Effects of atrial natriuretic factor, nitroprusside and acetylcholine on cGMP immunostaining in the isolated perfused rat kidney

1991 ◽  
Vol 96 (1) ◽  
pp. 13-19 ◽  
Author(s):  
H. S. Berkelmans ◽  
G. A. Burton ◽  
J. Schipper ◽  
J. de Vente
1992 ◽  
Vol 263 (5) ◽  
pp. F974-F978
Author(s):  
J. E. Greenwald ◽  
D. Ritter ◽  
E. Tetens ◽  
P. S. Rotwein

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.


1992 ◽  
Vol 263 (2) ◽  
pp. R273-R278
Author(s):  
M. R. Lebowitz ◽  
A. M. Moses ◽  
S. J. Scheinman

Atrial natriuretic peptide (ANP) antagonizes the release and action of arginine vasopressin (AVP) both in vivo and in vitro. We have reported that ANP increases the urinary and metabolic clearances of AVP in normal subjects (A. M. Moses et al. J. Clin. Endocrinol. Metab. 70: 222-229, 1990). To clarify this effect, we perfused isolated rat kidneys in vitro and measured the clearances of AVP for 30 min after the addition of rat ANP [rANP-(1-28), 10(-7) M]. In the perfused kidney, rANP increased the urinary clearance of AVP (UCAVP) from 321 +/- 19 to 417 +/- 20 microliters/min (P less than 0.01) and increased the glomerular filtration rate (GFR) from 558 +/- 28 to 696 +/- 28 microliters/min (P less than 0.01). Fractional excretion of AVP was unchanged. Rates of AVP reabsorption were directly related to filtered AVP, and this relationship was not altered by ANP. ANP did not affect the total organ clearance or the renal metabolic clearance of AVP. The increase in GFR was associated with increases in renal vascular resistance (P less than 0.05), filtration fraction (P less than 0.01), and sodium excretion (P less than 0.001). UCAVP also increased when GFR was raised without ANP by perfusing at higher pressures. The rat ANP clearance receptor agonist [cANP- (4-23), 10(-7) M] did not change GFR or UCAVP. ANP increases UCAVP in the isolated perfused rat kidney. This appears to be a hemodynamic effect of ANP, acting through its biological receptor and not the clearance receptor.(ABSTRACT TRUNCATED AT 250 WORDS)


2006 ◽  
Vol 136 (1-3) ◽  
pp. 14-22 ◽  
Author(s):  
Messias S. Santos-Neto ◽  
André F. Carvalho ◽  
Helena S.A. Monteiro ◽  
Leonard R. Forte ◽  
Manassés C. Fonteles

1987 ◽  
Vol 28 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Shosaku NARUMI ◽  
Toshiyuki YASUI ◽  
Mamoru YOSHIZAWA ◽  
Minako KAWAMURA ◽  
Hiromichi SUZUKI ◽  
...  

Hypertension ◽  
1989 ◽  
Vol 13 (4) ◽  
pp. 334-340 ◽  
Author(s):  
M Horiuchi ◽  
N Kohashi ◽  
H Nishiyama ◽  
J Hama ◽  
T Takenaka ◽  
...  

1990 ◽  
Vol 258 (5) ◽  
pp. F1266-F1272 ◽  
Author(s):  
W. Lieberthal ◽  
A. M. Sheridan ◽  
C. R. Valeri

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.


Peptides ◽  
1988 ◽  
Vol 9 (1) ◽  
pp. 173-180 ◽  
Author(s):  
J.L. Sonnenberg ◽  
Y. Sakane ◽  
A.Y. Jeng ◽  
J.A. Koehn ◽  
J.A. Ansell ◽  
...  

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