Elevated Plasma C-Type Natriuretic Peptide Concentrations in Patients with Chronic Renal Failure

1994 ◽  
Vol 87 (3) ◽  
pp. 319-322 ◽  
Author(s):  
Kazuhito Totsune ◽  
Kazuhiro Takahashi ◽  
Osamu Murakami ◽  
Fumitoshi Satoh ◽  
Masahiko Sone ◽  
...  

1. C-type natriuretic peptide is a neuropeptide, which is also produced by the vascular endothelial cells. Plasma immunoreactive C-type natriuretic peptide concentrations in patients with various diseases have not yet been studied. 2. Plasma immunoreactive C-type natriuretic peptide concentrations were studied by radioimmunoassay in normal subjects, patients with congestive heart failure, non-dialysed patients with chronic renal failure and haemodialysis patients with chronic renal failure. The C-type natriuretic peptide levels were compared with the levels of atrial natriuretic peptide and brain natriuretic peptide. 3. Plasma immunoreactive C-type natriuretic peptide concentrations were greatly elevated in patients with chronic renal failure [non-dialysed, 13.0 ± 4.2 pmol/l (mean ± SEM), n = 9, P < 0.01) compared with normal subjects (4.4 ± 0.4 pmol/l, n = 26); haemodialysis, 16.1 ± 2.1 pmol/l, n = 13, P < 0.01], but not in patients with congestive heart failure (New York Heart Association Class II-IV, 3.0 ± 0.7 pmol/l, n = 11, P > 0.05). Plasma immunoreactive atrial natriuretic peptide and brain natriuretic peptide concentrations were elevated both in patients with congestive heart failure and in haemodialysis patients with chronic renal failure. 4. Reverse-phase high performance liquid chromatography showed that immunoreactive C-type natriuretic peptide in plasma from normal subjects and haemodialysis patients was eluted in the positions of C-type natriuretic peptide −22 and −53. 5. These findings suggest that C-type natriuretic peptide is a non-cardiac circulating hormone and participates in the cardiovascular regulation in a different manner from atrial natriuretic peptide and brain natriuretic peptide.

2001 ◽  
Vol 49 (10) ◽  
pp. 1293-1300 ◽  
Author(s):  
Gad M. Bialik ◽  
Zaid A. Abassi ◽  
Ilan Hammel ◽  
Joseph Winaver ◽  
Dina Lewinson

The natriuretic peptides are believed to play an important role in the pathophysiology of congestive heart failure (CHF). We utilized a quantitative cytomorphometric method, using double immunocytochemical labeling, to assess the characteristics of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in atrial granules in an experimental model of rats with CHF induced by aortocaval fistula. Rats with CHF were further divided into decompensated (sodium-retaining) and compensated (sodium-excreting) subgroups and compared with a sham-operated control group. A total of 947 granules in myocytes in the right atrium were analyzed, using electron microscopy and a computerized analysis system. Decompensated CHF was associated with alterations in the modal nature of granule content packing, as depicted by moving bin analysis, and in the granule density of both peptides. In control rats, the mean density of gold particles attached to both peptides was 347.0 ± 103.6 and 306.3 ± 89.9 gold particles/μm2 for ANP and BNP, respectively. Similar mean density was revealed in the compensated rats (390.6 ± 81.0 and 351.3 ± 62.1 gold particles/μm2 for ANP and BNP, respectively). However, in rats with decompensated CHF, a significant decrease in the mean density of gold particles was observed (141.6 ± 67.3 and 158.0 ± 71.2 gold particles/μm2 for ANP and BNP, respectively; p < 0.05 compared with compensated rats, for both ANP and BNP). The ANP:BNP ratio did not differ between groups. These findings indicate that the development of decompensated CHF in rats with aortocaval fistula is associated with a marked decrease in the density of both peptides in atrial granules, as well as in alterations in the quantal nature of granule formation. The data further suggest that both peptides, ANP and BNP, may be regulated in the atrium by a common secretory mechanism in CHF.


1989 ◽  
Vol 77 (5) ◽  
pp. 573-579 ◽  
Author(s):  
M. G. Buckley ◽  
G. A. Sagnella ◽  
N. D. Markandu ◽  
D. R. J. Singer ◽  
G. A. MacGregor

