The effect of chronic and acute changes in plasma composition on vasopressin secretion and cerebrospinal fluid in the rat

1992 ◽  
Vol 127 (2) ◽  
pp. 174-178 ◽  
Author(s):  
Timothy Wells ◽  
Richard J Balment
Keyword(s):  
Cerebrospinal Fluid ◽  
New Zealand ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Fluid Composition ◽  
Plasma Composition ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Acute Changes ◽  
Hypertonic Saline Injection

The effects of chronic and acute changes in plasma composition on the osmolality and sodium concentration of cerebrospinal fluid and plasma vasopressin (AVP) concentration have been examined. Chronic elevation of plasma osmolality in three strains of genetically AVP-deflcient rats (Brattleboro and New Zealand hypertensive and normotensive Brattleboro) was associated with increased cerebrospinal fluid osmolality by comparison with AVP-replete controls (Long Evans and New Zealand genetically hypertensive and normotensive rats). The linear correlation between plasma and cerebrospinal fluid osmolality did not reflect a similar relationship between plasma and cerebrospinal fluid sodium concentration. Hypertensive animals exhibited a threefold higher plasma AVP concentration in association with significantly elevated cerebrospinal fluid osmolality by comparison with normotensive controls. Although ip hypertonic saline injection elicited parallel increases in plasma and cerebrospinal fluid osmolality and sodium concentration in both hypertensive and normotensive rats, only in the normotensives did this result in an increase in plasma AVP concentration. These results indicate that cerebrospinal fluid is subject to modest chronic and acute changes in osmolality and sodium concentration which may contribute to the osmotic control of AVP secretion. The disturbed control of vasopressin secretion in hypertensive rats may in part be related to the abnormal cerebrospinal fluid composition in these animals.

Acute suppression of plasma vasopressin and thirst after drinking in hypernatremic humans

1987 ◽  
Vol 252 (6) ◽  
pp. R1138-R1142 ◽  
Author(s):  
C. J. Thompson ◽  
J. M. Burd ◽  
P. H. Baylis
Keyword(s):  
Sodium Chloride ◽  
Hypertonic Saline ◽  
Analogue Scale ◽  
Chloride Solution ◽  
Sodium Chloride Solution ◽  
Plasma Osmolality ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
The Mean ◽  
Hypertonic Saline Infusion

Drinking rapidly abolishes thirst and vasopressin secretion in dehydrated humans before major changes in plasma osmolality are observed. We studied the effects of drinking on plasma vasopressin and thirst in seven healthy volunteers rendered hypernatremic by the infusion of hypertonic (855 mmol/l) sodium chloride solution. Thirst was measured on a visual analogue scale (0-10 cm). Infusion of hypertonic saline caused linear increases in plasma osmolality (289 +/- 1 to 306 +/- 1 mosmol/kg, mean +/- SE, P less than 0.001), plasma vasopressin (0.6 +/- 0.2 to 6.4 +/- 1.9 pmol/l, P less than 0.001), and thirst (1.4 +/- 0.4 to 7.4 +/- 0.5 cm, P less than 0.001). Water was allowed 15 min after cessation of the infusion, and within 5 min of drinking both plasma vasopressin and thirst were significantly lower than postinfusion. After 20 min of drinking, plasma vasopressin had fallen from 6.5 +/- 0.9 to 1.3 +/- 0.3 pmol/l (P less than 0.001) and thirst from 7.7 +/- 0.5 to 1.0 +/- 0.2 cm (P less than 0.001) despite no significant change in plasma osmolality (306 +/- 0.9 to 304 +/- 0.8 mosmol/kg, P = 0.17), and the drinking of 1,200 +/- 60 ml of water, over 85% of the mean cumulative water intake in the 30-min drinking period. Control studies in the same subjects showed comparable rises in plasma vasopressin, plasma osmolality, and thirst during hypertonic saline infusion but no fall in any of these parameters during an equivalent 30-min period after the infusions, during which water was withheld.(ABSTRACT TRUNCATED AT 250 WORDS)

