scholarly journals Regulation of aldosterone receptor in rat kidney cytosol by atrial natriuretic factor.

Hypertension ◽  
1989 ◽  
Vol 13 (4) ◽  
pp. 334-340 ◽  
Author(s):  
M Horiuchi ◽  
N Kohashi ◽  
H Nishiyama ◽  
J Hama ◽  
T Takenaka ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Rat Kidney ◽  
Natriuretic Factor ◽  
Aldosterone Receptor ◽  
Rat Kidney Cytosol ◽  
Atrial Natriuretic

Renal expression of the gene for atrial natriuretic factor

1992 ◽  
Vol 263 (5) ◽  
pp. F974-F978
Author(s):  
J. E. Greenwald ◽  
D. Ritter ◽  
E. Tetens ◽  
P. S. Rotwein
Keyword(s):  
Epithelial Cells ◽  
Atrial Natriuretic Factor ◽  
Rat Kidney ◽  
Pcr Amplification ◽  
Northern Analysis ◽  
Mammalian Kidney ◽  
Natriuretic Factor ◽  
Normal Rat ◽  
Gene Transcripts ◽  
Atrial Natriuretic

To date, atrial natriuretic factor (ANF) mRNA has eluded detection in the mammalian kidney, although we and others have identified ANF protein in the kidney using immunohistochemical and immunoassay techniques. Furthermore, we have demonstrated the synthesis and secretion of the ANF prohormone in the distal cortical nephron of the intact rat kidney and from rat primary cultured renal distal cortical tubular epithelial cells. In the present study, we show that the ANF gene is expressed in the kidney. Amplification of RNA isolated from rat distal cortical tubular epithelial cultures using ANF specific primers produced a 213-bp fragment that specifically hybridized to a 32P-labeled ANF cDNA. We had previously demonstrated these cultures to be enriched for the renal ANF synthetic and secretory cell type. However, we were unable to detect an ANF gene transcript in total rat kidney RNA using the above-mentioned polymerase chain reaction (PCR) conditions. Reanalysis of normal rat kidney PCR products by a second round of PCR amplification using nested primers successfully identified ANF mRNA. Similar to cultured kidney epithelial cells, normal rat kidney expresses ANF mRNA, but at a very low abundance, thus necessitating two rounds of PCR amplification. Further characterization of rat cortical distal tubular epithelia poly(A)+ RNA by Northern analysis revealed two ANF gene transcripts. A 1.0-kb message that comigrated with rat atrial ANF mRNA, and a second larger 1.4-kb transcript. These studies further substantiate the synthesis of ANF in the mammalian kidney. Unlike the mammalian heart, the kidney contains two ANF gene transcripts.

Protective effect of atrial natriuretic factor and mannitol following renal ischemia

1990 ◽  
Vol 258 (5) ◽  
pp. F1266-F1272 ◽  
Author(s):  
W. Lieberthal ◽  
A. M. Sheridan ◽  
C. R. Valeri
Keyword(s):  
Atrial Natriuretic Factor ◽  
Rat Kidney ◽  
Ischemic Injury ◽  
Ischemic Group ◽  
Natriuretic Factor ◽  
Ischemia Group ◽  
Renal Vascular ◽  
Isolated Kidneys ◽  
Atrial Natriuretic

We have examined the effect of atrial natriuretic factor (ANF) administered with and without mannitol on renal function following ischemic injury in both the isolated erythrocyte-perfused rat kidney and in the rat in vivo. ANF, administered alone after 25 min ischemia in the isolated kidney, reversed postischemic vasoconstriction but did not improve glomerular filtration rate (GFR). Mannitol alone had no effect on either renal vascular resistance or GFR. However, in isolated kidneys treated with the combination of both ANF and mannitol following reflow, GFR (0.65 +/- 0.04 ml.min-1.g-1) was markedly improved compared with GFR in the untreated ischemia group (0.20 +/- 0.04 ml.min-1.g-1) and was not different from GFR in the nonischemic controls (0.68 +/- 0.05 ml.min-1.g-1). Comparable results were obtained in studies performed in vivo. In rats subjected to 45 min ischemia, GFR (0.15 +/- 0.05 ml/min) was reduced compared with the GFR in sham-operated animals (0.95 +/- 0.07 ml/min). ANF or mannitol administered alone following ischemia and reflow did not improve GFR compared with the untreated ischemic group. However, in rats subjected to ischemia and treated with a combination of ANF and mannitol postreflow, GFR (0.69 +/- 0.10 ml/min) was 4.6-fold higher than GFR in the untreated ischemic group. Thus the combination of ANF and mannitol appear to act synergistically to improve GFR following ischemic injury.

Identification of protease 3.4.24.11 as the major atrial natriuretic factor degrading enzyme in the rat kidney

Peptides ◽  
1988 ◽  
Vol 9 (1) ◽  
pp. 173-180 ◽  
Author(s):  
J.L. Sonnenberg ◽  
Y. Sakane ◽  
A.Y. Jeng ◽  
J.A. Koehn ◽  
J.A. Ansell ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Rat Kidney ◽  
Degrading Enzyme ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Effect of a purified atrial natriuretic factor on rat and rabbit vascular strips and vascular beds

1984 ◽  
Vol 247 (1) ◽  
pp. R34-R39 ◽  
Author(s):  
R. Garcia ◽  
G. Thibault ◽  
M. Cantin ◽  
J. Genest
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Relaxant Effect ◽  
Natriuretic Factor ◽  
Specific Granules ◽  
Vascular Beds ◽  
Dose Dependent ◽  
Atrial Natriuretic

Rat atrium cardiocytes contain a powerful natriuretic and diuretic peptide that has been localized in the specific granules. This atrial natriuretic factor (ANF) produced a potent, dose-dependent relaxant effect on rabbit and rat arterial strips previously made to contract by application of either norepinephrine (NE) or angiotensin II. The effect was not seen if KCl was used as contractile agent or under any conditions with rabbit mesenteric strips. After the application of ANF the vascular strips were refractory to subsequent stimulation by either NE or angiotensin II. The infusion of ANF into a high-resistance isolated perfused rat kidney produced a rapid decrease (33 +/- 5 mmHg) in perfusion pressure that lasted for 18 +/- 3 min. This effect was not seen in the isolated rat mesenteric arterial preparation, even when the perfusion pressure was raised by the infusion of NE. These effects of ANF on vascular smooth muscle are not mediated by prostaglandins, by alpha- and beta-adrenergic and muscarinic receptors, or by an impairment of Ca2+ influx, but they are mimicked by sodium nitroprusside. A low- and a high-molecular-weight ANF produced the same effects. The existence of specific receptive sites for these peptides is suggested.

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