1. Plasma levels of immunoreactive N-terminal pro-atrial natriuretic peptide (N-terminal ANP) have been measured in 25 normal subjects, 29 patients with essential hypertension, six cardiac transplant recipients, seven patients with dialysis-independent chronic renal failure and 11 patients with haemodialysis-dependent chronic renal failure. Plasma was extracted on Sep-Pak cartridges and N-terminal ANP immunoreactivity was measured using an antibody directed against pro-ANP (1–30). 2. Plasma levels of TV-terminal ANP (means ± sem) were 235.3 ± 19.2 pg/ml in normal subjects and were significantly raised in patients with essential hypertension (363.6 ± 36.3 pg/ml), in cardiac transplant recipients (1240.0 ± 196.2 pg/ml), in patients with chronic renal failure not requiring dialysis (1636.6 ± 488.4 pg/ml) and patients with chronic renal failure on maintenance haemodialysis (10 336.1 ± 2043.7 pg/ml). 3. There were positive and significant correlations between the plasma levels of TV-terminal ANP and α-human ANP (α-hANP) with individual correlation coefficients of 0.68 within the normal subjects, 0.47 in patients with essential hypertension, 0.78 in patients with dialysis-independent chronic renal failure and 0.68 in patients with haemodialysis-dependent chronic renal failure (P < 0.05 in every case). 4. Gel filtration behaviour on Sephadex G-50 of the immunoreactive N-terminal ANP from Sep-Pak extracts of plasma from normal subjects or patients was consistent with a single peak having an elution volume corresponding to that of human pro-ANP (1–67) standard. 5. These studies demonstrate that the N-terminal pro-ANP peptide is co-secreted with α-hANP in both normal subjects and patients with cardiovascular/renal disease. The higher levels of the N-terminal ANP may reflect differences in the rate of elimination from the circulation but the exact structure and functional significance of the circulating N-terminal ANP remains to be established.


Renal Failure ◽  
1998 ◽  
Vol 20 (5) ◽  
pp. 717-723 ◽  
Author(s):  
Koichi Seta ◽  
Takahiro Hayashi ◽  
Akira Sugawara ◽  
Kenji Kasuno ◽  
Satoshi Watanabe ◽  
...  

1994 ◽  
Vol 87 (3) ◽  
pp. 311-317 ◽  
Author(s):  
M. G. Buckley ◽  
N. D. Markandu ◽  
G. A. Sagnella ◽  
G. A. MacGregor

1. The aim of this study was to determine plasma levels of N-terminal atrial natriuretic peptide and atrial natriuretic peptide in normal subjects and in patients with essential hypertension, cardiac transplant and chronic renal failure, using radioimmunoassays directed towards the mid-portion pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) of the N-terminal atrial natriuretic peptide and atrial natriuretic peptide (99-126). The circulating form(s) of the immunoreactive N-terminal atrial natriuretic peptide in plasma extracts has been investigated using all three radioimmunoassays by means of gel filtration chromatography to further clarify the major immunoreactive molecular circulating form(s) of N-terminal atrial natriuretic peptide in man. 2. The plasma level (mean ± SEM) of N-terminal pro-atrial natriuretic peptide (31-67) in the normal subjects was 547.2 ± 32.7 pg/ml (n = 36) and was significantly elevated in patients with essential hypertension (730.2 ± 72.3 pg/ml, P < 0.025, n = 39), in cardiac transplant recipients (3214.0 ± 432.2 pg/ml, P < 0.001, n = 9) and in patients with chronic renal failure (3571.8 ± 474.1 pg/ml, P < 0.001, n = 11). Plasma levels of N-terminal pro-atrial natriuretic peptide (1-30) and atrial natriuretic peptide were similarly elevated in the same patient groups when compared with the mean plasma values in the normal subjects. 3. There were positive associations between pro-atrial natriuretic peptide (31-67) and atrial natriuretic peptide, pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) and between pro-atrial natriuretic peptide (1-30) and atrial natriuretic peptide in the normal subjects, hypertensive patients, cardiac transplant recipients and patients with chronic renal failure. The correlation coefficient for all groups taken together was 0.86 (P < 0.001. n = 95) for pro-atrial natriuretic peptide (31-67) and atrial natriuretic peptide, 0.93 (P < 0.001, n = 95) for pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30), and 0.82 (p < 0.001, n = 95) for pro-atrial natriuretic peptide (1-30) and atrial natriuretic peptide. 4. Gel filtration of extracted plasma from cardiac transplant patients and patients with chronic renal failure indicated a single peak of immunoreactivity for N-terminal atrial natriuretic peptide using both the pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) radioimmunoassays, suggesting a major single high-molecular-mass circulating immunoreactive N-terminal atrial natriuretic peptide, probably pro-atrial natriuretic peptide (1-98). Atrial natriuretic peptide immunoreactivity, as measured by the radioimmunoassay for atrial natriuretic peptide (99-126), showed a separate and distinct peak from that of the N-terminal atrial natriuretic peptide, which co-eluted with the synthetic human standard atrial natriuretic peptide (99-126). 5. These results show that immunoreactive N-terminal atrial natriuretic peptide and atrial natriuretic peptide are elevated in patients with essential hypertension, in cardiac transplant recipients and in patients with chronic renal failure. The major immunoreactive form of N-terminal atrial natriuretic peptide cross-reacting in both the pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30) radioimmunoassays is of a high molecular mass, probably pro-atrial natriuretic peptide (1-98). Since pro-atrial natriuretic peptide (1-98) is unlikely to cross-react identically with antibodies for pro-atrial natriuretic peptide (31-67) or pro-atrial natriuretic peptide (1-30), this could account for the differences in plasma levels obtained by the assays for pro-atrial natriuretic peptide (31-67) and pro-atrial natriuretic peptide (1-30).


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