Effects of plasma volume and osmolality on secretion of atrial natriuretic peptide and vasopressin in man

1988 ◽  
Vol 118 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Kyuzi Kamoi ◽  
Fujio Sato ◽  
Okuhiro Arai ◽  
Miyuki Ishibashi ◽  
Tohru Yamaji
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Water Load ◽  
Healthy Men ◽  
Parallel Increase ◽  
Osmotic Change ◽  
Atrial Natriuretic

Abstract. To clarify the role of blood volume and osmolality in the mediation of the release of atrial natriuretic peptide (ANP) and to examine the relationship between plasma ANP and plasma AVP levels in man, the effects of hypertonic saline and hypertonic mannitol infusion, and of water load on plasma levels of ANP and AVP were studied. Infusion of 5% saline to 7 healthy men at a rate of 0.05 ml min−1·kg−1 for 2 h resulted in a parallel rise in plasma sodium, osmolality, plasma ANP and plasma AVP, indicating that plasma hyperosmolality stimulates secretion of both ANP and AVP. Infusion of 20% mannitol to 6 healthy men at the same rate resulted in a parallel increase in plasma osmolality, plasma ANP and AVP, whereas plasma sodium decreased, indicating that plasma hyperosmolality stimulates secretion of both ANP and AVP. Water load (20 ml/kg) into 7 healthy men produced a prompt and parallel fall in plasma sodium, plasma osmolality and plasma AVP. In contrast, plasma ANP and plasma volume, calculated from the changes in hematocrit, increased concomitantly, which indicates that expanded plasma volume stimulates secretion of plasma ANP. These results suggest that secretion of ANP in man is regulated principally by plasma volume, which may be modulated by a change in plasma osmolality. AVP secretion, on the other hand, is controlled mainly by osmotic change and secondarily by plasma volume.

Central oxytocin and ANP receptors mediate osmotic inhibition of salt appetite in rats

1995 ◽  
Vol 269 (2) ◽  
pp. R245-R251 ◽  
Author(s):  
R. E. Blackburn ◽  
W. K. Samson ◽  
R. J. Fulton ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Salt Appetite ◽  
Saline Ingestion ◽  
A Chain ◽  
Anp Receptors ◽  
Atrial Natriuretic

These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.

Effects of an oral water load and intravenous administration of isotonic glucose, hypertonic saline, mannitol and furosemide on the release of atrial natriuretic peptide in men

1988 ◽  
Vol 119 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Yasuhiro Yamasaki ◽  
Takeshi Nishiuchi ◽  
Akihiro Kojima ◽  
Haruhiko Saito ◽  
Shiro Saito
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Hypertonic Saline ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Normal Subjects ◽  
Water Load ◽  
Age Related ◽  
The Mean ◽  
Hypertonic Saline Infusion ◽  
Atrial Natriuretic

Abstract. The effects of an oral water load and iv administration of isotonic glucose, hypertonic saline, mannitol and furosemide on release of human atrial natriuretic peptide (hANP) were examined in normal subjects to determine the main factors causing its release. In addition, the influence of age on hANP secretion was investigated. The mean plasma hANP level in normal subjects, 0–89 years old, was 20.6 ± 1.1 ng/l (mean ± sem) and showed age-related change. The plasma hANP level did not change significantly after a water load or infusion of isotonic glucose, but rose significantly from 11.4 ± 1.4 to 15.6 ± 3.2 ng/l after infusion of hypertonic saline and from 10.9 ± 1.6 to 17.8 ± 4.1 ng/l after infusion of 20% mannitol in parallel with the increase in plasma volume. The plasma hANP level decreased from 17.3 ± 2.5 to 9.0 ± 2.5 ng/l after injection of 40 mg of furosemide. A positive correlation was found between change in the plasma hANP level and percent change in the plasma volume (P < 0.001) on these treatments. The response of plasma hANP to hypertonic saline infusion was greater in older than in young men. These results indicate that 1) the secretion of hANP shows an age-related change and 2) increase in the circulating plasma volume is an important factor regulating hANP secretion.

