Acute effect of an alpha1-adrenoceptor antagonist on urinary sodium excretion, plasma atrial natriuretic peptide, arginine vasopressin, and the renin-aldosterone system in healthy subjects

1992 ◽  
Vol 43 (1) ◽  
pp. 17-21 ◽  
Author(s):  
T. Tomiyama ◽  
T. Baba ◽  
S. Murabayashi ◽  
T. Ishizaki
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Sodium Excretion ◽  
Healthy Subjects ◽  
Urinary Sodium Excretion ◽  
Acute Effect ◽  
Urinary Sodium ◽  
Plasma Atrial Natriuretic Peptide ◽  
Adrenoceptor Antagonist

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.

Increased renal atrial natriuretic peptide synthesis in rats with deoxycorticosterone acetate-salt treatment

1996 ◽  
Vol 271 (4) ◽  
pp. F779-F789 ◽  
Author(s):  
Y. J. Lee ◽  
S. J. Shin ◽  
M. S. Tan ◽  
T. J. Hsieh ◽  
J. H. Tsai
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Excretion Rate ◽  
Rat Kidney ◽  
Urinary Sodium Excretion ◽  
Treated Group ◽  
Urinary Sodium ◽  
Deoxycorticosterone Acetate ◽  
Low Salt

To investigate the role of renal synthesis of atrial natriuretic peptide (ANP) as a contributor to the water-sodium homeostasis, we studied the effects of electrolyte-water imbalance on renal ANP mRNA levels, plasma ANP concentrations, and urinary ANP excretion rates by using reverse transcription-polymerase chain reaction (PCR) and radioimmunoassay. Male Wistar rates divided into the following three groups: 1) the control group, 2) deoxycorticosterone acetate (DOCA)-salt-treated group, and 3) low-salt-treated group. The urinary sodium excretion rate and urine volume in the DOCA-salt rats were significantly elevated at 2 days and for the 10-day study. The urinary ANP excretion rate in DOCA-salt rats was significantly increased at 2 days after treatment and was well correlated to the urinary sodium excretion rate (r = 0.76, P < 0.01). Plasma ANP levels in the DOCA-salt rats were elevated on the day of death. In contrast, plasma renin activities were markedly suppressed in DOCA-salt rats and increased in low-salt rats. By immunohistochemical study, immunoreactive ANP materials were mainly localized in the proximal and distal cortical tubules of the kidney. With the PCR cloning and sequencing technique, ANP cDNA was cloned from the rat kidney, and the sequences were identical to that of ANP identified in the atria. By semiquantitative PCR technique, the expression of ANP mRNA in the ventricle and renal cortex tissues was significantly enhanced in the DOCA-salt rats. Our results confirm that the rat kidney is a site of ANP synthesis and indicate that renal ANP synthesis is enhanced in a volume-expansion state. We propose that renal synthesized natriuretic peptide participates in the intrarenal regulation of water-electrolyte homeostasis and may contribute to renal adaptation during the mineralocorticoid escape phenomenon.

Atrial natriuretic peptide – cyclic GMP coupling and urinary sodium excretion during acute volume expansion in man

1990 ◽  
Vol 68 (4) ◽  
pp. 535-538 ◽  
Author(s):  
Giuseppe A. Sagnella ◽  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Graham A. MacGregor ◽  
David G. Shirley ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cyclic Gmp ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Atrial Natriuretic

The present study examines hormonal and renal responses to acute volume expansion in normal man, with particular emphasis on the atrial natriuretic peptide (ANP) – cyclic GMP coupling. Two liters of isotonic saline were infused into eight normotensive male subjects over a 1-h period. Plasma and urinary measurements were made before, during, and up to 300 min after the start of the saline infusion. With the initial increase in urinary sodium excretion there were increases in plasma ANP and plasma cyclic GMP, which reached maximum levels at 15 min after the end of the saline infusion. Urinary cyclic GMP increased gradually during saline infusion up to approximately 60 min after the end of the infusion. Plasma ANP and plasma and urinary cyclic GMP excretion gradually declined thereafter. By contrast, urinary sodium excretion remained elevated up to the end of the observation period. The saline infusion was associated with marked reductions in plasma renin activity and aldosterone, which persisted up to the end of the study. These results suggest a coupling between the increases in plasma ANP, the production of cyclic GMP, and urinary sodium excretion, in particular during the initial renal response to acute volume expansion. However, other mechanisms including the suppression of the rennin–angiotensin–aldosterone system may become increasingly important in the later natriuretic response to acute volume expansion.Key words: atrial natriuretic peptide, cyclic GMP, sodium, renal, human.

Atrial natriuretic peptide: Physiological release associated with natriuresis during water immersion in man

1986 ◽  
Vol 71 (3) ◽  
pp. 319-322 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Millar ◽  
J. P. O'Hare ◽  
J. C. MacKenzie ◽  
R. J. M. Corrall ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Natriuretic Hormone ◽  
The Mean ◽  
Atrial Natriuretic

1. Thermoneutral water immersion produces a physiological increase of thoracic blood volume, raises central venous pressure and increases urinary sodium excretion by a hitherto ill-understood mechanism. We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). 2. During water immersion there was a highly significant (P < 0.001) twofold increase of the mean plasma ANP concentration and a doubling of the mean urinary sodium excretion. Both were unchanged during the control experiments. 3. These results are consistent with the hypotheses (a) that ANP is released into plasma in response to central blood volume expansion and (b) that it functions as a natriuretic hormone in normal man under physiological conditions.

Dissociation between plasma atrial natriuretic peptide levels and urinary sodium excretion after intravenous saline infusion in normal man

1987 ◽  
Vol 73 (3) ◽  
pp. 285-289 ◽  
Author(s):  
Donald R. J. Singer ◽  
Angela C. Shore ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Giuseppe A. Sagnella ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Sodium Balance ◽  
Normal Male ◽  
Maximal Rise ◽  
Atrial Natriuretic

1. Plasma immunoreactive atrial natriuretic peptide (ANP) and urinary sodium excretion were measured in six normal male subjects before, during and for 195 min after a 60 min infusion of 2 litres of saline (0.9% NaCl, 308 mmol of Na+). 2. During the saline infusion, there was a significant increase in plasma ANP and urinary sodium excretion and a significant decrease in plasma renin activity, aldosterone, albumin, creatinine and packed cell volume. 3. The maximal rise in mean plasma ANP occurred 15 min after stopping the infusion and the maximal rise in mean urinary sodium excretion in the collection period 30 min later. 4. Plasma ANP then decreased so that by the end of the study the level was the same as before the saline infusion. However, at this time, 195 min after the saline infusion was stopped, there was still a net positive sodium balance of 220 mmol and urinary sodium excretion remained significantly elevated. 5. Our results are compatible with the concept that increased ANP secretion may play a role in the immediate increase in sodium excretion after a saline load. However, they also suggest that other mechanisms may be more important for the longer term increase in sodium excretion.

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