Normal Responses of Atrial Natriuretic Factor and Renal Tubular Function to Sodium Loading in Hypertension-Prone Humans

2000 ◽  
Vol 9 (4) ◽  
pp. 206-213 ◽  
Author(s):  
NIELS E. BRUUN
1986 ◽  
Vol 113 (1_Suppl) ◽  
pp. S165-S166 ◽  
Author(s):  
G. WAMBACH ◽  
S. GÖTZ ◽  
G. SUCKAU ◽  
G. BÖNNER ◽  
W. KAUFMANN

1994 ◽  
Vol 12 (4) ◽  
pp. 439???448
Author(s):  
Wilbert M.T. Janssen ◽  
Dick de Zeeuw ◽  
Gjalt K. van der Hem ◽  
Paul E. de Jong

1985 ◽  
Vol 249 (2) ◽  
pp. F315-F318
Author(s):  
T. G. Hammond ◽  
A. Haramati ◽  
F. G. Knox

Atrial natriuretic factor (ANF), a family of peptides isolated from cardiac atria, has marked effects on sodium excretion. A synthetic 26 amino acid sequence of ANF peptide has also been shown to be phosphaturic. However, it is difficult to assess whether the phosphaturia is due to changes in tubular reabsorption of phosphate without control of filtered load of phosphate. In the present study, the hypothesis that ANF peptide decreases tubular phosphate reabsorption was tested by using graded phosphate infusions of 0, 1, 2, and 3 mumol/min in thyroparathyroidectomized rats. Further, reabsorbed phosphate was similarly assessed in rats infused with parathyroid hormone (PTH) to allow comparison with a known phosphaturic hormone. ANF peptide decreased reabsorbed phosphate compared with saline controls (2.72 +/- 0.28 mumol/ml GFR compared with 3.35 +/- 0.35, P less than 0.05) but not as much as a maximally phosphaturic dose of PTH (2.04 +/- 0.13 mumol/ml GFR). We conclude that synthetic ANF peptide decreases tubular phosphate reabsorption in vivo.


1990 ◽  
Vol 79 (1) ◽  
pp. 57-65 ◽  
Author(s):  
H. Tuchelt ◽  
G. Eschenhagen ◽  
V. Bähr ◽  
G. Schwietzer ◽  
H. M. Thiede ◽  
...  

1. Sodium loading blunts the response of aldosterone to infusion of angiotensin II, whereas sodium depletion leads to an enhanced response. The hypothesis was tested that these changes in responsiveness of the zona glomerulosa are mediated in part by changes in plasma atrial natriuretic factor levels. 2. To this end, plasma renin activity and plasma aldosterone were measured in the upright and recumbent position and during incremental infusions of angiotensin II (1, 3 and 6 ng of angiotensin II amide min−1 kg−1 for 1 h each dose) after 6 days of sodium loading (study 1), after 5 days of sodium depletion (study 2) and after sodium depletion plus infusion of atrial natriuretic factor (0.13 μg/min for 8 h) on the test day (study 3). Six normal young males were investigated. 3. Plasma atrial natriuretic factor levels were around 5 pmol/l in study 2, 15 pmol/l in study 1 and 15 pmol/l in study 3 during infusion of atrial natriuretic factor. Two hours after the onset of atrial natriuretic factor infusion, plasma renin activity and plasma aldosterone (recumbent) were markedly and significantly lower in study 3 than in study 2, but still significantly higher than in study 1. The increase in plasma aldosterone after infusion of angiotensin II was slightly, but not significantly, blunted by infusion of atrial natriuretic factor in study 3 compared with study 2. The overall increase in plasma aldosterone was still significantly greater in study 3 than in study 1. 4. The fall in renal plasma flow, determined as p-aminohippurate clearance, during infusion of angiotensin II was greater in study 1 than in studies 2 and 3. Small differences between study 3 and study 2 were not significant. 5. It is concluded that infusions of atrial natriuretic factor in the low-sodium state that mimic plasma atrial natriuretic factor levels after sodium loading lead to a marked fall in recumbent plasma aldosterone, which is to a large extent secondary to a fall in plasma renin activity. A small direct effect of these physiologically elevated atrial natriuretic factor levels on the zona glomerulosa itself (the increase in plasma aldosterone during angiotensin II infusion) was only of borderline significance. Thus, atrial natriuretic factor at physiological plasma concentrations is a regulator of renin and aldosterone secretion, whereas a modulating effect on the renal vasoconstrictor action of angiotensin II could not be demonstrated.