Central infusion of vasopressin decreased plasma vasopressin concentration in dogs

1982 ◽  
Vol 243 (5) ◽  
pp. E365-E369
Author(s):  
B. C. Wang ◽  
L. Share ◽  
J. T. Crofton
Keyword(s):  
Cerebrospinal Fluid ◽  
Physiological Role ◽  
The Other ◽  
Intracerebroventricular Infusion ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Severe Hemorrhage ◽  
Anesthetized Dogs ◽  
Vasopressin Secretion ◽  
Hypertonic Saline Infusion

The effects of increasing the cerebrospinal fluid (CSF) vasopressin concentration (CSFADH) by intracerebroventricular infusion of vasopressin on the plasma vasopressin concentration (PADH) were studied in four groups of anesthetized dogs. One group received an intracerebroventricular infusion of artificial CSF (ACSF) alone for 90 min; the other groups were infused intracerebroventricularly with vasopressin at rates of 10, 20, or 50 microunits/min for 90 min. Arterial blood and CSF samples were taken just before infusion and at 30-min intervals for 210 min. Vasopressin infused intracerebroventricularly at 10, 20, and 50 microunits/min resulted in peak CSFADH of 32.2 +/- 5.3, 82.6 +/- 4.5, and 131.4 +/- 12.5 microunits/ml and reductions in PADH of 32, 47, and 51%, respectively. Only the latter two responses were significant (P less than 0.5-0.01). Because the peak increases in CSFADH after intracerebroventricular infusion of vasopressin ranged from values that were similar to or five times higher than those seen after severe hemorrhage or intracerebroventricular hypertonic saline infusion, we suggest that centrally acting vasopressin may play a physiological role in control of vasopressin secretion.

Thirst and vasopressin release in the dog: an osmoreceptor or sodium receptor mechanism?

1980 ◽  
Vol 238 (5) ◽  
pp. R333-R339 ◽  
Author(s):  
T. N. Thrasher ◽  
C. J. Brown ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Nacl Solution ◽  
Elevated Plasma ◽  
Vasopressin Release ◽  
Hypertonic Glucose ◽  
Hypertonic Solutions ◽  
Vasopressin Secretion ◽  
Plasma Arginine

The effects of intravenous infusion of hypertonic NaCl, sucrose, glucose, urea, or isotonic NaCl solution on thirst and plasma arginine vasopressin concentration (AVP) were studied in five conscious dogs. The changes in osmolality and sodium concentration of plasma and cerebrospinal fluid (CSF) were measured at the threshold of drinking, or after 45 min if no drinking occurred. Hypertonic NaCl and sucrose stimulated drinking in all dogs and significantly elevated plasma AVP. Equally hypertonic glucose, urea, or isotonic NaCl failed to stimulate any drinking or vasopressin secretion. All hypertonic solutions caused significant and similar increases in the osmolality and sodium concentration of CSF. Plasma osmolality was increased by the hypertonic solutions. Plasma sodium was increased by hypertonic NaCl, decreased by sucrose and glucose, and not changed by urea. Isotonic NaCl had no effect on either plasma or CSF composition. These data are not consistent with either a sodium or an osmoreceptor mechanism located within the blood-brain barrier (BBB) or with a peripheral sodium receptor mechanism. An intracranial osmoreceptor located on the blood side of the BBB is proposed to explain these results.

