Impaired aldosterone production by long-term infusion of atrial natriuretic factor

1990 ◽  
Vol 258 (1) ◽  
pp. E51-E56
Author(s):  
M. Nagano ◽  
E. L. Bravo
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Plasma Concentrations ◽  
In Vivo Studies ◽  
In Vitro Production ◽  
Natriuretic Factor ◽  
Pressor Responses ◽  
Atrial Natriuretic

This study assessed the effect of chronic infusions of atrial natriuretic factor (ANF) on in vivo and in vitro production of aldosterone. Vehicle (saline) or rat ANF-(99-126) was intravenously infused at 100 ng.kg-1.h-1 for 5 consecutive days into male New Zealand White rabbits. At 5 days plasma ANF was 18 +/- 4.1 pg/ml in vehicle-infused and 48.5 +/- 9.0 in ANF-infused rabbits (P less than 0.01). Plasma renin activity was significantly less in ANF-infused rabbits (2.99 +/- 0.35 vs. 0.77 +/- 0.12 ng.ml-1.h-1, P less than 0.01); however no differences were observed in the basal plasma concentrations of aldosterone, corticosterone, potassium, or hematocrit. In in vivo studies, chronically administered ANF attenuated plasma aldosterone, but not pressor, responses to acutely infused angiotensin II given at doses of 4, 16, and 64 ng.kg-1.min-1 for 20 min each. In in vitro experiments, collagenase-dispersed adrenal capsular cells from ANF-infused rabbits exhibited significantly reduced maximal responses to adrenocorticotropic hormone, angiotensin II, and potassium. These results suggest that chronic small increases in circulating ANF can blunt selectively adrenocortical responses to aldosterone secretagogues without affecting pressor responses to angiotensin II.

Atrial natriuretic factor binding sites in the jejunum

1989 ◽  
Vol 256 (2) ◽  
pp. G436-G441 ◽  
Author(s):  
C. Bianchi ◽  
G. Thibault ◽  
A. De Lean ◽  
J. Genest ◽  
M. Cantin
Keyword(s):  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Specific Binding ◽  
Rat Tissues ◽  
Rat Jejunum ◽  
Specific Binding Sites ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

We have studied the localization and the characterization of atrial natriuretic factor (ANF) binding sites by radioautographic techniques. Quantitative in vitro radioautography with a computerized microdensitometer demonstrated the presence of high-affinity, low-capacity 125I-ANF-(99-126) binding sites (Kd, 48 pM; Bmax, 63 fmol/mg protein) mainly in the villi of 20-microns slide-mounted transverse sections of the rat jejunum. Competition curves showed 50% inhibitory concentrations of 55 and 1,560 pM for ANF-(99-126) and ANF-(103-123), respectively. In vivo electron microscope radioautography showed that 80% of the silver grains were localized on the lamina propria fibroblast-like cells, 18% on mature enterocytes, and 2% on capillaries. Bradykinin and adrenocorticotropin did not compete with ANF binding. These results demonstrate that ANF binding sites in the rat jejunum possess the pharmacological characteristics of functional ANF receptors encountered in other rat tissues, and ultrastructural radioautographs show their cellular distribution. Taken together, these results demonstrate the presence and the localization of specific binding sites for ANF in the jejunal villi of the rat small intestine.

In vitro secretion of atrial natriuretic factor: receptor-mediated release of prohormone

1988 ◽  
Vol 254 (5) ◽  
pp. R809-R814 ◽  
Author(s):  
A. T. Veress ◽  
S. Milojevic ◽  
C. Yip ◽  
T. G. Flynn ◽  
H. Sonnenberg
Keyword(s):  
Atrial Natriuretic Factor ◽  
Active Form ◽  
High Concentration ◽  
Natriuretic Factor ◽  
Rat Hearts ◽  
Agonist Concentration ◽  
Atrial Natriuretic Factor Receptor ◽  
Atrial Natriuretic

