Trout vascular and renal responses to atrial natriuretic factor and heart extracts

1986 ◽  
Vol 251 (3) ◽  
pp. R639-R642 ◽  
Author(s):  
D. W. Duff ◽  
K. R. Olson

Dorsal aortic pressure (DAP), urine flow rate, and urinary K+, Na+, and Cl- were monitored in chronically catheterized unanesthetized rainbow trout before and after injection of saline, tissue extracts, or synthetic (rat, Ile-26) atrial natriuretic factor (ANF). Synthetic ANF (1.0 and 10.0 micrograms/kg body wt) and extracts from trout atria and ventricles increased DAP, urine flow rate, and electrolyte excretion. Saline, skeletal muscle extracts, and 0.1 microgram/kg body wt synthetic ANF had no effect on DAP and only minor effects on renal water and ion excretion. The slow-onset long-duration pressor response to ANF and heart extracts contrasted with a rapid short-acting pressor effect of epinephrine. Synthetic ANF (10 micrograms/kg body wt) and ventricular extracts produced marked increases in Na+ and Cl- excretion but only a mild diuresis. Much of the increase in urine flow rate appears to be due to solvent injection. These results show that trout hearts contain an ANF-like material and that mammalian and piscine ANF produce hemodynamic and renal effects upon intra-arterial injection.

1987 ◽  
Vol 253 (4) ◽  
pp. R561-R567 ◽  
Author(s):  
R. A. Brace ◽  
C. Y. Cheung

Presently little is known about the effects of atrial natriuretic factor (ANF) in the fetus. In this study we explored the effects of ANF on vascular pressures and fluid dynamics in the chronically catheterized sheep fetuses averaging 133 days gestation (term = 145-150 days). Under resting conditions plasma ANF concentration was positively correlated with fetal heart rate (P less than 0.001) and was not correlated with arterial pressure, venous pressure, or plasma osmolality. The weight-normalized fetal urine flow rate correlated positively with ANF concentration (P less than 0.01). After a bolus injection of 8 micrograms/kg of synthetic human ANF into the inferior vena cava, fetal arterial pressure decreased by 2 mmHg and remained at this level for 60 min, venous pressure was unchanged, and heart rate increased transiently by 15 beats/min. Urine flow rate increased to 250% of control 5 min after the injection and returned to control at 20 min even though ANF was four times control levels. Fetal blood volume decreased significantly by 5% within 10 min and remained low for 60 min. This decrease in blood volume was greater than the increase in urine flow. A kinetic analysis revealed that ANF disappearance from the plasma could not be adequately characterized with a single rate constant due to exchange between plasma and interstitial fluid.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 257 (4) ◽  
pp. F565-F573
Author(s):  
J. Ohanian ◽  
M. A. Young ◽  
Y. T. Shen ◽  
R. Gaivin ◽  
S. F. Vatner ◽  
...  

