Influence of atrial natriuretic factor on uptake, intracellular distribution, and release of norepinephrine in rat adrenal medulla

1993 ◽  
Vol 71 (3-4) ◽  
pp. 195-200 ◽  
Author(s):  
M. S. Vatta ◽  
L. G. Bianciotti ◽  
B. E. Fernández
Keyword(s):  
Adrenal Medulla ◽  
Atrial Natriuretic Factor ◽  
Muscle Tone ◽  
Intracellular Distribution ◽  
Dependent Manner ◽  
High Potassium ◽  
Norepinephrine Uptake ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Several studies have demonstrated that atrial natriuretic factor can bind to adrenal medulla cells. Furthermore, atrial natriuretic factor immunoreactivity has been identified in chromaffin cells. The aim of the present work was to investigate atrial natriuretic factor effects on the uptake, intracellular distribution, and release of norepinephrine in the rat adrenal medulla. Results showed that 100 nM atrial natriuretic factor induced a rapid increase of norepinephrine uptake during the first minute of the incubation period. This increase was maintained for up to 60 min. In addition, only neuronal norepinephrine uptake was increased by the natriuretic factor; non-neuronal norepinephrine uptake was unaltered. Atrial natriuretic factor modified the intracellular distribution of the amine store: the granular fraction of norepinephrine increased, while the cytosolic fraction decreased. On the other hand, different concentrations (10, 50, and 100 nM) of the atrial factor decreased spontaneous [3H]norepinephrine output in a concentration-dependent manner. Furthermore, atrial natriuretic factor (10 nM) also reduced high potassium solution evoked secretion of norepineprhine. These results suggest that atrial natriuretic factor modulates sympathetic activity in the rat adrenal medulla. These effects of atrial natriuretic factor may be related to the catecholamine peripheral mechanism involved in the regulation of arterial blood pressure, smooth muscle tone, metabolic activity, etc.Key words: adrenal medulla, atrial natriuretic factor, intracellular norepinephrine distribution, norepinephrine release, norepineprhine uptake.

scholarly journals Kinetic analysis of internalization, recycling and redistribution of atrial natriuretic factor-receptor complex in cultured vascular smooth-muscle cells. Ligand-dependent receptor down-regulation

1992 ◽  
Vol 288 (1) ◽  
pp. 55-61 ◽  
Author(s):  
K N Pandey
Keyword(s):  
Smooth Muscle ◽  
Cell Surface ◽  
Atrial Natriuretic Factor ◽  
Dependent Manner ◽  
Receptor Complex ◽  
Down Regulation ◽  
Surface Receptors ◽  
Natriuretic Factor ◽  
Metabolic Degradation ◽  
Atrial Natriuretic

The kinetics of internalization, sequestration and metabolic degradation of atrial natriuretic factor (ANF)-receptor complex were studied in rat thoracic aortic smooth-muscle (RTASM) cells. These parameters were directly determined by measuring 125I-ANF binding to total, intracellular and cell-surface receptors. Pretreatment of cells with the lysosomotropic agent chloroquine and the energy depleter dinitrophenol led to an increase in the intracellular 125I-ANF radioactivity. After 60 min incubation at 37 degrees C, cell-associated 125I-ANF radioactivity fell rapidly in chloroquine-treated cells (> 85%) compared with the controls (< 45%). 125I-ANF radioactivity increased to a peak of 65% of the initial level within 15 min in chloroquine-treated cells compared with only 22% in the control cells. During the initial incubation period at 37 degrees C, chloroquine inhibited the release of both intact and degraded 125I-ANF in a time-dependent manner. However, at later incubation times, the effect of chloroquine was diminished and release of both degraded and intact ligand was resumed. Extracellular unlabelled ANF did not affect the release of degraded 125I-ANF but it accelerated the release of intact ANF by a retroendocytotic mechanism. After the endocytosis, about 30-40% of ANF receptors were restored to the cell surface from the internalized pool of receptors. The restoration was blocked by chloroquine or dinitrophenol but not by cycloheximide. Exposure of RTASM cells to unlabelled ANF resulted in a time- and concentration-dependent loss of ANF receptors. Unlabelled ANF (10 nM) induced a loss of more than 52% of 125I-ANF binding, and a complete loss occurred at micromolar concentrations. It is inferred that ANF-induced down-regulation of its receptor resulted primarily from an increased rate in internalization and metabolic degradation of ligand-receptor complex by receptor-mediated endocytotic mechanisms.

