Atrial natriuretic factor and blood pressure control: role of sodium and aldosterone

1990 ◽  
Vol 259 (5) ◽  
pp. R973-R980 ◽  
Author(s):  
C. A. Gaillard ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
M. W. Brands ◽  
D. A. Hildebrandt ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Sodium Intake ◽  
Control Period ◽  
Hypotensive Effect ◽  
Long Term Effects ◽  
High Sodium ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

This study examined the long-term actions of atrial natriuretic factor (ANF), at physiological levels, on renal function and mean arterial pressure (MAP) and the importance of Na intake and the renin-angiotensin-aldosterone system in modulating those effects. After a control period, ANF was infused intravenously at a rate of 10 ng.kg-1.min-1 for 7 days, followed by 7 days of 20 ng.kg-1.min-1 and 7 days of recovery. After 7 days of ANF at 10 ng.kg-1.min-1, MAP decreased from 87 +/- 3 to 80 +/- 2 mmHg in normal dogs on low sodium intake (LS, 7 meq Na/day) and from 89 +/- 2 to 79 +/- 2 mmHg in adrenalectomized dogs (ADX, 7 meq Na/day) given constant mineralocorticoid replacement. In both groups, no significant change in glomerular filtration rate (GFR) was observed, although sodium excretion increased transiently. ANF failed to cause significant changes in MAP, GFR, or sodium excretion in normal dogs on high sodium intake (HS, 269 meq Na/day). In LS and HS no long-term effects of ANF on plasma renin activity (PRA) and aldosterone were observed. In ADX, as expected, no change in aldosterone was observed. Thus, in normal and adrenalectomized dogs on LS, chronic ANF infusion caused sustained reductions in MAP. HS markedly attenuated the hypotensive effect of ANF. Our data suggest that the long-term effect of ANF is salt sensitive but that decreases in PRA and aldosterone are not essential for the long-term hypotensive effect of ANF.

Aldosterone, atrial natriuretic factor and sodium intake as determinants of the natriuretic response to head-out water immersion in healthy subjects

1991 ◽  
Vol 80 (5) ◽  
pp. 475-480 ◽  
Author(s):  
Leonard C. Warner ◽  
Gilles A. Morali ◽  
Judith A. Miller ◽  
Alexander G. Logan ◽  
Karl L. Skorecki ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Sodium Intake ◽  
Water Immersion ◽  
Factor Level ◽  
Baseline Serum ◽  
Aldosterone Level ◽  
Natriuretic Factor ◽  
Serum Aldosterone ◽  
Atrial Natriuretic

1. The effect of sodium intake on the natriuresis and hormonal changes induced by head-out water immersion was studied in seven normal subjects during head-out water immersion and on a control day while successively on 20 mmol of sodium/day and 100 mmol of sodium/day diets. The effects of head-out water immersion were compared with those seen on the control day for both diets. 2. The natriuresis on the 100 mmol of sodium/day diet was significantly greater than on the 20 mmol of sodium/day diet (natriuretic peak: 10.3 ± 2.2 versus 3.9 ± 1 mmol of sodium/h; P < 0.01). The total sodium excretion during the 3 h of head-out water immersion was 26.2 ± 2.0 mmol on the 100 mmol of sodium/day diet and 9.9 ± 0.9 mmol on the 20 mmol of sodium/day diet (P < 0.01). In contrast, the increase in the plasma atrial natriuretic factor level was similar on both diets (peak plasma atrial natriuretic factor level 23.1 ± 1.9 versus 26.2 ± 1 pg/ml; not significant). As expected, the baseline serum aldosterone level was higher on the 20 mmol of sodium/day diet and, despite a significant suppression, remained significantly higher at the end of the third hour of head-out water immersion (peak serum aldosterone level: 495 ± 130 versus 197 ± 26 pmol/l, P < 0.06). Furthermore, there was an inverse relationship between the serum aldosterone level and the urinary sodium excretion at the time of peak natriuresis (r = −0.59, P < 0.01). 3. We conclude that the effect of sodium intake on the natriuresis induced by head-out water immersion is more dependent upon anti-natriuretic agents, such as aldosterone, than on natriuretic factors, such as atrial natriuretic factor.

