Osmotic and volaemic regulation of atrial and ventricular natriuretic peptide secretion in conscious eels

Abstract The effects of acute manipulation of plasma osmolality and blood volume on plasma atrial and ventricular natriuretic peptide (ANP and VNP) levels were examined in conscious freshwater eels, Anguilla japonica. A bolus injection of hypertonic NaCl (0·85 m and 1·7 m, 2·5 ml/kg body weight) through a catheter into the ventral aorta produced increases in plasma Na concentration and osmolality with parallel concentration-dependent, transient increases in plasma ANP and VNP levels. Plasma ANP and VNP levels also increased after injection of 1·7 m mannitol solution which produced an increase in plasma osmolality but a decrease in plasma Na concentration. However, injection of a 2·0 m solution of urea, which does not cause cellular dehydration in mammals, produced only small increases in plasma ANP and VNP levels, although plasma osmolality increased. A bolus injection of 10 or 25 ml/kg isotonic saline supplemented with 2% dextran for colloidal osmotic pressure, which theoretically increased blood volume by 29% or 71%, produced volume-dependent, transient increases in plasma ANP and VNP levels without changes in plasma Na concentration and osmolality. Similar volume expansion with dialysed eel plasma caused greater increases than with dextran-saline. However, these increases were much smaller than those after osmotic stimuli. These results indicate that secretion of ANP and VNP is regulated by two receptor mechanisms: osmoreceptors activated by cellular dehydration, not specifically by hypernatraemia, and volume or stretch receptors activated by hypervolaemia. The relative importance of the osmoreceptive mechanism is greater in eels than in mammals where volaemic regulation dominates over osmotic regulation for ANP secretion. Journal of Endocrinology (1996) 149, 441–447

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Acute and chronic increases in osmolality increase excitatory amino acid drive of the rostral ventrolateral medulla in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00104.2004 ◽

2004 ◽

Vol 287 (6) ◽

pp. R1359-R1368 ◽

Cited By ~ 30

Author(s):

Virginia L. Brooks ◽

Korrina L. Freeman ◽

Theresa L. O’Donaughy

Keyword(s):

Amino Acid ◽

Arterial Pressure ◽

Blood Volume ◽

Excitatory Amino Acid ◽

Isotonic Saline ◽

Plasma Osmolality ◽

Saline Infusion ◽

Ventrolateral Medulla ◽

Depressor Response ◽

Hypertonic Saline Infusion

Water deprivation is associated with increased excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), but the mechanism is unknown. This study tested the hypotheses that the increased EAA activity is mediated by decreased blood volume and/or increased osmolality. This was first tested in urethane-anesthetized rats by determining whether bilateral microinjection of kynurenate (KYN, 2.7 nmol) into the RVLM decreases arterial pressure less in water-deprived rats after normalization of blood volume by intravenous infusion of isotonic saline or after normalization of plasma osmolality by intravenous infusion of 5% dextrose in water (5DW). Water-deprived rats exhibited decreased plasma volume and elevated plasma osmolality, hematocrit, and plasma sodium, chloride, and protein levels (all P < 0.05). KYN microinjection decreased arterial pressure by 24 ± 2 mmHg ( P < 0.05; n = 17). The depressor response was not altered following isotonic saline infusion but, while still present ( P < 0.05), was reduced ( P < 0.05) to −13 ± 2 mmHg soon after 5DW infusion. These data suggest that the high osmolality, but not low blood volume, contributes to the KYN depressor response. To further investigate the action of increased osmolality on EAA input to RVLM, water-replete rats were also studied after hypertonic saline infusion. Whereas KYN microinjection did not decrease pressure immediately following the infusion, a depressor response gradually developed over the next 3 h. Lumbar sympathetic nerve activity also gradually increased to up to 167 ± 19% of control ( P < 0.05) 3 h after hypertonic saline infusion. In conclusion, acute and chronic increases in osmolality appear to increase EAA drive of the RVLM.

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Cellular dehydration acutely degrades mood mainly in women: a counterbalanced, crossover trial

British Journal Of Nutrition ◽

10.1017/s0007114520003475 ◽

2020 ◽

pp. 1-9

Author(s):

HyunGyu Suh ◽

Harris R. Lieberman ◽

Lisa T. Jansen ◽

Abigail T. Colburn ◽

J. D. Adams ◽

...