Effect of atrial natriuretic peptide on thirst and arginine vasopressin release in humans

1991 ◽  
Vol 260 (3) ◽  
pp. R475-R479 ◽  
Author(s):  
L. M. Burrell ◽  
H. J. Lambert ◽  
P. H. Baylis
Keyword(s):  
Steady State ◽  
Atrial Natriuretic Peptide ◽  
Hypertonic Saline ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Normal Male ◽  
Vasopressin Release ◽  
Atrial Natriuretic

We investigated the effect of human alpha-atrial natriuretic peptide (alpha-hANP) on osmotically stimulated arginine vasopressin (AVP) secretion and thirst appreciation. Seven normal male volunteers were studied on two occasions: synthetic alpha-hANP-(99-126) (2 pmol.kg-1.min-1) or control was infused intravenously for 30 min before and for the first 60 min of a 120-min hypertonic saline (855 mmol/l) infusion (0.06 ml.kg-1.min-1). Plasma ANP did not alter significantly during infusion of control and hypertonic saline (C+HS) but rose to steady-state concentrations of 17.4 +/- 3.2 pmol/l during infusion of ANP and hypertonic saline (ANP+HS). Plasma osmolality increased on both study days [ANP+HS: 284.4 +/- 0.6 to 299.7 +/- 1.1 mosmol/kgH2O (P less than 0.01)], C+HS: 283.6 +/- 1.2 to 299.1 +/- 1.6 mosmol/kgH2O (P less than 0.01)], as did plasma sodium [ANP+HS: 139.0 +/- 0.6 to 148.0 +/- 0.4 mmol/l (P less than 0.01), C+HS: 137.6 +/- 0.75 to 145.8 +/- 0.7 mmol/l (P less than 0.01)] and blood volume (ANP+HS: 7.7 +/- 0.6%, C+HS: 9.4 +/- 1.0%). The increase in plasma osmolality was accompanied by an increase in plasma AVP [ANP+HS: 1.4 +/- 0.3 to 8.3 +/- 1.2 pmol/l (P less than 0.01), C+HS: 1.6 +/- 0.4 to 7.8 +/- 1.5 pmol/l (P less than 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 138-143 ◽  
Author(s):  
EM Renkin ◽  
VL Tucker
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
Interstitial Fluid Volume ◽  
Atrial Natriuretic

Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.

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.

Assessment of atrial natriuretic peptide resistance in cirrhosis with head-out water immersion and atrial natriuretic peptide infusion

1993 ◽  
Vol 71 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Louis Legault ◽  
Leonard C. Warner ◽  
Wai Ming Leung ◽  
Alexander G. Logan ◽  
Laurence M. Blendis ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Collecting Duct ◽  
Water Immersion ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Sodium Retention ◽  
Serum Aldosterone ◽  
Atrial Natriuretic

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.

Atrial natriuretic peptide inhibits osmolality-induced arginine vasopressin release in man

1988 ◽  
Vol 75 (1) ◽  
pp. 35-39 ◽  
Author(s):  
M. J. Allen ◽  
V. T. Y. Ang ◽  
E. D. Bennett ◽  
J. S. Jenkins
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Random Order ◽  
Vasopressin Release ◽  
Plasma Arginine ◽  
Placebo Infusion ◽  
Atrial Natriuretic

1. Eight normal volunteers were infused with 5% saline (5 g of NaCl/100 ml) at a rate of 0.06 ml min−1 kg−1 for 120 min to increase plasma osmolality and plasma arginine vasopressin. Human atrial natriuretic peptide (α-hANP; 100 μg) or placebo was given in random order in a double-bind cross-over design for the last 20 min of the saline infusion. 2. Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. 3. Mean plasma immunoreactive ANP did not increase in response to changes in osmolality and rose to a peak of 118 pg/ml during the α-hANP infusion. α-hANP produced significant suppression of mean plasma arginine vasopressin over the 60 min after the infusions. 4. We conclude that ANP is not released in response to increased osmolality in vivo, and that it inhibits osmolality-induced arginine vasopressin release in man.

Atrial Natriuretic Peptide and Response to Changing Plasma Volume in Diabetic Nephropathy

Diabetes ◽  
1991 ◽  
Vol 40 (7) ◽  
pp. 893-901 ◽  
Author(s):  
J. S. Lieberman ◽  
L. Parra ◽  
L. Newton ◽  
J. D. Scandling ◽  
N. Loon ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Atrial Natriuretic
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