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.

Synthesis and renal activity of rat atrial granules depend on extracellular volume

1984 ◽  
Vol 247 (4) ◽  
pp. R750-R752
Author(s):  
U. Ackermann ◽  
T. G. Irizawa
Keyword(s):  
Atrial Natriuretic Factor ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Deoxycorticosterone Acetate ◽  
Natriuretic Factor ◽  
Specific Granules ◽  
Atrial Specific Granules ◽  
Natriuretic Effect

Extracellular fluid volume (by 22Na) and extent of 4-h [3H]fucose incorporation into atrial-specific granules were measured in deoxycorticosterone acetate (DOCA)/salt-loaded or Na-deficient rats. The natriuretic potency of extracts from their atria was also measured in assay rats. DOCA/salt-treated animals had a significantly greater extracellular volume, a significantly greater degree of fucose uptake, and a significantly more potent diuretic and natriuretic effect than did Na-deficient rats. These observations, together with the known decrease in atrial granularity with DOCA treatment, suggest that a chronic increase in extracellular fluid volume is associated with increased synthesis and metabolism of atrial natriuretic factor. They also confirm the finding reported by others that granularity and natriuretic potency are not always directly related. It may be that visible granules represent a peptide storage form that requires further processing to become natriuretic.

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)

Role of renal arterial pressure in the regulation of extracellular volume in conscious dogs

1992 ◽  
Vol 82 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Gabriele Kaczmarczyk ◽  
Klaus Schröder ◽  
Dirk Lampe ◽  
Rainer Mohnhaupt
Keyword(s):  
Body Weight ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Central Venous ◽  
Infusion Period

1. This study in conscious dogs examined the quantitative effects of a reduction in the renal arterial pressure on the renal homoeostatic responses to an acute extracellular fluid volume expansion. 2. Seven female beagle dogs were chronically instrumented with two aortic catheters, one central venous catheter and a suprarenal aortic cuff, and were kept under standardized conditions on a constant high dietary sodium intake (14.5 mmol of Na+ day−1 kg−1 body weight). 3. After a 60 min control period, 0.9% (w/v) NaCl was infused at a rate of 1 ml min−1 kg−1 body weight for 60 min (infusion period). Two different protocols were applied during the infusion period: renal arterial pressure was maintained at 102 ± 1 mmHg by means of a servo-feedback control circuit (RAP-sc, 14 experiments) or was left free (RAP-f, 14 experiments). 4. During the infusion period, in the RAP-sc protocol as well as in the RAP-f protocol, the mean arterial pressure increased by 10 mmHg, the heart rate increased by 20 beats/min, the central venous pressure increased by 4 cmH2O and the glomerular filtration rate (control 5.1 ± 0.3 ml min−1 kg−1 body weight, mean ± sem) increased by 1 ml min−1 kg−1. 5. Plasma renin activity [control 0.85 ± 0.15 (RAP-f) and 1.08 ± 0.23 (RAP-sc) pmol of angiotensin I h−1 ml−1] decreased similarly in both protocols. 6. Renal sodium excretion, fractional sodium excretion and urine volume increased more in the RAP-f experiments than in the RAP-sc experiments (P<0.05), renal sodium excretion from 8.2 to 70.1 (RAP-f) and from 7.7 to 47.4 (RAP-sc) μmol min−1 kg−1 body weight, fractional sodium excretion from 1.1 to 8.0 (RAP-f) and from 1.0 to 5.4 (RAP-sc)% and urine volume from 39 to 586 (RAP-f) and from 38 to 471 (RAP-sc) μl min−1 kg−1 body weight. 7. In the RAP-f experiments as well as in the RAP-sc experiments, urinary sodium excretion increased with expansion of the extracellular fluid volume, which increased by a maximum of 21% (fasting extracellular fluid volume: 206 ± 4 ml/kg body weight, six dogs, 28 days). 8. The increase in renal arterial pressure contributed significantly to the renal homoeostatic response, as 21% less urine and 31% less sodium were excreted when the extracellular fluid volume was expanded and the renal arterial pressure was kept constant below control pressure rather than being allowed to rise. The differences in sodium and water excretion were mainly due to the effect of renal arterial pressure on tubular reabsorption. However, the striking increase in sodium and urine excretion which occurred despite the reduction in renal arterial pressure emphasizes the importance of other homoeostatic factors involved in body fluid regulation.