Secretion of atrial natriuretic factor (ANF) in vivo is thought to be mediated by atrial distension. We have shown previously that nonstretched atria can release natriuretic activity in vitro when stimulated by certain agonists. In the present study atrial appendages from freshly excised rat hearts were incubated at 37 degrees C for up to 1 h in the presence of either vasopressin (5 X 10(-9) mol/l) or angiotensin II (2.5 X 10(-7) mol/l). Aliquots of postincubation media were injected intravenously into anesthetized bioassay rats to determine natriuretic activity. Control media, in which atria had been incubated without agonist, did not cause natriuresis. Significant increases in sodium excretion were seen after injection of media in which atria had been incubated in the presence of either agonist. Injection of medium with the same agonist concentration did not result in comparable natriuresis. Radioimmunoassay (RIA) indicated a high concentration of immunoactive ANF in the natriuretic media. However, radioreceptor assay (RRA) of the same media gave apparent ANF concentrations that were lower by about three orders of magnitude. Because the antibody used in the RIA cross reacts with ANF prohormone, whereas the RRA is sensitive only to the active form, we concluded that agonist-induced, stretch-independent release of ANF is in the form of prohormone, which can be converted to the active hormone in the circulation of the bioassay animal. The conclusion of prohormone release was confirmed by liquid chromatography. The data thus suggest that receptor-mediated as well as stretch-induced ANF secretion may be important in regulating the activity of the ANF system.

scholarly journals Degradation of atrial natriuretic factor in the rat

1986 ◽  
Vol 240 (2) ◽  
pp. 461-469 ◽  
Author(s):  
K K Murthy ◽  
G Thibault ◽  
R Garcia ◽  
J Gutkowska ◽  
J Genest ◽  
...  
Keyword(s):  
Whole Blood ◽  
Atrial Natriuretic Factor ◽  
Mesenteric Artery ◽  
Biologically Active ◽  
Prolonged Incubation ◽  
Amino Acid Peptide ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The biologically active circulating form of atrial natriuretic factor (ANF) in the rat is the 28-amino-acid peptide ANF-(Ser-99-Tyr-126). Degradation of this peptide in vivo as well as in vitro, in whole blood, in plasma and by the isolated mesenteric artery was investigated. Studies in vivo in the rat demonstrated that the elimination and degradation of ANF was extremely fast: within 3 min more than 95% of the injected immunoreactive material was eliminated from circulation. The production of a short C-terminal peptide was detected on injection of 125I-ANF-(Ser-99-Tyr-126) into the rat. This peptide increased proportionately with incubation time. Experiments in vitro in the presence of whole blood or plasma did not cause any major destruction of ANF even after incubation for 60 min. After this prolonged incubation in plasma, ANF-(Ser-99-Tyr-126) was partially converted into ANF-(Ser-103-Tyr-126), a less potent peptide. Isolated mesenteric-artery preparation appeared to degrade ANF in a manner very similar to the system in vivo. These results suggest that degradation of ANF may occur either after internalization in the vascular cells or by a membrane-bound enzyme in the vasculature.

Atrial natriuretic factor inhibits central angiotensin II pressor responses.

Hypertension ◽  
1987 ◽  
Vol 9 (5) ◽  
pp. 473-477 ◽  
Author(s):  
R Casto ◽  
J Hilbig ◽  
G Schroeder ◽  
G Stock
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Pressor Responses ◽  
Atrial Natriuretic

Human heart LIM protein activates atrial-natriuretic-factor gene expression by interacting with the cardiac-restricted transcription factor Nkx2.5

