Increase in Plasma Atrial Natriuretic Polypeptide (ANP) Following Sodium Load in Anesthetized Rats

1987 ◽  
Vol XXXI (2) ◽  
pp. 75
Author(s):  
J. KATO ◽  
O. KIDA ◽  
T. HIGA ◽  
A. SASAKI ◽  
K. DONDO ◽  
...  
Life Sciences ◽  
1986 ◽  
Vol 39 (6) ◽  
pp. 493-497 ◽  
Author(s):  
Johji Kato ◽  
Osamu Kida ◽  
Toshinobu Higa ◽  
Akira Sasaki ◽  
Koichi Kondo ◽  
...  

1988 ◽  
Vol 254 (4) ◽  
pp. F540-F546
Author(s):  
Y. Nishida ◽  
A. Miyata ◽  
H. Morita ◽  
N. Uemura ◽  
K. Kangawa ◽  
...  

The hypothesis that an increase in plasma sodium concentration (PNa) causes an increase in circulating atrial natriuretic polypeptide (ANP) was examined in conscious dogs. NaCl solution in small volume (0.3 ml/kg body wt) and at high concentration (20%) was injected intravenously within 2 s to rapidly increase PNa. PNa rapidly increased to 5.1 +/- 0.3 meq/l. Urinary excretion of sodium and water increased to 4.1 and 2.5 times the control levels, respectively. Plasma vasopressin level increased to 3.7 times the control level. Plasma ANP level (PANP) did not change significantly. PANP corrected for sodium-induced hemodilution did not change either. On a different day, a double amount of sodium (0.6 ml/kg body wt of 20% NaCl solution) was intravenously injected into the dogs. PNa increased by 7.3 +/- 0.4 meq/l, which was significantly more than the increase after the 0.3 ml/kg injection. PANP with or without correction for hemodilution again did not change. These results indicate that a rapid increase in PNa within the physiological range does not cause elevation of circulating ANP. This suggests that ANP does not contribute to the regulation of plasma sodium concentration.


Life Sciences ◽  
1986 ◽  
Vol 39 (26) ◽  
pp. 2623-2627 ◽  
Author(s):  
Johji Kato ◽  
Osamu Kida ◽  
Shigeru Nakamura ◽  
Akira Sasaki ◽  
Kenro Takiguchi ◽  
...  

1985 ◽  
Vol 109 (3) ◽  
pp. 405-407 ◽  
Author(s):  
Akira Sasaki ◽  
Osamu Kida ◽  
Kenji Kangawa ◽  
Hisayuki Matsuo ◽  
Kenjiro Tanaka

1988 ◽  
Vol 6 (4) ◽  
pp. S309-313 ◽  
Author(s):  
Hiroshi Itoh ◽  
Kazuwa Nakao ◽  
Masashi Mukoyama ◽  
Kiminori Hosada ◽  
Shozo Shiono ◽  
...  

Life Sciences ◽  
1987 ◽  
Vol 40 (2) ◽  
pp. 119-125 ◽  
Author(s):  
Satoshi Akabane ◽  
Shunichi Kojima ◽  
Yuichiro Igarashi ◽  
Minoru Kawamura ◽  
Yohkazu Matsushima ◽  
...  

Burns ◽  
1990 ◽  
Vol 16 (3) ◽  
pp. 169-175 ◽  
Author(s):  
G. Wakabayashi ◽  
M. Ueda ◽  
N. Aikawa ◽  
O. Abe

1988 ◽  
Vol 75 (3) ◽  
pp. 243-249 ◽  
Author(s):  
Stanislas Czekalski ◽  
Catherine Michel ◽  
Jean-Claude Dussaule ◽  
Philippe Touraine ◽  
Francoise Mignon ◽  
...  

1. In order to examine the potential role of endogenous atrial natriuretic peptide (ANP) in modulating the increased sodium excretion per nephron in chronic renal failure, we studied healthy subjects with normal renal function (group I) and patients with moderate (group II) or severe chronic renal failure (group III) before, during and after administration of an intravenous sodium load. All subjects had been on a controlled diet containing 120 mmol of sodium per day for 5 days before the study. 2. Under basal conditions, plasma ANP and fractional excretion of sodium (FENa) were highest in group III. Both parameters increased in response to the sodium load in the three groups studied (P < 0.001). Changes with time differed from group to group (P < 0.05), the more marked response for both parameters being observed in group III. After adjustment with respect to plasma ANP (analysis of covariance), FENa was no longer modified in response to the sodium load, whereas adjustment of FENa with respect to mean blood pressure was without consequence on the significance of its change with time. This demonstrates that plasma ANP, but not mean blood pressure, represents the main factor producing variation in FENa during and after the sodium load. 3. These results suggest an important role for plasma ANP in promoting adaptation of short-term sodium excretion in response to an acute sodium load in patients with chronic renal failure who ingest a normal sodium intake.


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