We studied the effects of 30-min infusions of the synthetic 25-amino acid atrial natriuretic factor [ANF-(102-126)] and the 28-amino acid ANF-(99-126) at 0.1 and 0.3 micrograms.kg-1.min-1 on urine flow rate, sodium excretion, and arterial pressure in conscious dogs. Each dose was administered on a separate day following a 1-h stabilization period. We also compared the effects of 60-min infusions of ANF, 0.01 micrograms.kg-1.min-1, or water infusion on separate days in conscious dogs. Arterial pressure was reduced in a dose-dependent fashion, reaching statistical significance at a dose of 0.3 micrograms.kg-1.min-1. During the 0.01-micrograms.kg-1.min-1 infusion, the plasma concentration of ANF rose approximately threefold (from 68 +/- 7 to 207 +/- 14 pg/ml), with no change in urine flow rate, sodium excretion, or arterial pressure. At a dose of 0.1 micrograms.kg-1.min-1, urine flow increased (P less than 0.05) by 0.41 +/- 0.15 ml/min, and sodium excretion rose by 72 +/- 24 mu eq/min, but not significantly, whereas plasma ANF levels rose to 1,236 +/- 229 pg/ml. At the highest dose of ANF (0.3 micrograms.kg-1.min-1) urine flow rose by 0.62 +/- 0.16 ml/min, P less than 0.05, and sodium excretion rose by 139 +/- 30 mu eq/min, P less than 0.05, whereas plasma levels of ANF rose to 2,436 +/- 320 pg/ml. In contrast, volume loading with dextran increased urine flow by 3.5 +/- 1.3 ml/min, P less than 0.05, and sodium excretion by 439 +/- 147 mu eq/min, P less than 0.05, whereas ANF rose to only 320 +/- 69 pg/ml. These results suggest that, in the conscious dog, ANF does not cause significant diuretic or natriuretic effects until plasma levels are markedly above those observed in physiological conditions. A possible explanation for the difference between this and previous studies is that the renal effects of ANF, at physiological plasma levels, are indirect and thus dependent on autonomic and hormonal (angiotensin, vasopressin, and aldosterone levels) factors governing the renal function of the animal.


1987 ◽  
Vol 252 (3) ◽  
pp. R498-R502 ◽  
Author(s):  
J. R. Dietz

These experiments examined the effects of altering venous return, aortic pressure, or perfusate sodium concentration on the release of atrial natriuretic factor (ANF) from a rat heart-lung preparation. Changes in perfusate ANF concentration during each time period (delta ANF) were used as an index of ANF secretion. Raising the height of the venous return reservoir from 2-3 to 5-7 cm above the heart increased delta ANF from 88 +/- 19 to 748 +/- 154 pg X ml-1 X 10 min-1 (P less than 0.01, n = 7). In control experiments where the height of the reservoir was not increased, delta ANF was unchanged (65 +/- 35 vs. 43 +/- 26 pg X ml-1 X 10 min-1, n = 6). Increasing aortic pressure from 60 to 100 mmHg increased ANF from 43 +/- 10 to 107 +/- 20 pg X ml-1 X 15 min-1 (P less than 0.05, n = 6). Separate groups of heart-lung preparations were perfused with solutions with sodium concentrations of 132 +/- 1, 144 +/- 2, or 166 +/- 1 meq/l (n = 8/group). delta ANF was 45 +/- 14, 50 +/- 17, and 52 +/- 22 pg X ml-1 X 10 min-1, respectively. These values were not significantly different. These results suggest that ANF plays a role in the control of blood volume and blood pressure but do not support a role for ANF in the control of plasma sodium concentration.


1989 ◽  
Vol 35 (7) ◽  
pp. 1519-1523 ◽  
Author(s):  
M Wencker ◽  
S Hauptlorenz ◽  
W Moll ◽  
B Puschendorf

Abstract The significance of increased atrial natriuretic factor (ANF) in relation to blood pressure and age is still controversial. We investigated the influence of blood pressure, age, and some other variables on ANF and its putative second messenger, cGMP. Samples for ANF and cGMP detection were taken from 124 ostensibly healthy individuals who were donating blood. Samples were also collected from 27 volunteers before and after blood donation, to study the influence of bleeding. During blood donation, ANF increased from 78.9 to 87.4 ng/L (P = 0.0035), whereas cGMP remained unchanged. ANF concentrations in 124 healthy individuals, corrected for the influence of bleeding, were 61.5 (SD 26.1) ng/L, with a 95% confidence interval of 10.0 to 112.1 ng/L. Mean cGMP concentrations in plasma were 2.9 (SD 1.45) nmol/L, with a 95% confidence interval of 0.4 to 5.75 nmol/L. Multivariance analysis revealed no significant influence of blood pressure, age, heart rate, or sex on concentrations of either ANF or cGMP in plasma.


