Atrial natriuretic peptide levels during acute and chronic saline loading in conscious dogs

1986 ◽  
Vol 251 (3) ◽  
pp. R499-R503 ◽  
Author(s):  
F. J. Salazar ◽  
J. C. Romero ◽  
J. C. Burnett ◽  
S. Schryver ◽  
J. P. Granger
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Urinary Excretion ◽  
Natriuretic Peptide ◽  
Sodium Intake ◽  
Plasma Concentrations ◽  
Isotonic Saline ◽  
Saline Infusion ◽  
Plasma Aldosterone Concentration ◽  
Saline Loading ◽  
Atrial Natriuretic

The purpose of the present study was to determine if acute and chronic increases in sodium intake by isotonic saline infusion are accompanied by changes in plasma concentrations of atrial natriuretic peptide (PANP). Acute saline loading (5% body wt) over a 30-min period in seven conscious chronically instrumented dogs produced a significant increase in PANP (48 +/- 5 to 119 +/- 24 pg/ml, P less than 0.05). However, chronic and progressive increments of sodium intake from 5 to 75 to 300 meq/day for 7 days, each by isotonic saline infusion, were examined in the same group of dogs and had no significant effect on PANP. PANP's were 37 +/- 7, 39 +/- 8, and 33 +/- 5 pg/ml when sodium intake was changed from 5 to 75 to 300 meq/day, respectively. The increase of sodium intake from 5 to 75 meq/day produced decreases of plasma renin activity (PRA) (2.5 +/- 0.5 to 1.5 +/- 0.4 ng angiotensin I X ml-1 X h-1, P less than 0.05), plasma aldosterone concentration (PAC) (19.3 +/- 5.4 to 2.9 +/- 0.4 pg/ml, P less than 0.05), and urinary excretion of prostaglandin E2 (760 +/- 131 to 320 +/- 58 pg/min, P less than 0.05). Further increase of sodium intake to 300 meq/day induced decreases of PRA and PAC to undetectable levels and an increase of urinary excretion of 6-ketoprostaglandin F1 alpha (649 +/- 95 to 1,056 +/- 148 pg/min, P less than 0.05). Before the completion of the study, sodium intake was decreased from 300 to 75 meq/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Isotonic Saline Infusion Stimulates Plasma Release of Atrial Natriuretic Peptide (ANP) in Man

1986 ◽  
Vol 70 (s13) ◽  
pp. 74P-74P ◽  
Author(s):  
JV Anderson ◽  
J Donckier ◽  
W McKenna ◽  
ACR Burns ◽  
SR Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Isotonic Saline ◽  
Saline Infusion ◽  
Atrial Natriuretic

Effects of an acute saline infusion on fluid and electrolyte metabolism in humans

1992 ◽  
Vol 262 (5) ◽  
pp. F744-F754 ◽  
Author(s):  
C. Drummer ◽  
R. Gerzer ◽  
M. Heer ◽  
B. Molz ◽  
P. Bie ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Urinary Excretion ◽  
Natriuretic Peptide ◽  
Body Fluid ◽  
Urine Flow ◽  
Saline Infusion ◽  
Electrolyte Excretion ◽  
Renal Response ◽  
Atrial Natriuretic

Several hormonal systems participating in body fluid and electrolyte homeostasis were investigated in six healthy volunteers in a supine body position during a period of 9 days and nights. Under strictly controlled conditions, striking circadian rhythms were observed for plasma levels of vasopressin, renin, aldosterone, guanosine 3',5'-cyclic monophosphate, cortisol, and epinephrine. Nocturnal decreases and diurnal increases in urine flow rate and urinary excretion of electrolytes were observed and closely paralleled the urinary excretion of urodilatin. During 48 h after an acute isotonic saline infusion (2 liters within 25 min) and after a 48-h control experiment the urinary excretion of H2O and electrolytes, and simultaneously the alterations in endocrine systems participating in body fluid homeostasis, were determined. Urine flow and urinary electrolyte excretion rates were significantly increased during 2 days after the saline infusion. The largest increase in urinary fluid and electrolyte excretion was observed between 3 and 22 h postinfusion. These long-term changes were paralleled by altered H2O and Na balances and also by elevated body weights that returned to baseline values with an approximate half-life of 7 h. These data suggest that vasopressin, atrial natriuretic peptide, and catecholamines are unlikely to be of major importance for the renal response to this hypervolemic stimulus. The renin-aldosterone system was suppressed during 2 days postinfusion. This suppression correlated with the effects of saline load on Na excretion. However, the closest relation with Na excretion was observed for the kidney-derived member of the atrial natriuretic peptide family, urodilatin, which was considerably increased during the long-term period up to 22 h postinfusion. Thus these data show that the human body in supine position requires approximately 2 days to regulate the amount of Na and H2O provided by an acute saline infusion. The data also suggest that urodilatin and the renin-aldosterone system might participate in the long-term renal response to an acute saline infusion and also in the mediation of circadian urinary excretion rhythms.

