Effect of water immersion on renal natriuretic peptide (urodilatin) excretion in humans

1993 ◽  
Vol 74 (6) ◽  
pp. 2881-2885 ◽  
Author(s):  
P. Norsk ◽  
C. Drummer ◽  
L. B. Johansen ◽  
R. Gerzer

We examined 1) the effect of thermoneutral (34.5 +/- 0.5 degrees C) water immersion to the neck (WI) in humans on the temporal profile of renal urodilatin [atrial natriuretic peptide- (ANP) (95–,126)] excretion and 2) the relationship between urodilatin and urinary fluid (V) and sodium (UNaV) excretion. Eight normal subjects underwent 12 h of WI, and another group of eight were studied during seated control conditions. The subjects ingested 200 ml of tap water hourly. WI induced an increase in renal urodilatin and guanosine 3′,5′-cyclic monophosphate (cGMP) excretion, V, and UNaV. After peak values were attained between the 2nd and 5th h of WI, urodilatin and cGMP excretion, V, and UNaV returned toward preimmersion and control levels. At the 12th h of WI, urodilatin and cGMP excretion and V were indistinguishable from preimmersion values but were significantly elevated compared with the control values. UNaV was maintained elevated compared with both preimmersion and control values. During WI, positive and statistically significant linear correlations could be established between V and renal urodilatin excretion in six subjects and between UNaV and urodilatin excretion in four subjects. We conclude that WI induces an increase in the rate of renal urodilatin excretion, attaining a peak value at the 3rd h followed by an attenuation toward preimmersion and control levels. Furthermore, urodilatin might participate as one of several mechanisms of the natriuresis and diuresis of WI in humans.

1995 ◽  
Vol 78 (1) ◽  
pp. 217-224 ◽  
Author(s):  
K. Nagashima ◽  
H. Nose ◽  
T. Yoshida ◽  
T. Kawabata ◽  
Y. Oda ◽  
...  

To assess the relationship between atrial natriuretic peptide (ANP) and the reduction in plasma volume (PV) during exercise, we measured changes in PV and ANP in seven male volunteers during treadmill exercise in air (AE) and with water immersion (WE) together with time control studies of rest in air and in water. Blood samples were collected from a catheter in the antecubital vein at exercise intensities of 32, 49, 65, and 78% of peak oxygen consumption (VO2). Plasma ANP in AE increased significantly from the resting value [15 +/- 1 (SE) pg/ml] only at 78% of peak VO2 (29 +/- 5 pg/ml), whereas ANP in WE increased significantly at exercise levels of > 49% of peak VO2 and reached 68 +/- 9 pg/ml at 78% of peak VO2. Although PV in AE and WE decreased significantly with VO2 of > 49% of peak VO2 (P < 0.01), the decrease from the resting value in WE was significantly greater than that in AE of > 65% of peak VO2 (P < 0.01) and the decreases at 78% of peak VO2 were -9.7 +/- 0.8 and -6.1 +/- 1.7%, respectively. The difference in the decrease in PV between AE and WE at corresponding VO2 correlated strongly with that in the increase in ANP (r = -0.97; P < 0.01). These results are consistent with the hypothesis that ANP may be involved in the fluid shift from the intra- to extravascular space during exercise.


1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S235-S236
Author(s):  
G. MÜLLER-ESCH ◽  
J. POTRATZ ◽  
W. KLINGLER ◽  
R. GERZER ◽  
R. LAWRENZ ◽  
...  

Author(s):  
M D Penney ◽  
D Hampton ◽  
D A Oleesky ◽  
C Livingstone ◽  
E Mulkerrin

A rapid vacuum-driven procedure, using pre-treated Sep-Pak C18 cartridges, has been developed for the simultaneous extraction of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) from plasma. Non-specific interference was removed by fractional elution with an aqueous methanol/trifluoroacetic acid (TFA) mixture. AVP and ANP were coeluted under positive pressure with a methanol/TFA mixture and the eluates air-dried before measurement using separate radioimmunoassays. Assay ranges for AVP and ANP were 0·12–29·5 pmol/L and 0·65–162 pmol/L, respectively, with mean recoveries (standard deviation in parentheses) for AVP of 96·4% (5·5%) at a level of 11·8 pmol/L and for ANP of 94·8% (5·9%) at a level of 32·4 pmol/L. The extraction and assay procedures were validated by observing the changes in plasma AVP and ANP concentrations in normal subjects at different stages of hydration and in elderly patients during treatment for congestive cardiac failure.


1990 ◽  
Vol 36 (6) ◽  
pp. 855-859 ◽  
Author(s):  
J E Tattersall ◽  
A Dawnay ◽  
C McLean ◽  
W R Cattell

Abstract We have developed and validated a two-site liquid-phase immunoradiometric assay (IRMA) of atrial natriuretic peptide (ANP) in unextracted human plasma. Both radiolabeled rabbit anti-ANP IgG and polyclonal mouse anti-ANP must bind to ANP for detection, and the assay is specific for peptides with both an intact C-terminus and a disulfide bridge. The assay sensitivity (detection limit) is 0.96 pmol/L, and the working range is 2.3-300 pmol/L, with the hook effect occurring above 500 pmol/L. Results for diluted plasma from normal subjects and from patients with renal failure paralleled the standard curve; analytical recovery of ANP added to such samples averaged 94%. The between- and within-assay CVs at 8 pmol/L were 10% and 5%, respectively. The assay is sufficiently sensitive and precise to detect the postural change in ANP concentrations in normal subjects.


