scholarly journals Atrial natriuretic factor mRNA and binding sites in the adrenal gland

1990 ◽  
Vol 271 (2) ◽  
pp. 555-558 ◽  
Author(s):  
D J R Nunez ◽  
A P Davenport ◽  
M J Brown
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Adrenal Medulla ◽  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Zona Glomerulosa ◽  
Aldosterone Secretion ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The factor inhibiting aldosterone secretion produced by the adrenal medulla may be atrial natriuretic factor (ANF), since the latter abolishes aldosterone release in response to a number of secretagogues, including angiotensin II and K+. In this study we have shown that cells in the adrenal medulla contain ANF mRNA and therefore have the potential to synthesize this peptide. The presence of binding sites for ANF predominantly in the adrenal zona glomerulosa suggests that, if ANF is synthesized in the medulla and transferred to the cortex, it may affect mineralocorticoid status.

Distinct localization of atrial natriuretic factor and angiotensin II binding sites in the glomerulus

1986 ◽  
Vol 251 (4) ◽  
pp. F594-F602 ◽  
Author(s):  
C. Bianchi ◽  
J. Gutkowska ◽  
G. Thibault ◽  
R. Garcia ◽  
J. Genest ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Comparative Study ◽  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Mesangial Cells ◽  
Ang Ii ◽  
Half Maximum ◽  
Natriuretic Factor ◽  
Glomerular Size ◽  
Atrial Natriuretic

A comparative study of the localization of 125I-labeled atrial natriuretic factor (ANF) and 125I-labeled angiotensin II (ANG II) binding sites in the glomerulus of the rat, after an intravascular injection, has been done by ultrastructural radioautography. 125I-ANF binding sites are localized predominantly on the podocytes of the visceral epithelium (63%) followed by the endothelium of capillaries (14%), the parietal epithelium (13%), and finally mesangial cells (10%). In a comparative study, it was confirmed that 125I-ANG II uptake is localized predominantly on mesangial cells (60%) followed by epithelial visceral cells (23%) and the endothelium of capillaries (16%). Using isolated rat glomeruli, it was confirmed that ANG II decreases glomerular size (maximum effect of 15%) with an apparent half maximum effective concentration (EC50) between 10(-9) and 10(-8) M. Although ANF alone has no apparent effect on glomerular size, it inhibits the contractile effect of ANG II with a half maximum inhibitory concentration (IC50) between 10(-11) and 10(-10) M. These results suggest that an intraglomerular mechanism other than glomerular arteriolar resistance may be involved in the modulation of glomerular filtration rate by ANF. The presence of 125I-ANF uptake mainly in foot processes of visceral epithelial cells of glomeruli in vivo and the inhibition of ANG II decrease in glomerular size by ANF in vitro raise the possibility that ANF may regulate the ultrafiltration coefficient by two mechanisms: modulation of glomerular permeability, and surface area.

Atrial natriuretic factor binding sites in experimental congestive heart failure

1989 ◽  
Vol 257 (4) ◽  
pp. F515-F523
Author(s):  
C. Bianchi ◽  
G. Thibault ◽  
E. Wrobel-Konrad ◽  
A. De Lean ◽  
J. Genest ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Severe Heart Failure ◽  
Zona Glomerulosa ◽  
Renal Glomeruli ◽  
Natriuretic Factor ◽  
Cardiomyopathic Hamsters ◽  
Atrial Natriuretic

A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor [(Ser99, Tyr126)ANF] binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF [des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2] (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.

Autoradiographic localization of binding sites for atrial natriuretic factor

1985 ◽  
Vol 63 (11) ◽  
pp. 1373-1377 ◽  
Author(s):  
H. P. von Schroeder ◽  
E. Nishimura ◽  
C. H. S. McIntosh ◽  
A. M. J. Buchan ◽  
N. Wilson ◽  
...  
Keyword(s):  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Renal Medulla ◽  
Rabbit Aorta ◽  
Wistar Rat ◽  
Iliac Vein ◽  
Zona Glomerulosa ◽  
Rat Tissues ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The distribution of atrial natriuretic factor (ANF) binding sites in Wistar rat tissues, as well as tissues from other species was studied. Using autoradiography of slide mounted tissue sections incubated with 125I-labelled ANF, high densities of binding sites were found in the renal glomeruli and papilla, aortic smooth muscle, iliac vein, choroid plexus, anterior pituitary, lung, and adrenal zona glomerulosa. Results from renal, aortic, adrenal, and lung tissues from spontaneously hypertensive rats did not differ from those of Wistar rats. Binding sites were also observed in guinea pig glomeruli, renal medulla, and aorta as well as in the rabbit aorta.

Atrial Natriuretic Factor and Angiotensin Ii Stimulate Nitric Oxide Release from Human Proximal Tubular Cells

1995 ◽  
Vol 89 (5) ◽  
pp. 527-531 ◽  
Author(s):  
J. S. McLay ◽  
P. K. Chatterjee ◽  
S. K. Mistry ◽  
R. P. Weerakody ◽  
A. G. Jardine ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Nitric Oxide Production ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Oxide Production ◽  
Natriuretic Factor ◽  
Proximal Tubular ◽  
Atrial Natriuretic

1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase. 2. The ability of angiotensin II, atrial natriuretic factor and c(4–23) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells. 3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence. Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c(4–23) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor NG-monomethyl-l-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT, and AT2 receptor antagonists DuP 753 and PD 123319. 4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c(4–23) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of NG-monomethyl-l-arginine. A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c(4–23) atrial natriuretic factor. 5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT1 or AT2 receptor antagonists DuP 753 or PD 123319. 6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II. Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.

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