Atrial natriuretic peptide: Evidence of action as a natriuretic hormone at physiological plasma concentrations in man

1987 ◽  
Vol 72 (3) ◽  
pp. 305-312 ◽  
Author(s):  
J. V. Anderson ◽  
J. Donckier ◽  
N. N. Payne ◽  
J. Beacham ◽  
J. D. H. Slater ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Natriuretic Hormone ◽  
Plasma Aldosterone Concentration ◽  
Water Excretion ◽  
Physiological Range ◽  
Atrial Natriuretic

1. The administration of exogenous atrial natriuretic peptide (ANP) causes a natriuresis and diuresis in man, but this has, to date, only been demonstrated at plasma ANP concentrations within the high pathological or pharmacological ranges. Evidence that ANP acts physiologically requires the demonstration of a natriuretic effect when it is infused to recreate plasma concentrations similar to those observed after physiological stimuli. 2. We infused human α-ANP (1–28) at a calculated rate of 1.2 pmol min−1 kg−1 for 3 h into seven water-loaded normal subjects, achieving plasma ANP concentrations within the upper part of the physiological range. The subjects' resting plasma ANP concentration increased from 3.8 ± 1.5 to 20.9 ± 1.9 pmol/l. 3. The infusion of ANP caused a 60% increase of mean urinary sodium excretion from 111 ± 18 to 182 ± 30 μmol/min (P < 0.001) and a 28% increase of mean water excretion from 10.8 ± 0.8 to 13.8 ± 1.6 ml/min (P < 0.01). 4. The infusion suppressed mean plasma renin activity from 1.55 ± 0.10 to 1.17 ± 0.06 pmol of ANG I h−1 ml−1 (P < 0.001). Mean plasma aldosterone concentration (242 ± 16 basally and 215 ± 15 pmol/l at the end of ANP infusion) did not change significantly. Pulse rate and blood pressure were unchanged throughout the study. 5. No significant change in any of the variables mentioned above occurred during the infusion of the vehicle alone on a separate study day. 6. The demonstration that recreation of plasma concentrations of ANP within the physiological range by intravenous infusion induces a natriuresis provides new evidence supporting the role of ANP as a natriuretic hormone.

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

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.

scholarly journals Urinary Excretion of Atrial Natriuretic Peptide during Saline Infusion and Supraventricular Tachycardia

Nephron ◽  
1989 ◽  
Vol 51 (2) ◽  
pp. 283-284 ◽  
Author(s):  
Shunichi Kojima ◽  
Satoshi Akabene ◽  
Takashi Fujii ◽  
Tohru Ohe ◽  
Hiroki Yoshimi ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Urinary Excretion ◽  
Supraventricular Tachycardia ◽  
Natriuretic Peptide ◽  
Saline Infusion ◽  
Atrial Natriuretic

Response of atrial natriuretic peptide to acute saline loading in essential hypertension

1988 ◽  
Vol 255 (6) ◽  
pp. F1085-F1090 ◽  
Author(s):  
A. Mimran ◽  
J. Nussberger ◽  
J. Ribstein ◽  
B. Waeber ◽  
H. R. Brunner
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Normal Subjects ◽  
Saline Loading ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.

How important are suppression of aldosterone and stimulation of atrial natriuretic peptide secretion in the natriuretic response to an acute sodium load in man?

1991 ◽  
Vol 80 (4) ◽  
pp. 293-299 ◽  
Author(s):  
D. R. J. Singer ◽  
D. G. Shirley ◽  
N. D. Markandu ◽  
M. A. Miller ◽  
M. G. Buckley ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Lithium Clearance ◽  
Saline Loading ◽  
Sodium Load ◽  
Atrial Natriuretic

1. Aldosterone is suppressed by sodium loading. We studied the contribution of this decrease in plasma aldosterone to the natriuresis after acute sodium loading in healthy volunteers. 2. Two litres of saline [0.9% (w/v) NaCl] were infused during the second hour of a 6 h infusion of aldosterone (3 pmol min−1 kg−1) or placebo in eight healthy young men. On the placebo day, plasma aldosterone decreased by 30 min after the start of saline infusion and remained suppressed. During aldosterone infusion, plasma aldosterone was maintained at around 400 pmol/l. 3. Urinary sodium excretion, lithium clearance and plasma atrial natriuretic peptide increased and plasma renin activity decreased after saline infusion, whether or not aldosterone was infused. However, from 60 to 240 min after saline infusion, natriuresis was significantly less during aldosterone infusion than on the placebo day. In addition, saline loading led to a progressive increase in the ratio of sodium clearance to lithium clearance, used as an index of the fractional distal tubular rejection of sodium, and in the ratio of urinary sodium to potassium. These increases were prevented by the infusion of aldosterone. 4. This study suggests that there are differences in the mechanisms determining the early and the later responses to an acute sodium load. Suppression of aldosterone may explain much of the later increase in natriuresis after saline infusion. In addition, the results are consistent with a role for atrial natriuretic peptide in the immediate increase in sodium excretion after saline loading.

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.

Sign in / Sign up

Export Citation Format

Share Document