Platelet-activating factor stimulates the release of atrial natriuretic factor from the rat heart

1991 ◽  
Vol 130 (2) ◽  
pp. 281-288 ◽  
Author(s):  
T. E. Rayner ◽  
M. F. Menadue ◽  
J. R. Oliver
Keyword(s):  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Isolated Heart ◽  
Platelet Activating Factor ◽  
Natriuretic Factor ◽  
Paf Receptor ◽  
Factor Α ◽  
Paf Receptor Antagonist ◽  
Atrial Natriuretic

ABSTRACT Atrial natriuretic factor (α-ANF(99–126); ANF) is released from atrial cells following atrial distension, myocardial infarction and periods of ischaemic or tachyarrhythmias. In this report we demonstrate that platelet-activating factor (PAF) stimulates ANF release from the isolated perfused rat heart and following i.v. injection to conscious unrestrained rats. ANF release peaked at 145% above baseline following injection of 2·5 nmol PAF into the isolated heart while administration of 2 nmol in vivo produced a 135% increase in plasma ANF levels. The PAF receptor antagonist BN52021 (10 μmol/l) attenuated this stimulated release, with the results suggesting a role for PAF in ANF secretion following release from damaged myocardium or as a humoral factor originating from the kidney. Journal of Endocrinology (1991) 130, 281–288

Insulin-like growth factor-I stimulates myofibrillar genes and modulates atrial natriuretic factor mRNA in rat heart

1997 ◽  
pp. 309-315 ◽  
Author(s):  
MY Donath ◽  
MA Gosteli-Peter ◽  
C Hauri ◽  
ER Froesch ◽  
J Zapf
Keyword(s):  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Gh Treatment ◽  
Natriuretic Factor ◽  
Igf I ◽  
Hypophysectomized Rats ◽  
Actin Expression ◽  
Alpha Actin ◽  
Atrial Natriuretic

We have investigated the effect of a 6-day infusion of recombinant human (rh) IGF-I (0.3-1.0 mg/day) or rhGH (200 mU/day) into normal and hypophysectomized rats on the ventricular expression of myofibrillar genes (alpha- and beta-myosin heavy chain (MHC), skeletal and cardiac alpha-actin) and of atrial natriuretic factor (ANF). In normal rats, beta-MHC was not detectable either before or after IGF-I or GH, but alpha-MHC mRNA increased significantly (twofold) with GH (not statistically significant for IGF-I). In contrast to normal rats, hypophysectomized rats did not express alpha-MHC either before or after IGF-I or GH, but beta-MHC was strongly expressed and significantly stimulated (1.8-fold) by IGF-I (not statistically significantly with GH). Skeletal alpha-actin expression remained unchanged during IGF-I or GH treatment of normal rats, but was enhanced by both IGF-I and GH (2.5- and 2.8-fold respectively) in hypophysectomized rats. Expression of cardiac alpha-actin in normal and hypophysectomized rats was not altered by either treatment. IGF-I and GH decreased ventricular expression of ANF in normal rats by 63% and 45% respectively, but did not influence ANF expression in hypophysectomized rats. Our results show that IGF-I and GH (possibly via IGF-I) stimulate expression of myofibrillar genes and modulate ANF mRNA concentrations in rat heart ventricles in vivo, depending on the hormonal status of the animals. However, neither IGF-I nor GH caused a shift from the beta- to the alpha-MHC isoform in hypophysectomized rats.

Homologous IRCM-Serine Protease 1 from pituitary, heart atrium and ventricle: A common pro-hormone maturation enzyme?

1986 ◽  
Vol 6 (9) ◽  
pp. 835-844 ◽  
Author(s):  
Nabil G. Seidah ◽  
James A. Cromlish ◽  
Josée Hamelin ◽  
Gaétan Thibault ◽  
Michel Chrétien
Keyword(s):  
Serine Protease ◽  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Cleavage Sites ◽  
Heart Atrium ◽  
Natriuretic Factor ◽  
Heart Atria ◽  
Atrial Natriuretic