Centrally administered atrial natriuretic factor increases renal water excretion

1987 ◽  
Vol 252 (6) ◽  
pp. F1011-F1015 ◽  
Author(s):  
J. Lee ◽  
J. Q. Feng ◽  
R. L. Malvin ◽  
B. S. Huang ◽  
R. J. Grekin
Keyword(s):  
Intravenous Infusion ◽  
Atrial Natriuretic Factor ◽  
Renal Plasma Flow ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Free Water ◽  
Water Excretion ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.

Atrial natriuretic factor enhances norepinephrine uptake in circumventricular organs, locus coeruleus and nucleus tractus solitarii of the rat

1995 ◽  
Vol 197 (1) ◽  
pp. 29-32 ◽  
Author(s):  
Marcelo Vatta ◽  
Martín Rodriquez-Fermepín ◽  
Liliana Bianciotti ◽  
Juan Perazzo ◽  
Alejandro Monserrat ◽  
...  
Keyword(s):  
Locus Coeruleus ◽  
Atrial Natriuretic Factor ◽  
Circumventricular Organs ◽  
Nucleus Tractus Solitarii ◽  
Norepinephrine Uptake ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Mechanism of atrial natriuretic factor-induced inhibition of rat mesangial cell mitogenesis.

1990 ◽  
Vol 259 (3) ◽  
pp. E312 ◽  
Author(s):  
R G Appel
Keyword(s):  
Atrial Natriuretic Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Maximal Response ◽  
Thymidine Uptake ◽  
Dependent Manner ◽  
Cyclic Monophosphate ◽  
3T3 Fibroblasts ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Recent observations suggest that atrial natriuretic factor (ANF) may have growth-inhibitory activity. The present studies were performed to further define this action in rat mesangial cells (which have both biological and clearance ANF receptors) and in 3T3 fibroblasts (which have only clearance ANF receptors). Both cell types were made quiescent by removal of serum and then reactivated by exposure to a serum-free defined medium. ANF inhibited [3H]thymidine uptake in a dose-dependent manner in mesangial cells (half-maximal response 10(-11) M; 47% maximal inhibitory effect) but had no effect in 3T3 fibroblasts. Exogenous 8-bromoguanosine 3',5'-cyclic monophosphate (0.1 mM) inhibited [3H]thymidine uptake by 33% in mesangial cells but had no effect in 3T3 fibroblasts. Counts in mesangial cells exposed to 0.1 mM sodium nitroprusside, which stimulates guanosine 3',5'-cyclic monophosphate (cGMP), were inhibited by 76%. However, this represented a toxic effect, because excessive trypan blue uptake was noted in this condition. Mesangial cell number after 3 days of logarithmic proliferation was reduced by 33% in cells incubated with 1.0 nM ANF compared with vehicle. Incubation of mesangial cell monolayers with ANF caused a concentration-dependent increase in intracellular cGMP accumulation. Threshold responses occurred at concentrations one order of magnitude greater than that resulting in the antimitogenic action. In 3T3 fibroblast monolayers exposed to ANF, cGMP accumulation occurred but was markedly attenuated compared with mesangial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic factor does not affect norepinephrine catabolism in rat hypothalamus and adrenal medulla

1998 ◽  
Vol 253 (3) ◽  
pp. 151-154 ◽  
Author(s):  
Marcelo S Vatta ◽  
Modesto Rubio ◽  
Liliana G Bianciotti ◽  
Belisario E Fernandez
Keyword(s):  
Adrenal Medulla ◽  
Atrial Natriuretic Factor ◽  
Rat Hypothalamus ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial natriuretic factor and vasopressin during dehydration and rehydration in rats

1986 ◽  
Vol 251 (4) ◽  
pp. E497-E501 ◽  
Author(s):  
P. Januszewicz ◽  
G. Thibault ◽  
J. Gutkowska ◽  
R. Garcia ◽  
C. Mercure ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Tap Water ◽  
Control Level ◽  
Mixed Volume ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Sprague Dawley Rats ◽  
Osmotic Stimulus ◽  
Atrial Natriuretic

