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)

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.

The Antinatriuretic Effect of Dopaminergic Blockade during Volume Expansion is Independent of Circulating Atrial Natriuretic Factor

1989 ◽  
Vol 77 (5) ◽  
pp. 479-484 ◽  
Author(s):  
Paolo Coruzzi ◽  
Almerico Novarini ◽  
Luisa Musiari ◽  
Carlo Ravanetti ◽  
Salvatore Ghielmi ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Water Immersion ◽  
Urinary Sodium Excretion ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Natriuretic Factor ◽  
Group I ◽  
Group Ii ◽  
Atrial Natriuretic

1. Ten normal subjects were subjected to 2 h water immersion with and without pharmacological dopaminergic blockade with either metoclopramide (group I) or domperidone (group II). 2. In group I, urinary sodium excretion showed a marked increase during water immersion alone, whereas it was blunted during water immersion plus dopaminergic blockade with metoclopramide (P < 0.05 vs water immersion alone, n = 5). Plasma aldosterone was significantly suppressed by water immersion alone (P < 0.05), but remained unchanged during water immersion plus metoclopramide. Plasma atrial natriuretic factor showed similar augmentation during water immersion alone and during water immersion plus metoclopramide. 3. Another five subjects (group II) were studied during water immersion alone and during water immersion plus dopaminergic blockade with domperidone. In this group the increase in urinary sodium excretion was similarly blunted by dopaminergic blockade. Plasma atrial natriuretic factor was equally elevated during water immersion alone and during water immersion plus domperidone, but aldosterone was suppressed by both water immersion alone and water immersion plus domperidone. 4. Our findings suggest that water immersion-induced atrial natriuretic factor release is independent of dopaminergic activity. Dopamine blockade is able to blunt significantly both water immersion-induced natriuresis and plasma aldosterone suppression, independently of the marked elevation of circulating atrial natriuretic factor, via a mechanism involving type 2 dopaminergic receptors.

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.

Role of vasopressin and atrial natriuretic factor in response to head-out water immersion

1993 ◽  
Vol 75 (4) ◽  
pp. 1917-1918
Author(s):  
R. M. Thornton ◽  
J. A. Krasney ◽  
S. K. Hong
Keyword(s):  
Atrial Natriuretic Factor ◽  
Water Immersion ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Role of potassium channels in stretch-promoted atrial natriuretic factor secretion

2009 ◽  
Vol 3 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Tsuneo Ogawa ◽  
Monica Forero ◽  
Patrick G. Burgon ◽  
Mercedes L. Kuroski de Bold ◽  
Tina Georgalis ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Factor Secretion ◽  
Atrial Natriuretic

Effects of clonidine and dihydralazine on atrial natriuretic factor and cGMP in humans

1989 ◽  
Vol 67 (3) ◽  
pp. 938-944 ◽  
Author(s):  
M. Wehling ◽  
T. Muller ◽  
J. M. Heim ◽  
R. Lorenz ◽  
H. Witzgall ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Soluble Guanylate Cyclase ◽  
Normal Subjects ◽  
Treated Group ◽  
Base Line ◽  
Hemodynamic Effects ◽  
Volume Loading ◽  
Natriuretic Factor ◽  
Basal Plasma ◽  
Atrial Natriuretic

The effects of a 1-wk treatment with clonidine (75 micrograms/day twice a day) and dihydralazine (25 mg/day twice a day) on base-line levels of plasma atrial natriuretic factor (ANF) and plasma and urinary guanosine 3′,5′-cyclic monophosphate (cGMP) and their changes by acute saline infusion (2 liters) in eight normal subjects were evaluated. Basal ANF was decreased to 65% in the clonidine group compared with both the control and dihydralazine groups. Volume loading increased plasma ANF levels by 30–40% of base-line values in the control and the dihydralazine groups and by 15% in the clonidine group. Basal plasma and urinary cGMP levels were raised by 30 and 90% in the dihydralazine group compared with both other groups. Volume loading increased plasma cGMP levels by 40% in the control and clonidine-treated groups and by 25% in the dihydralazine-treated group. It is concluded that ANF may contribute to hemodynamic effects of clonidine but not to those of dihydralazine. Dihydralazine increases plasma and urinary cGMP, supposedly by direct activation of the soluble guanylate cyclase.

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