Regulation of plasma vasopressin in insulin-dependent diabetes mellitus

1985 ◽  
Vol 249 (3) ◽  
pp. E317-E325 ◽  
Author(s):  
R. L. Zerbe ◽  
F. Vinicor ◽  
G. L. Robertson
Keyword(s):  
Diabetes Mellitus ◽  
Plasma Osmolality ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Plasma Sodium ◽  
Diabetic Patients ◽  
Plasma Vasopressin ◽  
Insulin Dependent ◽  
Vasopressin Secretion

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be accounted for totally by recognized osmotic or nonosmotic stimuli. To investigate the possibility that regulation of vasopressin secretion is abnormal in this disease, we characterized the vasopressin response to osmotic and hemodynamic stimuli in five uncomplicated, well-controlled insulin-dependent diabetics, and compared the results with those found in nondiabetic volunteers. During osmotic stimulation with hypertonic saline, plasma vasopressin increased in close linear correlation with plasma osmolality or sodium in both groups. However, in the diabetics, the lines describing the relationships between plasma sodium and vasopressin were shifted significantly to the left of normal, suggesting resetting of the osmostat. This shift was not due to abnormal stimulation by hyperglycemia, because increasing plasma glucose and osmolality by intravenous infusion of hypertonic dextrose produced no increase in plasma vasopressin in diabetics or normals. Tilt tests produced a slightly exaggerated increase in plasma vasopressin in diabetics, but their basal and upright pulse rate, blood pressure, plasma renin activity, norepinephrine, and hematocrit were all normal. The results indicate that in diabetic patients the osmoreceptor for osmotic regulation of vasopressin secretion is reset in such a way that higher plasma vasopressin levels are observed at comparable levels of plasma sodium. The exact cause and consequence of this abnormality remain to be determined.

Splanchnic control of vasopressin secretion in conscious rats

1990 ◽  
Vol 259 (1) ◽  
pp. E19-E26 ◽  
Author(s):  
S. Choi-Kwon ◽  
R. McCarty ◽  
A. J. Baertschi
Keyword(s):  
Plasma Osmolality ◽  
Cholinergic Receptor ◽  
Hemodynamic Changes ◽  
Maximal Increase ◽  
Tail Artery ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Saline Solutions ◽  
Intragastric Tube

Saline solutions (NaCl, 2 ml, pH 7.4, 10-598 mosmol/kgH2O) were infused over 4 min in conscious rats, via tail artery catheter or intragastric tube. Intragastric infusions of hyper- and hypotonic solutions caused, within 14.4 +/- 2.2 min, a maximal increase and decrease, respectively, of plasma vasopressin (AVP) relative to time controls (r = 0.97; P less than 0.00001) without affecting systemic plasma osmolality (r = -0.09; P less than 0.92). Mean changes of plasma AVP between 11 and 21 min were also correlated with the osmolality of gastric infusion (r = 0.72; P less than 0.000001), whereas systemic osmolality was unchanged (r = 0.14; P less than 0.42). Systemic infusions caused within 9.0 +/- 2.0 min a maximal change in both plasma AVP (r = 0.82; P less than 0.00001) and systemic osmolality (r = 0.97; P less than 0.00001). However, mean changes of plasma AVP between 11 and 21 min weakly correlated with the osmolality of systemic infusions (r = 0.27; P less than 0.20), although correlations between mean changes of systemic osmolality and the osmolality of systemic infusions were significant (r = 0.72; P less than 0.00001). Lack of correlations with mean arterial pressure and heart rate suggest that hemodynamic changes did not mediate the AVP responses. Pretreatment with atropine methyl bromate (2 mg/kg) abolished the AVP response to gastric but not systemic infusions of hypertonic saline. These results indicate that a splanchnic cholinergic receptor mechanism modulates AVP secretion during a moderate gastric intake of salt or water.