2008 ◽  
Vol 409 (3) ◽  
pp. 683-690 ◽  
Author(s):  
Bin Zheng ◽  
Mei Han ◽  
Jin-kun Wen ◽  
Rui Zhang
Keyword(s):  
Transcription Factor ◽  
Atrial Natriuretic Factor ◽  
Human Heart ◽  
Specific Expression ◽  
Human Embryonic Kidney Cells ◽  
Factor Gene ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

hhLIM [human heart LIM (Lin-11/IsI-1/Mec-3) protein] is a muscle-specific LIM-only protein that consists of two LIM motifs. hhLIM functions as a positive regulator for cardiac hypertrophy. Here we report that hhLIM serves as a cofactor regulating the expression of the ANF (atrial natriuretic factor) gene in H9c2 rat cardiomyoblast cells. We found that hhLIM promoted the expression of the ANF gene in H9c2 cells, but not in A293 human embryonic kidney cells. Furthermore, we showed that hhLIM interacted with Nkx2.5 (a cardiac-restricted transcription factor) in vivo and in vitro using its N-terminal LIM domain and enhanced the binding ability of Nkx2.5 to the NKE (Nkx2.5-binding element) boxes in the ANF promoter. These results suggest that hhLIM promotes the specific expression of the ANF gene by co-operating with Nkx2.5.

Inhibition of Neutral Endopeptidase (EC 3.4.24.11) Leads to An Atrial Natriuretic Factor-Mediated Natriuretic, Diuretic and Antihypertensive Response in Rodents

1991 ◽  
Vol 80 (3) ◽  
pp. 265-269 ◽  
Author(s):  
N. B. Shepperson ◽  
P. L. Barclay ◽  
J. A. Bennett ◽  
G. M. R. Samuels
Keyword(s):  
Atrial Natriuretic Factor ◽  
Neutral Endopeptidase ◽  
Volume Loading ◽  
Natriuretic Factor ◽  
Anaesthetized Rats ◽  
Diuretic Response ◽  
Antihypertensive Response ◽  
Atrial Natriuretic

1. Atrial natriuretic factor is metabolized by neutral endopeptidase (atriopeptidase; EC 3.4.24.11) in vitro. Inhibitors of this enzyme have been reported to prolong the half-life of atrial natriuretic factor in vivo and to potentiate the renal and haemodynamic effects of exogenous atrial natriuretic factor. 2. (±)-Candoxatrilat, a selective neutral endopeptidase inhibitor, potentiated the natriuretic and diuretic response to volume loading in anaesthetized rats. Part of the response to volume loading and the potentiation by (±)-candoxatrilat was prevented by a polyclonal atrial natriuretic factor antiserum. The diuretic and natriuretic responses evoked by hydrochlorothiazide were not altered by the antiserum. 3. (±)-Candoxatrilat reduced systolic blood pressure of one-kidney deoxycorticosterone acetate-salt hypertensive rats for over 5 h. This response was abolished by pretreatment with atrial natriuretic factor antiserum. 4. These data demonstrate that the neutral endopeptidase inhibitor (±)-candoxatrilat has natriuretic/diuretic and antihypertensive effects in rodents, and that these effects are mediated via endogenous atrial natriuretic factor.

Atrial natriuretic factor inhibits the stimulated in-vivo and in-vitro release of vasopressin and oxytocin in the rat

1987 ◽  
Vol 112 (1) ◽  
pp. 97-102 ◽  
Author(s):  
C. J. M. Poole ◽  
D. A. Carter ◽  
M. Vallejo ◽  
S. L. Lightman
Keyword(s):  
Drinking Water ◽  
Atrial Natriuretic Peptide ◽  
Atrial Natriuretic Factor ◽  
Plasma Concentrations ◽  
In Vitro Release ◽  
Oxytocin Release ◽  
Vitro Release ◽  
Atrial Natriuretic

ABSTRACT The effect of an atrial natriuretic peptide on the secretion of the neurohypophysial peptides arginine vasopressin (AVP) and oxytocin has been studied in vivo and in vitro. Atriopeptin III was administered intracerebroventricularly to conscious rats and plasma concentrations of AVP and oxytocin were determined both in controls and in rats which had their drinking water replaced by 2% NaCl. The release of both AVP and oxytocin was inhibited when basal levels were increased by the saline treatment. The inhibition of AVP release lasted for 40 min whereas oxytocin release was inhibited for 10 min only. In a further experiment the stimulated release of AVP and oxytocin from the isolated neurointermediate lobe of the rat was also inhibited by atriopeptin III. J. Endocr. (1987) 112, 97–102

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