IRCM-Serine Protease 1 (IRCM-SP1) has recently been isolated and characterized from porcine pituitary anterior and neurointermediate lobes (Cromlish et al., 1986a, J. Biol. Chem.261:10850–10858; Cromlish et al., 1986b, J. Biol. Chem.261:10859–10870). This pituitary serine protease was shown to selectively cleave human proopiomelanocortin (POMC)-derived peptides at both pairs of basic residues and C-terminal to specific Arg residues, all known to be cleaved in vivo. Here, a similar enzyme was isolated from rat heart atria and ventricles. Rat IRCM-SP1 was shown to be highly specific for the same cleavage sites in POMC, as the porcine pituitary homologue. Furthermore, the rat and the porcine enzymes cleave rat pro-Atrial Natriuretic Factor (pro-ANF 1–126) to yield ANF 103–126, 102–126 and 99–126 in that order of preference. This suggests that in vitro the cleavage sites preferred in pro-ANF resemble those found in brain and hypothalamus. The enzyme is nine times more abundant in atria versus ventricles/mg protein. It is concluded that IRCM-SP1, could well represent a common pro-hormone maturation enzyme for POMC and Pro-ANF and possibly many other pro-hormones.

Control of atrial natriuretic factor release from a rat heart-lung preparation

1987 ◽  
Vol 252 (3) ◽  
pp. R498-R502 ◽  
Author(s):  
J. R. Dietz
Keyword(s):  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Venous Return ◽  
Sodium Concentration ◽  
Aortic Pressure ◽  
Plasma Sodium ◽  
Natriuretic Factor ◽  
Time Period ◽  
Lung Preparation ◽  
Atrial Natriuretic

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.

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.

Identification of the Released form of Atrial Natriuretic Factor by the Perfused Rat Heart

1986 ◽  
Vol 182 (1) ◽  
pp. 137-141 ◽  
Author(s):  
G. Thibault ◽  
R. Garcia ◽  
J. Gutkowska ◽  
C. Lazure ◽  
N. G. Seidah ◽  
...  
Keyword(s):  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Perfused Rat Heart ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Mechanisms of hypoxia-induced atrial natriuretic factor release from rat hearts

1989 ◽  
Vol 257 (1) ◽  
pp. H147-H156 ◽  
Author(s):  
R. A. Lew ◽  
A. J. Baertschi
Keyword(s):  
Atrial Natriuretic Factor ◽  
Isolated Heart ◽  
Inhibitory Effect ◽  
Atropine Sulfate ◽  
Base Line ◽  
Adrenergic Stimulation ◽  
Natriuretic Factor ◽  
Rat Hearts ◽  
6 Hydroxydopamine ◽  
Atrial Natriuretic

Potential mechanisms of hypoxia-induced atrial natriuretic factor (ANF) release [A.J. Baertschi, J.M. Adams, and M.P. Sullivan. Am. J. Physiol. 255 (Heart Circ. Physiol. 24): H295-H300, 1988] were investigated in Langendorff-perfused rat hearts. The ANF release was graded with stimulus intensity; 10 min of perfusion with Krebs-Henseleit solution equilibrated with 95, 20, 10, 5, and 0% oxygen led to peak ANF levels of 140 +/- 31 (SE), 202 +/- 20, 407 +/- 76, 659 +/- 119, and 516 +/- 83% of base-line ANF (159 +/- 14 pg/ml), respectively. Hypoxia-induced release of lactate dehydrogenase and creatine kinase did not correlate with ANF release; this finding, along with other experiments, rules out tissue damage as a significant factor. Phentolamine (1.3 microM) and propranolol (0.1 microM) each reduced peak hypoxia-induced (0% O2) ANF release to 333 and 310%, respectively, whereas atropine sulfate (15 microM) had no inhibitory effect. The three antagonists combined reduced the peak hypoxia-induced ANF release to the same extent (307%) as either phentolamine or propranolol alone. Earlier (24 h) catecholamine depletion of rats with 100 mg/kg 6-hydroxydopamine also significantly reduced peak hypoxia-induced ANF release to 330%. Neither the reduction of the ANF secretory responses by these interventions nor the remaining ANF response could be attributed to changes in atrial mechanics. Therefore, these studies demonstrate that alpha- and beta-adrenergic stimulation is responsible for approximately half the hypoxia-induced ANF release from the isolated heart, whereas an as yet undefined mechanism accounts for the remainder of the response.

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.

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