Central ANP does not influence osmotic thirst threshold in the dog

Appetite ◽  
1989 ◽  
Vol 12 (3) ◽  
pp. 218
Author(s):  
E. Kowalik-Borowka ◽  
J. Sobocińska ◽  
E. Szczepańska-Sadowska
Keyword(s):  
Osmotic Thirst

Neurokinin A and osmotic thirst: A behavioural and renal study

1988 ◽  
Vol 20 (7) ◽  
pp. 605-606
Author(s):  
C. Polidori ◽  
M. Perfumi ◽  
M. Massi ◽  
G. de Caro
Keyword(s):  
Neurokinin A ◽  
Osmotic Thirst

Convergence of signals in the zona incerta for angiotensin-mediated and osmotic thirst

1987 ◽  
Vol 407 (2) ◽  
pp. 332-340 ◽  
Author(s):  
David Mok ◽  
Gordon J. Mogenson
Keyword(s):  
Zona Incerta ◽  
Osmotic Thirst

Loss of osmotic thirst in multiple system atrophy: association with sinoaortic baroreceptor deafferentation

1994 ◽  
Vol 266 (6) ◽  
pp. R1752-R1758
Author(s):  
M. Bevilacqua ◽  
G. Norbiato ◽  
V. Righini ◽  
T. Vago ◽  
L. Castelli ◽  
...  
Keyword(s):  
Multiple System Atrophy ◽  
Plasma Osmolality ◽  
Group A ◽  
The Central Nervous System ◽  
Group B ◽  
Response Group ◽  
And Control ◽  
Osmotic Thirst ◽  
Afferent Control ◽  
Hypertonic Saline Infusion

We evaluated plasma osmolality (pOsm), thirst, and vasopressin response to hypertonic saline infusion in 14 patients with multiple system atrophy (MSA). This disease is characterized by the degeneration of noradrenergic neurons in the central nervous system and severe orthostatic hypotension. Seven patients were also characterized by the lack of vasopressin response to hypotension (group B) and seven by a preserved response (group A). In group A pOsm rose from 290 +/- 2 to 312 +/- 6 mosmol/kgH2O, vasopressin from 0.9 +/- 0.3 to 5.7 +/- 0.5 pmol/l, and thirst from 1.1 +/- 0.1 to 8.7 +/- 1.1 cm on the visual analog scale. After saline, patients drank 1,215 +/- 150 ml of water (no different from healthy controls). In group B patients' pOsm rose from 296 +/- 3 to 325 +/- 6 mosmol/kgH2O and vasopressin from 1.2 +/- 0.1 to 19.6 +/- 0.4 pmol/l (P < 0.01 vs. group A and controls). Group B patients had no thirst during saline and drank little after the challenge (175 +/- 50 ml; P < 0.01 vs. group A and control). Forced drinking decreased vasopressin in patients before changes in pOsm, showing that inhibitory afferents from oropharyngeal mucosa were intact. In MSA patients with altered afferent control of vasopressin there is a dissociation between the osmotic control of thirst and the osmotic control of vasopressin.

Osmotic thirst and vasopressin release in humans: a double-blind crossover study

1985 ◽  
Vol 248 (6) ◽  
pp. R645-R650 ◽  
Author(s):  
P. A. Phillips ◽  
B. J. Rolls ◽  
J. G. Ledingham ◽  
M. L. Forsling ◽  
J. J. Morton
Keyword(s):  
Hypertonic Saline ◽  
Water Intake ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Double Blind ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Plasma Sodium Concentration ◽  
Osmotic Thirst

Thirst is a subjective sensation. Therefore to investigate further the nature, intensity, and specificity of osmotic thirst, we studied the effects of double-blind infusions of hypertonic (0.45 M) and isotonic (0.15 M) saline on subjective ratings and sensations of thirst, water intake, plasma vasopressin, and body fluids in seven healthy volunteer young men. Only the hypertonic saline significantly increased plasma sodium concentration, plasma osmolality, plasma vasopressin concentration, and visual analog ratings of thirst sensations. Both infusions expanded blood volume, which was greater with the hypertonic saline infusion. Neither solution significantly altered mean arterial blood pressure nor plasma angiotensin levels. Throughout a 60-min drinking period after the infusions, water intake was always significantly greater after the hypertonic saline than after the isotonic saline. The subjects described the thirst sensations as mainly due to a dry unpleasant tasting mouth, which was promptly relieved by drinking. Visual analog rating changes confirmed the subjective reports. Finally, the effects on thirst and vasopressin secretion were observed at plasma sodium concentration and osmolality changes that are well within the physiological range.

