Fluid intake and renal excretion after icv atrial natriuretic peptide (ANP) in rats

1. The effect of atrial natriuretic peptide on osmotically stimulated thirst appreciation and consequent fluid intake was investigated in healthy man. 2. Six seated male subjects were studied on two occasions: synthetic α-human atrial natriuretic peptide (99–126) (2 pmol min−1kg−1) or placebo (saline, 150 mmol/l NaCl) was infused intravenously for 105 min; 30 min after the start of atrial natriuretic peptide/placebo infusion, hypertonic saline (855 mmol/l NaCl) was infused (0.06 ml min−1 kg−1) for 60 min. Subjects were then allowed free access to water for the next 2 h; infusion of atrial natriuretic peptide/ placebo continued for the first 15 min of the drinking period. 3. The plasma atrial natriuretic peptide concentration did not alter significantly during infusion of hypertonic saline and placebo; it rose to a steady state of 12.7 ± 1.1 pmol/l (mean ± SEM) during the infusion of atrial natriuretic peptide and hypertonic saline, and remained at this level during the first 15 min of the drinking period. During infusion of hypertonic saline and atrial natriuretic peptide or placebo, similar increases in plasma osmolality (P < 0.001) and plasma vasopressin concentration (P < 0.005) occurred. During infusion of hypertonic saline and atrial natriuretic peptide or placebo, thirst increased significantly over the time course of both studies (P<0.01), but the effect of atrial natriuretic peptide infusion compared with placebo infusion was to significantly decrease thirst at 60 min. 4. Drinking rapidly abolished thirst and vasopressin secretion before changes in plasma osmolality occurred. Subjects drank significantly less water after atrial natriuretic peptide infusion compared with after placebo infusion (P<0.01). 5. In conclusion, physiological increases in plasma atrial natriuretic peptide concentrations blunt osmotically stimulated thirst appreciation and attenuate subsequent fluid intake in hyperosmolar man.

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Atrial natriuretic peptide induces sustained natriuresis in conscious dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.258.6.r1445 ◽

1990 ◽

Vol 258 (6) ◽

pp. R1445-R1452

Author(s):

H. L. Mizelle ◽

D. A. Hildebrandt ◽

C. A. Gaillard ◽

M. W. Brands ◽

J. P. Montani ◽

...

Keyword(s):

Arterial Pressure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Renal Excretion ◽

Renal Plasma Flow ◽

Conscious Dogs ◽

Change In Mean ◽

Renal Responses ◽

Atrial Natriuretic

Although acute infusions of atrial natriuretic peptide (ANP) often cause natriuresis, these effects are not sustained, possibly because of reductions in arterial pressure or other compensatory adaptations. The aim of this study was to determine whether physiological increases in intrarenal ANP levels cause sustained natriuresis if changes in arterial pressure and other neurohumoral influences that might obscure the renal responses are controlled. Changes in renal function were quantitated during chronic unilateral renal arterial infusion of ANP at rates of 1, 2, and 4 ng.kg-1.min-1 in conscious dogs (n = 7) with the urinary bladder split to allow continuous measurement of renal excretion in the ANP-infused and contralateral, vehicle-infused kidneys. There was no change in mean arterial pressure at any infusion rate. During 1 ng.kg-1.min-1 infusion of ANP for 5 days, the renal excretory responses were small and variable. However, during 2 and 4 ng.kg-1.min-1 ANP infusion for 7 days, sodium excretion averaged 37.2 +/- 10.0 and 134.8 +/- 19.0% greater, respectively, in the ANP-infused kidneys compared with the vehicle-infused kidneys but there were no changes in glomerular filtration rate or effective renal plasma flow. These results demonstrate that when compensatory changes in arterial pressure and neurohumoral factors are controlled, ANP, at physiological concentrations, causes marked increases in renal excretion. This study supports the concept that ANP's effects to increase renal excretory capability could play a role in long-term control of arterial pressure and body fluid homeostasis.

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