Control of atrial natriuretic factor release in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. R947-R956 ◽  
Author(s):  
K. M. Verburg ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
D. Villarreal ◽  
R. C. Vari
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Base Line ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The aim of this study was to examine the changes in the concentration of plasma immunoreactive atrial natriuretic factor (iANF) that occur in response to expansion or depletion of the extracellular fluid volume in conscious dogs. The plasma iANF concentration was also measured postprandially after the ingestion of a meal containing 125 meq of sodium. Postprandial plasma iANF increased 45% (P less than 0.05) above the base-line concentration, and this increase was accompanied by a brisk natriuresis. After a low-sodium meal, however, plasma iANF and sodium excretion failed to increase. The plasma iANF concentration increased from 57 +/- 5 to 139 +/- 36 pg/ml (P less than 0.05) immediately after volume expansion with intravenous isotonic saline infusion (2.5% body wt) administered over a 30-min period; plasma iANF remained elevated at 90 +/- 14 pg/ml (P less than 0.05) for an additional 30 min before returning toward preinfusion levels. Plasma iANF decreased 45% from 78 +/- 17 to 43 +/- 7 pg/ml (P less than 0.05) in response to the administration of ethacrynic acid (2.0 mg/kg, iv bolus) that produced an estimated 15% depletion of intravascular volume. In additional experiments the infusion of synthetic alpha-human ANF at 100 and 300 ng X kg-1 X min-1 increased (P less than 0.05) both the plasma iANF concentration and the urinary excretion of iANF. This study demonstrates that the secretion of ANF is consistently influenced by changes in the extracellular fluid volume. Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

Central effects of atrial natriuretic factor on renal salt excretion

1991 ◽  
Vol 261 (2) ◽  
pp. F354-F359 ◽  
Author(s):  
P. Rohmeiss ◽  
G. Demmert ◽  
T. Unger
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Nerves ◽  
Urinary Flow ◽  
Renal Nerve ◽  
Ureteral Catheter ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial natriuretic factor (ANF) has been localized in periventricular brain areas involved in cardiovascular and fluid control. We investigated the effect of intracerebroventricular (icv) ANF (alpha-rat atriopeptin III) on renal sodium excretion in unilaterally nephrectomized, conscious unrestrained rats fitted with a chronic ureteral catheter. Isotonic NaCl (1 ml/h) was infused intravenously. ANF injected at doses (icv) of 1 ng (n = 6), 100 ng (n = 7), and 1 microgram (n = 7) reduced urinary sodium excretion (all values mumol/45 min, means +/- SE) from 111.6 +/- 24.4 to 83 +/- 20 (P less than 0.05), from 96.9 +/- 25.2 to 55 +/- 14 (P less than 0.01), and from 90.8 +/- 14.2 to 51 +/- 9 (P less than 0.01), respectively, whereas urinary flow rate did not change. The antinatriuretic effect was immediate in onset and lasted for greater than or equal to 60 min. Blood pressure remained unaltered. ANF (100 ng icv) increased efferent sympathetic renal nerve activity (+36%; n = 6, P less than 0.05), plasma renin activity (4.6 +/- 0.6 to 7.5 +/- 0.5 pmol angiotensin I.ml-1.h-1; n = 9, P less than 0.01), plasma angiotensin II (68.7 +/- 2.5 to 84.7 +/- 3.4 fmol/ml; n = 8, P less than 0.01), and aldosterone (22.3 +/- 3.6 to 37.2 +/- 4.0 ng/ml; n = 9, P less than 0.02). Renal denervation reduced the antinatriuretic effect of ANF by 37%. We conclude that brain ANF has antinatriuretic actions, which may be partly explained by activation of renal nerves.