Renal response to atrial natriuretic factor in conscious dogs with caval constriction

1985 ◽  
Vol 248 (4) ◽  
pp. R495-R500 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
R. C. Vari
Keyword(s):  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Conscious Dogs ◽  
Sodium Reabsorption ◽  
Renal Tubules ◽  
Potassium Excretion ◽  
Plasma Aldosterone Concentration ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Constriction of the thoracic inferior vena cava to decrease venous return and atrial filling markedly elevates plasma renin activity (PRA) and plasma aldosterone concentration (PAC) and produces chronic sodium retention and ascites in the dog. Infusion of a synthetic atrial natriuretic factor into conscious dogs with caval constriction and ascites at doses of 175 and 350 ng X kg-1 X min-1 for 30 min each produced striking increases (P less than 0.05) in creatinine clearance, diuresis, and kaliuresis but failed to increase urinary sodium excretion. Infusions of atrial natriuretic factor at these doses into conscious normal dogs, however, produced a striking increase in sodium excretion from 41 +/- 14 and 55 +/- 19 mu eq/min to 150 +/- 58 and 181 +/- 49 mu eq/min (P less than 0.05 for both values). Creatinine clearance and urine flow also increased in these normal dogs, but potassium excretion remained unchanged during the infusion periods. Atrial natriuretic factor produced parallel suppression (P less than 0.05) of the elevated levels of PRA and PAC in the caval dogs but failed to significantly decrease either PRA or PAC in the normal animals. Arterial pressure, heart rate, and PAH clearance were unchanged in both groups of dogs during infusion of atrial natriuretic factor. These results suggest that the pattern of renal electrolyte excretion elicited in response to the acute infusion of atrial natriuretic factor is dependent, at least partially, on the preexisting status of the renal tubules to facilitate sodium reabsorption and potassium excretion. The results also are consistent with the concept that atrial natriuretic factor might function to tonically inhibit the renin-angiotensin-aldosterone system.

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.

The Interrelationship between ECF Volume and ECF Anion Composition in the Regulation of Sodium Excretion

1970 ◽  
Vol 39 (4) ◽  
pp. 475-487
Author(s):  
J. J. Cohen ◽  
J. A. Chazan ◽  
S. Garella
Keyword(s):  
Hydrochloric Acid ◽  
Sodium Bicarbonate ◽  
Sodium Excretion ◽  
Extracellular Fluid ◽  
Progressive Increase ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Volume Depletion ◽  
Anion Composition ◽  
Bicarbonate Infusion

1. The interrelationship between extracellular fluid volume and extracellular anion composition as determinants of sodium excretion was studied in thirty-four dogs. In six, hypovolaemia, hypochloraemia and hyperbicarbonataemia were induced by the administration of ethacrynic acid and a low chloride diet. Isotonic sodium bicarbonate was then infused resulting in a progressive increase in sodium excretion. After 3 h while continuing the sodium bicarbonate infusion, an infusion of hydrochloric acid was given in order to return extracellular anion composition towards normal. This resulted in a prompt fall in sodium excretion without a change in GFR. 2. Ten studies were performed to determine whether this hydrochloric acid-induced enhancement of sodium conservation depends upon the presence of volume depletion and sodium avidity or whether it could also be demonstrated under circumstances of volume expansion. In these studies, hypervolaemia, hypochloraemia, hyperbicarbonataemia and a brisk natriuresis were induced by infusing isotonic sodium bicarbonate into normal dogs. The addition of hydrochloric acid returned anion composition to normal and, as before, resulted in a prompt suppression of sodium excretion despite continued sodium loading and enhanced glomerular filtration. 3. Results obtained from three related protocols (six animals each) confirmed that hypochloraemia and hyperbicarbonataemia were the necessary prerequisite conditions for this effect of hydrochloric acid in volume expanded animals. We interpret these findings as evidence that the response of the kidney to changes in extracellular fluid volume may be significantly affected by changes in the extracellular concentration of physiologic anions.

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.

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