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

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.

1988 ◽  
Vol 118 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Kyuzi Kamoi ◽  
Fujio Sato ◽  
Okuhiro Arai ◽  
Miyuki Ishibashi ◽  
Tohru Yamaji

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.


1991 ◽  
Vol 260 (3) ◽  
pp. R475-R479 ◽  
Author(s):  
L. M. Burrell ◽  
H. J. Lambert ◽  
P. H. Baylis

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)


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.


1987 ◽  
Vol 73 (5) ◽  
pp. 489-495 ◽  
Author(s):  
A. M. Richards ◽  
G. Tonolo ◽  
R. Fraser ◽  
J. J. Morton ◽  
B. J. Leckie ◽  
...  

1. Diurnal changes in plasma concentrations of atrial natriuretic peptide (ANP), renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were investigated in seven normal volunteers studied under standardized conditions of dietary sodium, posture and physical activity. After completion of the diurnal study serial measurements of these variables were continued during, and on recovery from, a 2 day period of severe sodium depletion. 2. Clear diurnal variations in plasma concentrations of renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were observed. 3. Plasma ANP concentrations also varied significantly over 24 h. Values peaked about mid-day and a distinct trough in peptide concentrations occurred in the early evening. However, variations in plasma ANP values were of relatively small amplitude and not clearly independent of modest parallel shifts in sodium balance. 4. Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. 5. No simple parallel or reciprocal relationships between plasma concentrations of ANP, on the one hand, and concurrent plasma concentrations of other hormones or in the rate of urinary sodium excretion, on the other, were observed during the 25 h of the diurnal study.


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.


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