Atrial natriuretic factor counteracts sodium-retaining actions of insulin in normal men

1993 ◽  
Vol 265 (3) ◽  
pp. R584-R590 ◽  
Author(s):  
J. A. Miller ◽  
S. Abouchacra ◽  
B. Zinman ◽  
K. L. Skorecki ◽  
A. G. Logan
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Low Dose ◽  
Diastolic Pressure ◽  
Sodium Reabsorption ◽  
Acute Administration ◽  
Sodium Retention ◽  
Natriuretic Factor ◽  
Normal Men ◽  
Atrial Natriuretic

It has been hypothesized that hyperinsulinemia is causally related to hypertension by its effect on renal sodium transport. To examine the relationship between the sodium-retaining actions of insulin and atrial natriuretic factor (ANF), 16 healthy subjects were studied on three occasions, approximately 1 wk apart, using standard clearance techniques to evaluate responses during the acute administration of insulin, low-dose ANF, or both. In study 1, the euglycemic clamp was used to increase plasma insulin 10-fold to an average of 320 +/- 14 (SE) pM. This maneuver produced an immediate and persistent fall in sodium excretion from 0.315 +/- 0.02 to 0.207 +/- 0.02 mmol/min (P < 0.001) independent of change in renal hemodynamics, lithium clearance, and catecholamines. The decline in sodium excretion was associated with a marked increase in fractional distal sodium reabsorption. Systolic and diastolic pressure did not change significantly. In study 2, low-dose ANF (0.3 pmol.kg-1.min-1) designed to raise plasma levels to twice baseline was administered simultaneously in a repeat of study 1. This maneuver abolished insulin-mediated sodium reabsorption. In study 3, low-dose ANF infusion alone produced no changes in tubular handling of sodium. Our findings indicate that insulin at levels found in hyperinsulinemic states caused sodium retention and that physiological increases in plasma ANF concentration abolished the sodium-retaining action of insulin. Our findings suggest that if hypertension is causally related to hyperinsulinemia, mechanisms besides renal sodium retention are responsible for the hypertensive properties of insulin.

Atrial natriuretic factor and renal function during head-out water immersion in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. R1000-R1004
Author(s):  
K. Miki ◽  
G. Hajduczok ◽  
M. R. Klocke ◽  
J. A. Krasney ◽  
S. K. Hong ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Time Course ◽  
Water Immersion ◽  
Base Line ◽  
Peripheral Tissues ◽  
Natriuretic Factor ◽  
Peak Value ◽  
Atrial Natriuretic

The potential role of atrial natriuretic factor (ANF) in the renal response to head-out water immersion (WI) was studied. Five female mongrel dogs, trained to stand for 100 min in air followed by 100 min of thermoneutral WI at 37 degrees C or 200 min in air (timed control, TC), were chronically instrumented with arterial and venous catheters. The animals were hydrated with a volume of 0.45% NaCl solution equivalent to 2% of their body weight. Prehydration levels of arterial ANF were 243 +/- 15 (SE), and venous ANF levels were 211 +/- 21 pg/ml. WI resulted in an increase in urine flow from 0.7 +/- 0.1 ml/min to a peak flow of 2.2 +/- 0.3 ml/min (P less than 0.05). On immersion, plasma venous and arterial ANF levels increased significantly by 29 and 21% from the preimmersion values of 183 +/- 14 and 222 +/- 20 pg/ml, respectively. The arterial-venous difference for plasma ANF was maintained at 35 +/- 14 pg/ml (P less than 0.05) during WI; therefore venous sampling may suffice as a measure of circulating ANF levels. Sodium excretion increased linearly during WI to a peak value of 228 +/- 32 mu eq/min from a base line of 52 +/- 12 mu eq/min (P less than 0.05). These data indicate that peripheral tissues extract ANF and that WI is a physiological stimulus for the release of ANF. However, the time course and magnitude of the changes in plasma ANF and urine sodium excretion during WI are not comparable, and other mechanisms are likely responsible for the WI natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Right atrial appendectomy reduces the renal response to acute hypervolemia in the rat

