Atrial Natriuretic Peptide-Cyclic Gmp Relationships in Normal Humans: Effects of Dietary Sodium Intake

1993 ◽  
Vol 85 (1) ◽  
pp. 13-17 ◽  
Author(s):  
G. A. Sagnella ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
D. R. J. Singer ◽  
G. A. MacGregor
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cyclic Gmp ◽  
Sodium Intake ◽  
Fractional Excretion ◽  
Dietary Sodium ◽  
High Sodium ◽  
High Sodium Intake ◽  
Normotensive Subjects ◽  
Atrial Natriuretic

1. The present study was designed to investigate the relationships between circulating atrial natriuretic peptide, plasma and urinary cyclic GMP and sodium excretion under basal conditions and in response to changes in dietary sodium intake. 2. Measurements of plasma atrial natriuretic peptide and plasma and urinary (24 h collections) cyclic GMP, sodium and creatinine were made in (i) 30 normotensive subjects on their normal sodium intake and (ii) 12 subjects on the 5th day of a low and on the 5th day of a high sodium intake. 3. Plasma cyclic GMP, urinary cyclic GMP and fractional excretion of cyclic GMP in 30 normotensive subjects on their normal sodium intake were (means ± SEM) 5.4 ± 0.5 pmol/ml, 434.5 ± 31.8 pmol/min and 86.9 ± 8.6%, respectively. There were significant correlations between urinary cyclic GMP and its corresponding filtered load (r = 0.55) and between the renal clearance of cyclic GMP and that of creatinine (r = 0.44), but there were no significant associations between circulating atrial natriuretic peptide and plasma cyclic GMP or the fractional excretion of cyclic GMP or between urinary sodium and the fractional excretion of cyclic GMP. 5. Plasma atrial natriuretic peptide was significantly raised on the 5th day of the high sodium intake compared with the low sodium intake (10.6 ± 1.6 versus 4.2 ± 0.9 pg/ml; P <0.05). Similarly, there were increases in urinary cyclic GMP excretion (692.3 ± 43.4 versus 427.4 ± 41.9 pmol/min, P <0.05), but there were no significant differences in the fractional excretion of cyclic GMP. 6. As neither plasma nor urinary cyclic GMP was strongly associated with circulating levels of atrial natriuretic peptide, the present study suggests that other factors may be more important than circulating atrial natriuretic peptide as determinants of extracellular cyclic GMP.

Role of atrial natriuretic peptide in sodium balance in conscious spontaneously hypertensive rats

1990 ◽  
Vol 258 (4) ◽  
pp. F916-F926 ◽  
Author(s):  
A. A. Seymour ◽  
J. N. Swerdel ◽  
S. A. Fennell ◽  
V. J. Kratunis ◽  
M. M. Asaad
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
Renal Responses ◽  
Atrial Natriuretic

Sodium and fluid intake were precisely regulated by 3 days of infusion of 0.07, 0.35, or 3.5 mu eq Na/min at rates of 25, 50, or 100 microliters/min in nine groups of conscious spontaneously hypertensive rats (SHR). At each level of sodium and volume intake, the acute depressor and renal responses to three doses of exogenous atrial natriuretic peptide (ANP)-(99-126) were determined in conscious, unrestrained SHR. The natriuretic responses to the highest dose of ANP-(99-126) (150 pmol/min) were independent of the rate of fluid infusion but were highly dependent on the sodium intake. The maximal increases in sodium excretion averaged 0.9 +/- 0.5 (253%), 2.6 +/- 0.5 (302%), and 15.4 +/- 2.1 mu eq.kg-1.min-1 (577%) in SHR maintained on 0.07, 0.35, and 3.5 mu eq Na/min, respectively. In addition, the diuretic but not the depressor responses to ANP-(99-126) were dependent on the sodium intake and were unrelated to the rate of fluid delivery. In separate groups of SHR, 3 days of infusions of 3.5 mu eq Na/min at 25 and 100 microliters/min significantly elevated plasma ANP from 89 +/- 16 to 200 +/- 60 and 159 +/- 24 fmol/ml, respectively. In conclusion, high sodium intake enhanced the renal responses to exogenous ANP-(99-126) despite increases in endogenous peptide concentrations in conscious SHR.

EFFECTS OF CHANGES IN DIETARY SODIUM INTAKE AND SALINE INFUSION ON IMMUNOREACTIVE ATRIAL NATRIURETIC PEPTIDE IN HUMAN PLASMA

The Lancet ◽  
1985 ◽  
Vol 326 (8466) ◽  
pp. 1208-1211 ◽  
Author(s):  
GiuseppeA. Sagnella ◽  
AngelaC. Shore ◽  
Nirmalad. Markandu ◽  
GrahamA. Macgregor
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Human Plasma ◽  
Natriuretic Peptide ◽  
Sodium Intake ◽  
Saline Infusion ◽  
Dietary Sodium ◽  
Atrial Natriuretic

Plasma atrial natriuretic peptide: Its relationship to changes in sodium intake, plasma renin activity and aldosterone in man

1987 ◽  
Vol 72 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Giuseppe A. Sagnella ◽  
Nirmala D. Markandu ◽  
Angela C. Shore ◽  
Mary L. Forsling ◽  
Graham A. MacGregor
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Activity ◽  
High Sodium ◽  
Sodium Diet ◽  
Atrial Natriuretic