Osmoregulation of thirst and vasopressin secretion in human subjects: effect of various solutes

1983 ◽  
Vol 244 (6) ◽  
pp. E607-E614 ◽  
Author(s):  
R. L. Zerbe ◽  
G. L. Robertson
Keyword(s):  
Hypertonic Saline ◽  
Human Subjects ◽  
Plasma Osmolality ◽  
Detectable Effect ◽  
Healthy Human ◽  
Hypertonic Glucose ◽  
Plasma Vasopressin ◽  
Human Volunteers ◽  
Vasopressin Secretion ◽  
High Degree

Various hypertonic solutions were infused in healthy human volunteers to determine their effect on thirst and vasopressin secretion. Hypertonic saline and mannitol produced prompt and parallel increases in plasma osmolality and vasopressin concentration. For both of these solutes, there was a high degree of correlation between these measurements. The slope describing this relationship varied considerably between individuals, but the same subjects showed similar slopes with either saline or mannitol. Both solutions stimulated thirst. Hypertonic urea infusions produced a comparable rise in osmolality but produced a smaller increase in plasma vasopressin and stimulated thirst in only one of the subjects. With urea, the correlation between plasma osmolality and vasopressin was significantly lower. Within individuals, the slope describing this relationship was significantly correlated with that seen during hypertonic saline. Hypertonic glucose significantly increased plasma osmolality but decreased plasma vasopressin and had no detectable effect on thirst. We conclude that osmoregulation of vasopressin in humans is mediated by a selective osmoreceptor that is located primarily outside of the blood-brain barrier and that individual differences in osmoregulatory sensitivity are not solute specific.

Vasopressin in plasma and ventricular cerebrospinal fluid during dehydration, postural changes, and nausea

1985 ◽  
Vol 248 (1) ◽  
pp. R78-R83 ◽  
Author(s):  
P. S. Sorensen ◽  
M. Hammer
Keyword(s):  
Cerebrospinal Fluid ◽  
Plasma Concentration ◽  
Plasma Osmolality ◽  
High Plasma ◽  
Base Line ◽  
Vasopressin Release ◽  
Modest Increase ◽  
Plasma Vasopressin ◽  
Postural Changes ◽  
Head Up Tilt

The responses of plasma and ventricular cerebrospinal fluid (CSF) vasopressin concentration to dehydration, postural changes, and induction of nausea were studied in 21 patients with hydrocephalus of various etiology. The 24-h dehydration test evoked a significant increase in plasma osmolality and vasopressin concentration, whereas the concentration of vasopressin in CSF was unchanged. Head-up tilt to 50 degrees for 45 min with a tilt bed resulted in a modest increase of plasma vasopressin in patients who did not develop presyncopal symptoms, but no changes were seen in CSF vasopressin. Induction of nausea by subcutaneously injected apomorphine provoked a marked (20- to 50-fold) rise in plasma vasopressin concentration within 15 min, and the plasma concentration was significantly increased above base-line values for 60-120 min. Despite the prolonged period of high plasma vasopressin concentration CSF vasopressin was not influenced by the apomorphine injection. The findings suggest that the concentration of vasopressin in the CSF is controlled by mechanisms other than the well-known osmotic and nonosmotic stimuli of vasopressin release into the blood.

Concentration thresholds for fetal swallowing and vasopressin secretion

1992 ◽  
Vol 262 (6) ◽  
pp. R1057-R1063 ◽  
Author(s):  
M. G. Ross ◽  
C. Agnew ◽  
Y. Fujino ◽  
M. G. Ervin ◽  
L. Day
Keyword(s):  
Control Period ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Threshold Concentration ◽  
Emg Activity ◽  
Thoracic Esophagus ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Vasopressin Secretion ◽  
Vascular Catheters