scholarly journals Central angiotensin-(1-7) increases osmotic thirst

2017 ◽  
Vol 102 (11) ◽  
pp. 1397-1404 ◽  
Author(s):  
Raoni Conceição dos-Santos ◽  
Lívia da Rocha Natalino Monteiro ◽  
Bruno Paes-Leme ◽  
Danilo Lustrino ◽  
José Antunes-Rodrigues ◽  
...  
Keyword(s):  
Osmotic Thirst

Contribution of zona incerta to osmotically induced drinking in rats

1986 ◽  
Vol 251 (5) ◽  
pp. R823-R832
Author(s):  
D. Mok ◽  
G. J. Mogenson
Keyword(s):  
Firing Rate ◽  
Fluid Intake ◽  
Preoptic Area ◽  
Third Ventricle ◽  
Zona Incerta ◽  
Single Neurons ◽  
Reduced Drinking ◽  
Osmotic Thirst ◽  
Extracellular Activity

Spontaneous extracellular activity was recorded from single neurons in the rostral zona incerta (ZI) of urethan-anesthetized rats. Ventricular injections of hyperosmotic saline (1 or 2 microliter of NaCl solutions with osmolarities of 0.6 or 1.2 osmol/l) and distilled water (1 or 2 microliter) at the level of the anteroventral third ventricle (AV3V) changed the firing rate of ZI neurons. By comparison, ventricular injections of osmotic solutions at the level of the dorsal third ventricle were relatively ineffective. Injections of osmotic solutions (0.2 or 0.5 microliter of 1.2 osmol/l NaCl) into the medial preoptic area (MPO) also changed the firing rate of ZI neurons, whereas control injections into the caudate putamen were ineffective. In another series of rats, injections of procaine into the region of the rostral ZI significantly reduced drinking to injections of hyperosmotic saline into the ipsi- but not the contralateral MPO. The ZI, AV3V, and MPO have previously been reported to contribute to the neural regulation of fluid intake. These findings provide additional evidence for a role of the ZI in drinking and suggest that part of the central pathway for osmotic thirst involves a projection to neurons in the ZI from osmoreceptors in the MPO.

Hyperactivity to quinine associated with osmotic thirst in the rat.

1972 ◽  
Vol 78 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Gene H. Burke ◽  
Douglas G. Mook ◽  
Elliott M. Blass
Keyword(s):  
Osmotic Thirst

Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy

1995 ◽  
Vol 132 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Marshall D Lindheimer ◽  
John M Davison
Keyword(s):  
Steady State ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Late Pregnancy ◽  
Metabolic Clearance ◽  
Hormone Release ◽  
Water Turnover ◽  
Osmotic Thirst ◽  
Term Data ◽  
In Pregnancy

Lindheimer MD, Davison JM. Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy. Eur J Endocrinol 1995;132:133–43. ISSN 0804–4643 This review stresses changes in osmoregulation as well as the secretion and metabolism of aŕginine vasopressin during pregnancy, focusing on human gestation. Pregnant women experience a decrease in body tonicity, plasma osmolality decreasing immediately after conception to a nadir ~ 10 mosmol/kg below non-pregnant levels early in pregnancy, after which a new steady state is maintained until term. Data from both human and rodent gestation have led to a formation of how these changes occur. The osmotic thresholds for thirst and antidiuretic hormone release decrease in parallel. Lowering the threshold to drink stimulates increased water intake and dilution of body fluids. Because arginine vasopressin (AVP) release is not suppressed at the usual level of body tonicity, the hormone continues to circulate and the ingested water is retained. Plasma osmolality declines until it is below the osmotic thirst threshold, and a new steady state with little change in water turnover is established. Pregnancy is characterized by increments in intravascular volume, but volume-sensing AVP release mechanisms appear to adjust as gestation progresses so that each new volume status is "sensed" as normal. The metabolic clearance of AVP increases fourfold, the rise paralleling that of circulating cystine aminopeptidase (vasopressinase), and enzyme produced by the placenta. Furthermore, the disposal rate of 1-deamino-8-d-AVP, and AVP analogue resistant to inactivation by vasopressinase, is unaltered in pregnancy. Thus, the increase in AVP's metabolism and the high circulating aminopeptidase levels have been implicated in certain forms of transient diabetes insipidus that occur in late pregnancy. Finally, mechanisms responsible for the altered osmoregulation in pregnancy are obscure, but chorionic gonadotropin and relaxin may be implicated in the changes. M Lindheimer, Section of Nephrology, MC 5100, University of Chicago Hospitals, 5841 S Maryland Ave, Chicago, IL, USA

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