary Na intake and appears to function independently of the ANF system for the prevention of Na loss.
KW - Arteriovenous fistula
KW - Postabsorptive
KW - Renin-angiotensin-aldosterone system
KW - Sodium depletion
KW - Volume regulation
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U2 - 10.1152/ajpregu.1990.258.1.r232
DO - 10.1152/ajpregu.1990.258.1.r232
M3 - Article
C2 - 2137300
AN - SCOPUS:0025190707
SN - 0002-9513
VL - 258
SP - R232-R239
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 1 27-1
ER -