To determine the effect of water deprivation (mixed volume and osmotic stimulus) on the secretion of atrial natriuretic factor (ANF) and arginine vasopressin (AVP), plasma immunoreactive ANF (IR-ANF), and plasma AVP were measured in normal conscious Sprague-Dawley rats. IR-ANF was decreased to 19.9 +/- 3.6 pg/ml (24 h dehydration), 9.8 +/- 2.5 pg/ml (48 h dehydration), and undetectable level (72 h dehydration) from the control level of 62.4 +/- 2.4 pg/ml. These decreases were accompanied by significant increase in plasma AVP, serum Na+, osmolality (osm), and hematocrit (Hct). In animals deprived of water for 3 days the secretion of ANF and AVP was monitored at seven time points during the 1st h after voluntary rehydration with tap water. After rehydration, IR-ANF was elevated dramatically within 3 min and gradually for up to 1 h after water was offered; AVP decreased within 3 min of rehydration and stayed at the water-repleted level during the next 1 h. Na+, osm, and Hct did not change until 15, 9, and 30 min after rehydration, respectively. The rapid modifications in plasma IR-ANF and AVP were accompanied by a transient but significant increase in arterial blood pressure for up to 15 min after water consumption. These results indicate that oropharyngeal-gastric stimuli contribute to the release of both ANF and AVP.

Does atrial natriuretic factor protect against right ventricular overload? I. Hemodynamic study

1989 ◽  
Vol 67 (4) ◽  
pp. 1606-1611 ◽  
Author(s):  
L. C. Ou ◽  
G. L. Sardella ◽  
N. S. Hill ◽  
C. D. Thron
Keyword(s):  
Atrial Natriuretic Factor ◽  
Base Line ◽  
Ang Ii ◽  
Vascular Effects ◽  
Pulmonary Vasoconstriction ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Pressor Responses ◽  
Intact Rats ◽  
Atrial Natriuretic

We studied the effects of synthetic atrial natriuretic factor (ANF, 28-amino acid peptide) on base-line perfusion pressures and pressor responses to hypoxia and angiotensin II (ANG II) in isolated rat lungs and on the following hemodynamic and renal parameters in awake, chronically instrumented rats: cardiac output (CO), systemic (Rsa) and pulmonary (Rpa) vascular resistances, ANG II- and hypoxia (10.5% O2)-induced changes in Rsa and Rpa, and urine output. Intra-arterial ANF injections lowered base-line perfusion pressures and blunted hypoxia- and ANG II-induced pressor responses in the isolated lungs. Bolus intravenous injection of ANF (10 micrograms/kg) into intact rats decreased CO and arterial blood pressures of both systemic and pulmonary circulations and increased Rsa. ANG II (0.4 micrograms/kg) increased both Rsa and Rpa, and hypoxia increased Rpa alone in the intact rats. ANF (10 micrograms/kg) inhibited both ANG II- and hypoxia-induced increases in Rpa but did not significantly affect the ANG II-induced increase in Rsa. The antagonistic effect of ANF on pulmonary vasoconstriction was reversible and dose-dependent. The threshold doses of ANF required to inhibit pulmonary vasoconstriction were in the same range as those required to elicit diuresis and natriuresis. The data demonstrate that ANF has a preferential relaxant effect on pulmonary vessels constricted by hypoxia or ANG II. Both the renal and the pulmonary vascular effects of ANF may represent fundamental physiological actions of ANF. These actions may serve as a negative feedback control system that protects the right ventricle from excessive mechanical loads.