1991 ◽  
Vol 260 (1) ◽  
pp. R39-R46 ◽  
Author(s):  
K. W. Cho ◽  
K. H. Seul ◽  
S. H. Kim ◽  
K. M. Seul ◽  
G. Y. Koh

It has been suggested in this laboratory that the principal stimulus for the secretion of atrial natriuretic peptide (ANP) is the reduction of atrial distension and that the secretion of ANP is dependent on both atrial reduction volume and reduction frequency. To investigate the relationship among the changes in atrial pressure, distension, pacing frequency, and ANP secretion, we performed a series of experiments in the isolated perfused rabbit atria. Increase in atrial pressure without changes in transmural pressure and thus without volume changes did not raise immunoreactive ANP (irANP) secretion. Atrial distension without changes in intracavitary atrial pressure increased irANP secretion with the reduction. Electrical stimulation with atrial distension resulted in an increase in irANP secretion in proportion to pacing frequency. Incremental response of irANP secretion to electrical stimulation was accentuated by increasing atrial distension. Neither atrial pacing without distension nor distension without pacing raised irANP secretion. These results suggest that the direct and principal stimulus for irANP secretion in response to atrial pacing and distension is the length shortening of atrial myocytes and that the incremental response of irANP secretion to increasing pacing frequency is the result of an increase in frequency of the length shortening of atrial myocytes.


1993 ◽  
Vol 71 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Louis Legault ◽  
Leonard C. Warner ◽  
Wai Ming Leung ◽  
Alexander G. Logan ◽  
Laurence M. Blendis ◽  
...  

The nature of sodium retention in cirrhosis complicated by ascites has been studied for the last 30 years. Resistance to the natriuretic action of atrial natriuretic peptide (ANP) may play a potential role in this sodium retention. To further evaluate this possibility, we studied 12 patients with biopsy-proven cirrhosis and ascites on 2 consecutive days after a 7-day period off diuretics while receiving a 20 mmol/day sodium restricted diet. Following a crossover design, patients underwent head-out water immersion (HWI) for 3 h and were infused with a α-human ANP for 2 h on 2 consecutive days. Blood and urine samples were collected hourly. Five patients displayed a natriuretic response to HWI, sufficient to achieve negative sodium balance, and these patients were termed responders. Each of these five patients also displayed a natriuretic response to ANP infusion. In contrast, the other seven patients (nonresponders) consistently failed to develop a natriuretic response to either maneuver. The two groups had similar elevations in plasma ANP concentrations, but at baseline differed in terms of plasma sodium, plasma renin activity, and serum aldosterone. Despite higher serum aldosterone concentrations, nonresponders excreted less potassium than responders during the peak effect of the interventions, suggesting greater sodium delivery to the aldosterone-sensitive nephron segment in responders. We conclude that the inability to mount an adequate sodium excretory response to HWI in patients with cirrhosis may be conveyed through increased antinatriuretic factors that decrease the sodium delivery to the medullary collecting duct and inhibit the natriuretic effect of ANP at that site.Key words: atrial natriuretic peptide, cirrhosis, ascites, sodium.


1989 ◽  
Vol 120 (4) ◽  
pp. 519-525 ◽  
Author(s):  
K. Olsson ◽  
B. E. Karlberg ◽  
L. Eriksson

Abstract. Plasma concentrations of atrial natriuretic peptide (ANP) were measured in 6 goats during pregnancy, lactation and a nonpregnant, nonlactating (= control) period before and during a rapid iv load of 0.9% NaCl. The volume of the load was 20% of blood volume. The infusions increased central venous pressure by 7 ± 1 mmHg during pregnancy and 8 ± 1 mmHg during lactation. Before infusions plasma ANP concentrations were 5.7 ± 0.7 pmol/l (control period), 10.8 ± 1.8 pmol/l (pregnancy;P< 0.05),and6.5 ± 1.5 pmol/l (lactation;NS).ANP increased significantly in all periods. Maximal values were 12.5 ± 1.5 (control period), 25.5 ± 2.3 (pregnancy; P< 0.01 vs control period, P<0.05 vs lactation), and 13.0 ± 1.6 (lactation; NS). Renal Na excretion increased similarly during pregnancy and control period, but slightly more during lactation. In 4 of the goats iv infusions of ANP (1 μg/min, 60 min) were given. The infusions caused natriuresis during the control period, but not during pregnancy and lactation, despite more than 10-fold increases of plasma ANP levels. In conclusion, our results indicate that although plasma ANP concentration rose to high levels during acute NaCl loading in pregnant goats, this effect was not important for the natriuresis. Instead, the natriuretic response to ANP appears attenuated during pregnancy, and also during lactation.


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