1. Plasma levels of immunoreactive atrial natriuretic peptide (IrANP), plasma renin activity, aldosterone and vasopressin were measured in 11 normotensive subjects on a low (10 mmol/day), a normal (150 mmol/day) and a high (350 mmol/day) sodium intake. 2. Plasma levels of IrANP increased significantly with increasing dietary sodium intake with levels (means ± sd) of 3.9 ± 2.1 pg/ml on the fifth day of the low sodium diet, 6.1 ± 3.4 pg/ml on the fifth day of the normal sodium diet and 11.4 ± 4.6 pg/ml on the fifth day of the high sodium diet. 3. Plasma renin activity and aldosterone decreased significantly with increasing sodium intake whereas plasma vasopressin was highest on the high sodium intake. 4. These results suggest that the atrial peptides may be a new and important component in the overall control of sodium and water balance during increased sodium intake.

scholarly journals Active kallikrein response to changes in sodium-chloride intake in essential hypertensive patients.

1996 ◽  
Vol 7 (3) ◽  
pp. 443-453 ◽  
Author(s):  
C Ferri ◽  
C Bellini ◽  
A Carlomagno ◽  
G Desideri ◽  
A Santucci
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Intake ◽  
Hypertensive Patients ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Sodium Load ◽  
Atrial Natriuretic

To evaluate the behavior of active kallikrein excretion in salt-sensitive and salt-resistant hypertensive patients during changes in sodium-chloride (NaCl) intake, 61 male, nonobese, nondiabetic outpatients affected by uncomplicated essential hypertension were given a diet that contained 140 mmol NaCl per day for 2 wk. Patients then received either a low- (20 mmol NaCl/day) or a high- (320 mmol NaCl/day) sodium diet for 2 wk, according to a randomized, double-blind, cross-over protocol. Hypertensive patients were classified as salt sensitive when their diastolic blood pressure rose by at least 10 mm Hg after the high-sodium diet, and decreased by at least 10 mm Hg after the low-sodium diet, considering as baseline blood pressure values those that were taken at the end of the 140 mmol NaCl/day intake period. The remaining patients were classified as salt resistant or, when diastolic blood pressure increased by 10 mm Hg or more after low-sodium intake, as counter-regulating. Twenty-three patients were therefore classified as salt sensitive, 28 as salt resistant, and 10 as counter-regulating. The baseline active kallikrein excretion was significantly lower (P < 0.0001) in salt-sensitive (0.62 +/- 0.31 U/24 h) patients than in salt-resistant (1.39 +/- 0.44 U/24 h) and counter-regulating patients (1.27 +/- 0.38 U/24 h). Surprisingly, the kallikrein response to changes in sodium intake was similar in all subgroups, although enzyme excretion was always at the lowest level in salt-sensitive hypertensive patients. This latter group also showed the highest plasma atrial natriuretic peptide levels (28.2 +/- 8.5 fmol/mL, P < 0.0001 versus salt-resistant and counter-regulating patients), and the greatest peptide increment with sodium load (P < 0.0001 versus salt-resistant and counter-regulating patients). Counter-regulating patients showed the steepest increase in plasma renin activity (from 0.24 +/- 0.18 to 0.83 +/- 0.21 ng/L per s, P < 0.001) and decrease of plasma atrial natriuretic peptide (from 26.1 +/- 6.3 to 6.8 +/- 3.1 fmol/mL, P < 0.001) when switched from a high to a low-sodium intake. In conclusion, salt-sensitive hypertensive patients excrete less active kallikrein than do salt-resistant and counter-regulating patients, but maintain a normal enzyme response to changes in dietary sodium intake. The exaggerated response of atrial natriuretic peptide to high-sodium intake that was observed in the same patients could be compensating for an impaired renal capability to excrete a sodium load.

scholarly journals Upregulation of atrial natriuretic peptide gene expression in remnant kidney of rats with reduced renal mass.

1998 ◽  
Vol 9 (9) ◽  
pp. 1613-1619
Author(s):  
K Totsune ◽  
H S Mackenzie ◽  
H Totsune ◽  
J L Troy ◽  
J Lytton ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Renal Mass ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Low Sodium Diet ◽  
Peptide Gene ◽  
Remnant Kidney ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) is synthesized in the kidney but its physiologic significance there is unclear. To determine whether renal expression of the ANP gene is regulated, renal ANP mRNA expression was assessed in remnant kidneys after 5/6 nephrectomy in Munich-Wistar rats. In normal sodium intake groups, ANP mRNA expression in the remnant kidney was significantly increased by 5.0 +/- 0.8-fold (n = 7, mean +/- SEM) at 4 d when compared with sham-operated controls (n = 6, all sham-operated groups) (*P < 0.001 by Scheffe's test) and by 28.3 +/- 5.1-fold at 14 d. This latter response was markedly diminished to 7.6 +/- 2.1-fold (n = 7, versus sham) in rats maintained on a low sodium diet. At 4 d, on the other hand, no significant downregulation was observed with dietary sodium restriction. Because natriuretic peptides have previously been shown by us to play a major role in the adaptive responses of remnant nephrons to renal mass ablation, these data suggest that ANP of renal origin may contribute to the overall mechanism for enhancing sodium excretion in the face of declining nephron number.

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