Angiotensin restores atrial natriuretic factor-induced decrease of baroreceptor sensitivity in normotensive rats, but not in spontaneously hypertensive rats

1989 ◽  
Vol 67 (6) ◽  
pp. 675-681 ◽  
Author(s):  
Uwe Ackermann ◽  
Terumi G. Irizawa ◽  
Brett Barber
Keyword(s):  
Atrial Natriuretic Factor ◽  
Spontaneously Hypertensive Rats ◽  
Baroreflex Sensitivity ◽  
Physiological Saline ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Wistar Kyoto ◽  
Atrial Natriuretic

The effect of atrial natriuretic factor (ANF) on baroreflex sensitivity was determined in unanesthetized normotensive (Wistar–Kyoto, WKY) or spontaneously hypertensive rats (SHR) during acute hypertensive stimuli (phenylephrine) or hypotensive stimuli (sodium nitroprusside). The i.v. dose of rat ANF ([Ser99, Tyr126]ANF) was 50 ng/min per rat, sufficient to decrease mean arterial blood pressure (ABP) by about 6 mmHg (1 mmHg = 133.3 Pa) in WKY. SHR showed no change in ABP with this ANF dose. During a control infusion of physiological saline, the mean heart rate (HR) response to increases in ABP was −1.30 ± 0.27 beats/min (bpm)/mmHg in WKY and −0.37 ± 0.22 in SHR (p < 0.05). These values were not affected significantly by ANF. However, ANF blunted chronotropic responses to ABP decreases. The control values of the ΔHR/ΔABP slope in WKY and SHR were −2.34 ± 0.57 and −2.01 ± 0.37 bpm/mmHg, respectively. In the presence of ANF, the slope changed to −0.36 ± 0.43 (i. e., bradycardia in response to hypotension) in WKY and to + 0.20 ± 0.21 in SHR (p < 0.005 for the difference from control for both). This ANF-induced loss of baroreflex sensitivity was reversed in WKY by the addition of angiotensin I (sufficient to increase ABP by 5 mmHg in control rats). Angiotensin did not restore baroreflex sensitivity in ANF-infused SHR, and ANF had no effect on the ABP increase caused by angiotensin in either group. The data suggest that ANF does not act on baroreceptor structures directly, but inhibits mechanisms involved in efferent sympathetic activation. Parasympathetic responses do not appear to be compromised.Key words: atrial natriuretic factor, cardiovascular regulation, baroreceptors.

Atrial natriuretic factor release and natriuresis in rats with high-output heart failure

1990 ◽  
Vol 259 (5) ◽  
pp. H1374-H1379 ◽  
Author(s):  
R. Garcia ◽  
D. Lachance ◽  
G. Thibault
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Left Ventricular ◽  
Heart Weight ◽  
Main Peak ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

We investigated whether rats with high-output heart failure [aortocaval (AC) shunts] release atrial natriuretic factor (ANF) and excrete sodium after moderate volume expansion (VE) as do sham-operated controls. Mean arterial blood pressure was lower (92.5 +/- 4.4 vs. 114.0 +/- 1.3 mmHg) and relative heart weight was higher (545.6 +/- 35.1 vs. 253.8 +/- 9.8 mg/100 g body wt) in animals with AC shunts than in their controls. Central venous pressure (CVP) was elevated (3.61 +/- 0.36 vs. 0.37 +/- 0.94 mmHg) and heart rate decreased (332.5 +/- 8 vs. 370.0 +/- 9.9 beats/min) in AC rats. This group also presented lower basal urinary sodium excretion (UNaV), urinary volume, and hematocrit than their sham-operated controls. Basal plasma COOH- and NH2-terminal ANF levels were greatly elevated in AC shunt animals (165.43 +/- 55.73 and 1,692.98 +/- 305.63 fmol/ml, respectively) when compared with the controls (14.27 +/- 1.49 and 331.67 +/- 29.84 fmol/ml, respectively). VE was performed in conscious rats 3 times at 15-min intervals with human plasma protein fraction. The effect of VE on CVP, left-ventricular end-diastolic pressure, the increases in plasma COOH- and NH2-terminal ANF, and the diuretic and natriuretic responses were similar in both experimental groups. U(NA)V was positively correlated with plasma COOH- (r = 0.50, P less than 0.01) and NH2- (r = 0.60, P less than 0.001) terminal ANF only in the controls. One main peak of immunoreactive ANF corresponding to the elution time of a small peptide such as ANF-(99-126) was detected in the plasma of AC animals after VE. We conclude that ANF release and natriuresis are conserved after moderate VE in a rat model of moderate high-output experimental heart failure.

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