1989 ◽  
Vol 257 (3) ◽  
pp. R580-R587 ◽  
Author(s):  
R. A. Brace ◽  
L. A. Bayer ◽  
C. Y. Cheung

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 65 (5) ◽  
pp. 1975-1983 ◽  
Author(s):  
S. Adnot ◽  
P. E. Chabrier ◽  
C. Brun-Buisson ◽  
I. Viossat ◽  
P. Braquet

The influence of endogenous and exogenous atrial natriuretic factor (ANF) on pulmonary hemodynamics was investigated in anesthetized pigs during both normoxia and hypoxia. Continuous hypoxic ventilation with 11% O2 was associated with a uniform but transient increase of plasma immunoreactive (ir) ANF that peaked at 15 min. Plasma irANF was inversely related to pulmonary arterial pressure (Ppa; r = -0.66, P less than 0.01) and pulmonary vascular resistance (PVR; r = -0.56, P less than 0.05) at 30 min of hypoxia in 14 animals; no such relationship was found during normoxia. ANF infusion after 60 min of hypoxia in seven pigs reduced the 156 +/- 20% increase in PVR to 124 +/- 18% (P less than 0.01) at 0.01 microgram.kg-1.min-1 and to 101 +/- 15% (P less than 0.001) at 0.05 microgram.kg-1.min-1. Cardiac output (CO) and systemic arterial pressure (Psa) remained unchanged, whereas mean Ppa decreased from 25.5 +/- 1.5 to 20.5 +/- 15 mmHg (P less than 0.001) and plasma irANF increased two- to nine-fold. ANF infused at 0.1 microgram.kg-1.min-1 (resulting in a 50-fold plasma irANF increase) decreased Psa (-14%) and reduced CO (-10%); systemic vascular resistance (SVR) was not changed, nor was a further decrease in PVR induced. No change in PVR or SVR occurred in normoxic animals at any ANF infusion rate. These results suggest that ANF may act as an endogenous pulmonary vasodilator that could modulate the pulmonary pressor response to hypoxia.


1987 ◽  
Vol 252 (4) ◽  
pp. F654-F660 ◽  
Author(s):  
N. Perico ◽  
F. Delaini ◽  
C. Lupini ◽  
G. Remuzzi

The aim of this study was to evaluate the renal response to atrial extracts (AE) and synthetic atrial natriuretic factor (ANF) in control rats and in rats with experimental nephrotic syndrome (NS). NS was obtained by a single intravenous injection of adriamycin (7.5 mg/kg). Bolus injection of AE from normal or NS rats resulted in marked increase of diuresis and natriuresis in bioassay control rats (AE from normal rats, urine flow rate, 14.87 +/- 2.94 to 186.18 +/- 55.86 microliters/min; Na excretion, 0.68 +/- 0.26 to 21.80 +/- 5.45 mu eq/min; AE from NS, urine flow rate, 13.49 +/- 4.30 to 167.14 +/- 51.44 microliters/min; Na excretion, 0.98 +/- 0.57 to 20.71 +/- 9.76 mu eq/min). In contrast, blunted diuretic (from 11.26 +/- 3.05 to 65.20 +/- 27.30 microliters/min) and natriuretic (from 0.58 +/- 0.15 to 4.52 +/- 1.59 mu eq/min) effect was observed when AE were injected in rats with NS. Injection of the vehicle in which AE were dissolved or ventricular extracts did not increase urinary flow rate or Na excretion in both control and NS animals. Bolus injection of synthetic ANF (Arg-101-Tyr-126) induced marked diuretic and natriuretic response in control but not in NS rats. Similar results were obtained when AE were infused by constant infusion in control or in NS bioassay rats. AE given by constant infusion induced comparable increase in glomerular filtration rate (GFR) over basal values both in control and NS animals (controls, 39%; NS rats, 40%).(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 252 (5) ◽  
pp. F865-F871 ◽  
Author(s):  
J. P. Koepke ◽  
G. F. DiBona

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.


Sign in / Sign up

Export Citation Format

Share Document