1984 ◽  
Vol 247 (3) ◽  
pp. R610-R613 ◽  
Author(s):  
A. T. Veress ◽  
H. Sonnenberg
Keyword(s):  
Atrial Natriuretic Factor ◽  
Control Period ◽  
Atrial Appendage ◽  
Right Atrial ◽  
Blood Flows ◽  
Natriuretic Factor ◽  
Right Atrial Appendage ◽  
The Right ◽  
Experimental Group ◽  
Atrial Natriuretic

We have shown previously that an extract of atrial tissue from rat heart contains a potent natriuretic factor. In this study anesthetized rats were connected to a respirator and the right atrial appendage was either excised, using a loop ligature (experimental group), or the loop was placed around the appendage and then removed (sham-operated group). After equilibration and control urine collection periods an isooncotic Ringers-albumin solution was infused intravenously (25% of estimated blood volume), and renal function was monitored over the next hour. There were no differences between groups in control period arterial or central venous pressures, heart rates, cardiac outputs, renal blood flows, or filtration rates. However, the diuretic and natriuretic responses to infusion in the experimental group were only one half of those in the sham-operated series (vol = 23.4 +/- 6.2 vs. 68.2 +/- 11.0 microliter X min-1 X g kidney wt-1, UNa V = 2,731 +/- 856 vs. 6,504 +/- 962 nmol X min-1 X g kidney wt-1). These differences were not affected by prior bilateral vagotomy. Administration of homologous atrial natriuretic factor or furosemide resulted in identical renal responses in both groups. We conclude therefore that acute hypervolemia is associated with release of atrial natriuretic factor into the bloodstream and that removal of the atrial appendage reduces the amount available for such release.

The response of atrial natriuretic factor and sodium excretion to dietary sodium challenges in patients with chronic liver disease

Hepatology ◽  
1990 ◽  
Vol 12 (3) ◽  
pp. 460-466 ◽  
Author(s):  
Leonard C. Warner ◽  
Peter J. Campbell ◽  
Gilles A. Morali ◽  
Alexander G. Logan ◽  
Karl L. Skorecki ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Chronic Liver ◽  
Dietary Sodium ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Regulation of atrial natriuretic factor release by endothelin in ovine fetuses

1994 ◽  
Vol 267 (2) ◽  
pp. R380-R386 ◽  
Author(s):  
C. Y. Cheung
Keyword(s):  
Urinary Excretion ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Direct Action ◽  
Venous Pressure ◽  
Recovery Period ◽  
Control Period ◽  
Natriuretic Factor ◽  
Potent Vasoconstrictor ◽  
Atrial Natriuretic

Endothelin is a potent vasoconstrictor synthesized by vascular endothelial cells. In the adult, endothelin has been shown to stimulate the release of atrial natriuretic factor (ANF) through a direct action on atrial cardiocytes. The present study was designed to investigate, in the fetus, whether endothelin would similarly release ANF into the circulation. In addition, the effects of endothelin on fetal cardiovascular and urinary functions were explored. Chronically catheterized ovine fetuses between 126 and 139 days gestation (term 147 days) were used for the study. After a 30-min control period, the fetuses were infused intravenously with vehicle (n = 6) or endothelin-1 (n = 9) at 25 ng.min-1.kg-1 for 30 min, and this was followed by a 60-min recovery period. In response to endothelin infusion, plasma ANF levels were significantly elevated. Endothelin infusion acutely increased fetal arterial pressure without affecting venous pressure. Fetal heart rate decreased, and blood volume was reduced. Fetal urine flow rate and urinary excretion of electrolytes did not change during the endothelin infusion but were elevated during the recovery period. The fetus developed hypoxia and acidemia. Thus our study demonstrates that endothelin is effective in stimulating ANF release in the fetus, and this effect appears to be unrelated to the venous pressure changes. In addition, the results suggest that endothelin is a potent vasoconstrictor of the fetal systemic and umbilical vascular beds. The decrease in blood volume and increase in urinary excretion of fluid and electrolytes in response to endothelin are consistent with the known actions of ANF, which is elevated during endothelin infusion.

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