1991 ◽  
Vol 25 (7) ◽  
pp. 558-564 ◽  
Author(s):  
H. Drexler ◽  
C. Hirth-Dietrich ◽  
J.-P. Stasch ◽  
D. Neuser ◽  
R. Gross ◽  
...  

1991 ◽  
Vol 260 (2) ◽  
pp. R346-R352 ◽  
Author(s):  
R. Castro ◽  
M. G. Ervin ◽  
R. D. Leake ◽  
M. G. Ross ◽  
D. J. Sherman ◽  
...  

The presence of atrial natriuretic factor (ANF) in fetal tissues and plasma early in gestation suggests that ANF may have a physiological role in cardiocirculatory homeostasis in utero. However, reported responsiveness of the fetal kidney to ANF varies markedly. To characterize the ontogeny of fetal renal responsiveness to ANF, chronically catheterized ovine fetuses at 114 +/- 1 days (n = 6) and 131 +/- 1 days (n = 6) received successive (30 min each) intravenous infusions of ANF at rates of 5, 25, and 100 ng.min-1.kg-1. Mean (+/- SE) fetal plasma ANF levels increased from 328 +/- 54 to 1,866 +/- 482 and 521 +/- 135 to 1,579 +/- 295 pg/ml in the younger and more mature fetuses, respectively. Mean urine volume (0.17 +/- 0.03 to 0.37 +/- 0.09 ml.min-1.kg-1) and GFR (0.9 +/- 0.2 to 1.8 +/- 0.4 ml.min-1.kg-1) increased in the early gestation fetuses but did not change in the older fetuses. Mean urine sodium excretion and osmolar clearance increased by 352 and 155% in the early gestation fetal lambs and 118 and 50% in the older animals. The fetal plasma ANF clearance rates (PCANF) were lower in the early vs. the late gestation fetuses (68 +/- 15 vs. 116 +/- 28 ml.min-1.kg-1, respectively). These results demonstrate a decrease in fetal renal responsiveness to ANF with advancing fetal age. Multiple factors appear to contribute, including changes in PCANF and maturational changes in glomerular filtration rate, renal tubular function and ANF receptor metabolism.


1994 ◽  
Vol 72 (10) ◽  
pp. 1168-1170 ◽  
Author(s):  
H. Sonnenberg ◽  
U. Honrath ◽  
C. K. Chong ◽  
L. J. Field ◽  
A. T. Veress

A transgenic mouse model in which atrial natriuretic factor (ANF) expression is targeted to the liver was used to study intrarenal adjustments to the chronically elevated hormone level. Such animals, designated TTR-ANF, are characterized by reduced arterial blood pressure but similar sodium excretion compared with nontransgenic siblings. Proximal tubular micro-puncture gave the following results: single-nephron filtration rate = 12.7 ± 1.1 vs. 15.6 ± 1.9 nL/min (TTR-ANF versus nontransgenic, ns); end-proximal tubular fluid/plasma concentration ratio of inulin = 1.93 ± 0.09 vs. 1.97 ± 0.15 (ns); fractional reabsorption of sodium = 45.5 ± 2.8 vs. 46.0 ± 3.8% (ns); fractional reabsorption of chloride = 33.6 ± 3.3 vs. 32.4 ± 4.1% (ns). These data indicate that life-long elevation of plasma ANF concentration was not associated with significant alteration in single-nephron filtration rate and proximal tubular function. We conclude that compensatory anti-natriuretic mechanisms, localized downstream from the proximal tubule, can prevent ANF natriuresis.Key words: micropuncture, single-nephron filtration rate, sodium chloride reabsorption.


Hypertension ◽  
1986 ◽  
Vol 8 (6_pt_2) ◽  
Author(s):  
A S Hollister ◽  
I Tanaka ◽  
T Imada ◽  
J Onrot ◽  
I Biaggioni ◽  
...  

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