Lack of effect of an inspiratory threshold load on plasma atrial natriuretic peptide levels

1990 ◽  
Vol 78 (3) ◽  
pp. 311-313 ◽  
Author(s):  
A. R. H. Warley ◽  
F. Fontes ◽  
M. Wilson ◽  
A. E. G. Raine ◽  
J. R. Stradling
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Urine Volume ◽  
Intrathoracic Pressure ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Plasma Atrial Natriuretic Peptide ◽  
Separate Control ◽  
Inspiratory Load ◽  
Atrial Natriuretic

1. After a run-in period, six healthy, recumbent, water-loaded male subjects breathed through an inspiratory threshold load for 90 min. To correct for prolonged recumbency, a similar protocol was followed on a separate control day, but without an inspiratory load. 2. A negative intrathoracic pressure of at least 30 cmH2O was required to overcome the threshold load. 3. Urine was collected every 30 min and analysed for sodium concentration. 4. Plasma samples were collected every 30 min and analysed for atrial natriuretic peptide concentration. 5. The inspiratory load had no effect on urine volume, urinary sodium excretion or plasma atrial natriuretic peptide levels.

Endocrine and renal response to water loading and water restriction in normal man

1988 ◽  
Vol 75 (2) ◽  
pp. 171-177 ◽  
Author(s):  
Angela C. Shore ◽  
Nirmala D. Markandu ◽  
Giuseppe A. Sagnella ◽  
Donald R. J. Singer ◽  
Mary L. Forsling ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Total Water ◽  
Water Restriction ◽  
Plasma Atrial Natriuretic Peptide ◽  
Plasma Vasopressin ◽  
Total Water Intake ◽  
Atrial Natriuretic

1. Nine normal subjects (eight male, one female) on a fixed daily intake of 150 mmol of sodium and 80 mnol of potassium, were randomized to receive either 3 days of 1.0 litre total water intake/24 h (food + fluid) or 4 days of 6.8 litres total water intake/24 h, and were then crossed over after a 3 day control period (2.7 litres water/24 h). 2. During water restriction, urine volume fell from 1.94 litres/24 h to less than 1 litre/24 h by the first day and was 0.77 litre/24 h on the final day. Plasma atrial natriuretic peptide levels were unchanged from baseline despite a large increase in plasma vasopressin and plasma and urine osmolality. Urinary sodium was unaltered throughout, while urinary potassium was increased on the final 2 days of water restriction. 3. During water loading, urine volume increased from 1.85 litres/24 h to 5.44 litres/24 h on the first day and remained at approximately 6 litres/24 h for the final 3 days. Plasma atrial natriuretic peptide showed no change. Plasma vasopressin and plasma and urine osmolality were reduced. Urinary sodium and potassium output were unchanged from baseline. 4. These results suggest that changes in plasma atrial natriuretic peptide are unlikely to be involved in the normal homoeostatic response to changes in water balance in man.

Ethanol Decreases Nocturnal Plasma Levels of Atrial Natriuretic Peptide (ANP 99-126) but Not the N-Terminal Fragment of Pro-Atrial Natriuretic Peptide (ANP 1-98) in Man

1994 ◽  
Vol 86 (3) ◽  
pp. 285-290 ◽  
Author(s):  
Ann-Charlotte Ekman ◽  
Olli Vakkuri ◽  
Olli Vuolteenaho ◽  
Juhani Leppäluoto
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Ethanol Intake ◽  
Serum Osmolality ◽  
Serum Sodium Concentration ◽  
Plasma Atrial Natriuretic Peptide ◽  
Terminal Fragment ◽  
Atrial Natriuretic

1. The aim of this study was to elucidate the role of atrial natriuretic peptides in the regulation of water and electrolyte balance after alcohol intake. To this end we measured the plasma concentrations of ethanol, atrial natriuretic peptide 99–126 and the N-terminal fragment of pro-atrial natriuretic peptide (atrial natriuretic peptide 1–98), serum osmolality and serum sodium concentration, and urine output, urine osmolality and urinary sodium excretion for 12 h after administration of ethanol (0, 0.5 and 1.0 g body weight/kg) and placebo drinks to nine healthy subjects according to a double-blind cross-over design. 2. Intake of ethanol (at 19.00–19.45 hours) inhibited the nocturnal increase in the plasma atrial natriuretic peptide 99–126 level dose-dependently (P < 0.05), but had no effect on the plasma atrial natriuretic peptide 1–98 level. Serum osmolality and serum sodium concentration were elevated dose-dependently for 2–5 h after the ethanol intake. Urine volume increased after the higher ethanol dose (net loss of 0.6 litre of water). 3. Since the plasma atrial natriuretic peptide 1–98 level was not changed after ethanol intake, we propose that the alcohol-induced inhibition of the nocturnal rise in the plasma atrial natriuretic peptide 99–126 level is not caused by an inhibition of release, but may rather reflect an increased peripheral elimination of atrial natriuretic peptide 99–126.

scholarly journals A role for atrial natriuretic peptide in endothelin-induced natriuresis.

1991 ◽  
Vol 1 (12) ◽  
pp. 1278-1283
Author(s):  
K A Munger ◽  
M Sugiura ◽  
K Takahashi ◽  
T Inagami ◽  
K F Badr
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Plasma Atrial Natriuretic Peptide ◽  
Peptide Antibody ◽  
Excretion Rates ◽  
Atrial Natriuretic

Systemic administration of low-dose endothelin increases urinary sodium excretion rate despite mild to moderate reductions in renal plasma flow and glomerular filtration rates. The role of atrial natriuretic peptide in endothelin-induced natriuresis was investigated. Administration of 2.50 pmol/min of endothelin to euvolemic rats resulted in increases in plasma atrial natriuretic peptide levels from 127 +/- 18 to 169 +/- 23 pg/mL. However, a lower dose of endothelin (0.63 pmol/min) or saline did not increase plasma levels of atrial natriuretic peptide. Mean arterial pressure was unchanged at the lower dose of endothelin and increased only slightly in rats receiving 2.5 pmol/min. To assess functional significance, renal responses to endothelin (2.5 pmol/min) in the absence and presence of a specific anti-rat atrial natriuretic peptide antibody were compared. Equivalent reductions in renal blood flow were observed. Urinary sodium excretion rates increased significantly in non-ANP-antibody-treated rats by 33 +/- 7 and 82 +/- 20% at 10 and 30 min, respectively. Atrial natriuretic peptide antibody blunted markedly endothelin-induced natriuresis: urinary sodium excretion rates changed insignificantly by 18 +/- 10 and 30 +/- 14%, respectively. Thus, endothelin infusion results in increases in plasma atrial natriuretic peptide levels, which may contribute to endothelin-induced natriuresis, providing evidence for potentially significant interactions between these peptide hormones in the regulation of sodium balance and renal vascular tone.

Effects of homologous atrial natriuretic peptide on drinking and plasma ANG II level in eels

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Drinking Rate ◽  
Plasma Sodium Concentration ◽  
Atrial Natriuretic

The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.

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