Keyword(s):

Heat Exposure ◽

Isotonic Saline ◽

Plasma Osmolality ◽

Acute Effect ◽

Short Version ◽

Female Age ◽

Cellular Dehydration ◽

Total Mood Disturbance ◽

Control Plasma ◽

Total Mood Disturbance Score

Abstract It is unclear if mild-to-moderate dehydration independently affects mood without confounders like heat exposure or exercise. This study examined the acute effect of cellular dehydration on mood. Forty-nine adults (55 % female, age 39 (sd 8) years) were assigned to counterbalanced, crossover trials. Intracellular dehydration was induced with 2-h (0·1 ml/kg per min) 3 % hypertonic saline (HYPER) infusion or 0·9 % isotonic saline (ISO) as a control. Plasma osmolality increased in HYPER (pre 285 (sd 3), post 305 (sd 4) mmol/kg; P < 0·05) but remained unchanged in ISO (pre 285 (sd 3), post 288 (sd 3) mmol/kg; P > 0·05). Mood was assessed with the short version of the Profile of Mood States Questionnaire (POMS). The POMS sub-scale (confusion-bewilderment, depression-dejection, fatigue-inertia) increased in HYPER compared with ISO (P < 0·05). Total mood disturbance score (TMD) assessed by POMS increased from 10·3 (sd 0·9) to 16·6 (sd 1·7) in HYPER (P < 0·01), but not in ISO (P > 0·05). When TMD was stratified by sex, the increase in the HYPER trial was significant in females (P < 0·01) but not in males (P > 0·05). Following infusion, thirst and copeptin (surrogate for vasopressin) were also higher in females than in males (21·3 (sd 2·0), 14·1 (sd 1·4) pmol/l; P < 0·01) during HYPER. In conclusion, cellular dehydration acutely degraded specific aspects of mood mainly in women. The mechanisms underlying sex differences may be related to elevated thirst and vasopressin.

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Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Brazilian Journal of Medical and Biological Research ◽

10.1590/s0100-879x2002000900011 ◽

2002 ◽

Vol 35 (9) ◽

pp. 1101-1109 ◽

Cited By ~ 34

Author(s):

R.R. Ventura ◽

D.A. Gomes ◽

W.L. Reis ◽

L.L.K. Elias ◽

M. Castro ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Blood Volume ◽

Volume Expansion ◽

Sodium Intake ◽

Blood Volume Expansion ◽

Peptide Secretion ◽

Atrial Natriuretic

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Atrial natriuretic peptide in multiple system atrophy

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.271.4.r1047 ◽

1996 ◽

Vol 271 (4) ◽

pp. R1047-R1053

Author(s):

M. Bevilacqua ◽

G. Norbiato ◽

V. Righini ◽

L. Castelli ◽

A. Rogolino ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Multiple System Atrophy ◽

Natriuretic Peptide ◽

Blood Volume ◽

Volume Expansion ◽

Plasma Osmolality ◽

Type A ◽

Type B ◽

Blood Volume Expansion ◽

Osmotic Load

Central nervous system feedback loops centered on hypothalamic neurons control atrial natriuretic peptide (ANP). We evaluated the ANP response to arterial hypotension, isotonic blood volume expansion, and increase in plasma osmolality in 14 patients with multiple system atrophy (MSA). Seven of the patients were characterized by a lack of vasopressin response to hypotension (MSA type B), suggesting chronic sinoaortic denervation, and seven by a preserved response (MSA type A). Orthostatic hypotension decreased ANP in controls and type A patients, whereas ANP in type B was not affected. Isotonic saline infusion increased ANP and diuresis in controls and type A patients, whereas it did not affect ANP in type B. Osmotic load increased plasma osmolality and vasopressin in controls and MSA patients and ANP in controls and type A but not in type B patients. In MSA patients with altered afferent control of vasopressin, ANP secretion is not stimulated by blood volume expansion, osmotic load, or blood pressure, suggesting that afferent excitatory control plays a role in the release of ANP.

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Physiological mechanisms for thirst in the nonhuman primate

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1982.242.5.r423 ◽

1982 ◽

Vol 242 (5) ◽

pp. R423-R428 ◽

Cited By ~ 3

Author(s):

R. J. Wood ◽

E. T. Rolls ◽

B. J. Rolls

Keyword(s):

Nonhuman Primate ◽

Rhesus Monkeys ◽

Water Deprivation ◽

Isotonic Saline ◽

Plasma Osmolality ◽

Physiological Mechanisms ◽

Cellular Dehydration ◽

Primary Determinant ◽

The Relationship ◽

Intravenous Sodium

The relationship between body fluid deficits and drinking has been investigated in a nonhuman primate. Intravenous sodium chloride infusions (0.93-3.25 M) given to rhesus monkeys caused drinking correlated with increases in plasma osmolality and sodium concentrations. Sucrose infusions (0.3 M in 0.15 M NaCl) also caused drinking while equiosmolal urea infusions did not. It was found that the drinking threshold corresponded to a 2.3% increase in plasma osmolality. Water deprivation for 24 h caused significant cellular dehydration, as indicated by a 5.8% elevation in plasma osmolality that exceeded the threshold for thirst, and a significant hypovolemia as indicated by elevated plasma protein and hematocrit values. Intravenous water preloads decreased plasma osmolality and produced a dose-related decrease in subsequent drinking. Infusions that restored plasma osmolality to predeprivation values, reduced intake by 85%. Intravenous isotonic saline preloads which abolished the hypovolemia did not have a consistent effect and reduced mean water intakes by only 3.2%. Thus in the rhesus monkey, cellular dehydration is an effective stimulus for thirst, and it is the primary determinant of drinking after water deprivation, used as an example of a natural thirst stimulus. In contrast to findings in nonprimates, the extracellular deficit contributes very little to drinking after water deprivation.

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