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 ◽  
...  

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.

1986 ◽  
Vol 251 (3) ◽  
pp. R499-R503 ◽  
Author(s):  
F. J. Salazar ◽  
J. C. Romero ◽  
J. C. Burnett ◽  
S. Schryver ◽  
J. P. Granger

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)


Nephron ◽  
1989 ◽  
Vol 51 (2) ◽  
pp. 283-284 ◽  
Author(s):  
Shunichi Kojima ◽  
Satoshi Akabene ◽  
Takashi Fujii ◽  
Tohru Ohe ◽  
Hiroki Yoshimi ◽  
...  

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei

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.


1988 ◽  
Vol 13 ◽  
pp. S62-S68
Author(s):  
Yasunobu Hirata ◽  
Masao Ishii ◽  
Kazushige Fukui ◽  
Hiroshi Hayakawa ◽  
Shin-ichiro Namba ◽  
...  

1988 ◽  
Vol 74 (4) ◽  
pp. 419-425 ◽  
Author(s):  
J. McMurray ◽  
A. D. Struthers

1. Atrial natriuretic peptide (ANP) has previously been shown to inhibit the renin–angiotensin–aldosterone system (RAAS) at several different levels. We have now investigated a further non-endocrine, renal interaction between ANP and the RAAS. 2. The effects of ANP and angiotensin II (ANG II) alone, and in combination, on urinary electrolyte and water excretion were studied in eight normal male subjects undergoing maximal water diuresis. 3. ANP caused a significant increase in urine flow and sodium excretion. ANG II alone was antidiuretic, antinatriuretic and antikaliuretic. When ANP was given against a background infusion of ANG II, urinary flow rate and electrolyte excretion increased from a new lower level to reach a value intermediate between that found with ANG II alone and ANP alone. 4. It is concluded that the renal effects of ANP are modified in the presence of simultaneously elevated levels of ANG II and that net water and electrolyte excretion reflect the sum of the opposing influences of each peptide. While this interplay may be non-specific, it is possible that ANP may exert some of its actions by specifically inhibiting the intrarenal effects of ANG II.


1986 ◽  
Vol 70 (s13) ◽  
pp. 74P-74P ◽  
Author(s):  
JV Anderson ◽  
J Donckier ◽  
W McKenna ◽  
ACR Burns ◽  
SR Bloom

1988 ◽  
Vol 254 (2) ◽  
pp. R161-R169 ◽  
Author(s):  
P. Bie ◽  
B. C. Wang ◽  
R. J. Leadley ◽  
K. L. Goetz

The effects of alpha-human atrial natriuretic peptide (alpha-hANP) on cardiovascular and renal function in conscious dogs were evaluated in two experimental protocols. In one protocol, alpha-hANP was infused intravenously at increasing rates of 50, 100, and 200 ng.min-1.kg-1 (stepup infusion) during successive 20-min periods. The greatest responses occurred during the final 20-min period of the stepup infusion when the plasma concentration of immunoreactive atrial natriuretic peptide (irANP) was increased by 44-fold over preinfusion values; pressures in the aorta and both atria were decreased at this time, whereas glomerular filtration rate, urine flow, and sodium excretion were increased. In a second protocol, alpha-hANP was infused for 1 h at constant rates of either 12.5, 25, or 50 ng.min-1.kg-1; these constant infusions increased plasma irANP by 3-, 7-, and 12-fold, respectively. Each infusion rate decreased left and right atrial pressures and increased urine flow and sodium excretion. The two lowest infusion rates elevated plasma irANP to levels that would be expected to occur only during unusual physiological, or perhaps pathophysiological, conditions. The two highest infusion rates decreased plasma renin activity. Nevertheless, the accompanying maximal increases in sodium excretion were modest (41-72%). These data imply that small changes in circulating atrial peptides that presumably occur under normal physiological conditions would not have a dominant effect on the regulation of sodium excretion; the peptides may, however, play a modulatory role on sodium excretion under these conditions. It remains to be determined whether the ability of atrial peptides to lower cardiac filling pressures is of physiological significance.


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