In adults, plasma osmolality thresholds for hypernatremia-induced arginine vasopressin (AVP) secretion are similar or less than thresholds for stimulation of thirst. In the fetus, the thresholds for swallowing stimulation and AVP secretion have not been defined. Fetal swallowing and AVP secretory responses to hypertonic NaCl and urea were determined in six fetuses (130 +/- 1 1 days) chronically prepared with thyrohyoid, nuchal and thoracic esophagus, and diaphragm electromyograms (EMG), an esophageal flow probe, and vascular catheters. Fetuses received intracarotid injections (0.15 ml/kg) of increasing concentrations of NaCl (0.15, 0.30, 0.45, 0.60, 0.75, and 0.90 M), administered at 2-min intervals. A swallow was defined as a coordinated time-sequence of fetal thyrohyoid, nuchal esophagus, and thoracic esophagus EMG activity. The threshold saline concentration for swallowing was defined as the minimum NaCl dose eliciting swallow responses (within 20 s) after four of five injections at each dose. During a 2-h control period swallowing averaged 25.0 +/- 10.1 ml/h and 39.4 +/- 14.6 swallows/h. The mean NaCl threshold concentration for swallowing stimulation was 0.56 +/- 0.06 M. Fetal plasma AVP (2.6 +/- 0.9 pg/ml) increased significantly at the maximum subthreshold (7.6 +/- 4.0 pg/ml) and the threshold NaCl concentration (8.2 +/- 4.0 pg/ml) that stimulated swallowing. On a subsequent day, equiosmolar urea injections increased plasma AVP (from 2.2 +/- 0.7 to 7.6 +/- 2.6 pg/ml) but had no effect on swallowing activity. Fetal mean arterial blood pressure increased after injections of threshold saline and urea concentrations. Fetal arterial blood osmolality and sodium concentration did not change during any study.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits

1994 ◽  
Vol 266 (2) ◽  
pp. H822-H828 ◽  
Author(s):  
M. Goyer ◽  
H. Bui ◽  
L. Chou ◽  
J. Evans ◽  
L. C. Keil ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Posterior Pituitary ◽  
Paraventricular Nuclei ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Posterior Pituitary Gland ◽  
Hypertonic Saline Infusion

NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)

Possible contribution of dopaminergic receptors in the anteroventral third ventricular region to hyperosmolality-induced vasopressin secretion in conscious rats

1996 ◽  
Vol 134 (2) ◽  
pp. 243-250 ◽  
Author(s):  
Ken'ichi Yamaguchi ◽  
Hitoshi Hama ◽  
Kazuo watanabe
Keyword(s):  
Arterial Pressure ◽  
Ventral Tegmental Area ◽  
Dopamine Receptors ◽  
Paraventricular Nucleus ◽  
Plasma Osmolality ◽  
Dopaminergic Receptors ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Ventral Tegmental

Yamaguchi K, Hama H, Watanabe K. Possible contribution of dopaminergic receptors in the anteroventral third ventricular region to hyperosmolality-induced vasopressin secretion in conscious rats. Eur J Endocrinol 1996;134:243–50. ISSN 0804–4643 We have reported previously that regions encompassing the cerebral ventricle may contain dopamine receptors responsible for facilitatory roles in the osmotic release of vasopressin in conscious rats. In order to explore the location of these receptors, we injected (0.5 μl) the dopamine antagonist haloperidol (13.3 nmol) or dopamine (26.4 nmol) topically into the anteroventral third ventricular region or the paraventricular nucleus of rats, and their effects on the levels of plasma vasopressin and its controlling factors were examined in the presence or absence of an osmotic stimulus. The effects of haloperidol injections into the ventral tegmental area were also tested to study whether information associated with drinking behavior may affect the osmotic vasopressin secretion. Intravenous infusion (0.1 ml kg−1 body wt min−1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin 15 and 30 min later, and this was accompanied by an augmentation of plasma osmolality, sodium and chloride, and by elevated or unaltered arterial pressure. The vasopressin response was abolished by haloperidol injection into the anteroventral third ventricular region 10 min before the beginning of the hypertonic saline infusion. The injection sites were confirmed histologically to have been in or near the organum vasculosum of the laminae terminalis and a ventral part of the median preoptic nucleus. Similarly, a partial but significant reduction of the vasopressin response was noted after bilateral injections of haloperidol into the ventral tegmental area, whereas bilateral haloperidol injections into the paraventricular nucleus had no appreciable effect. The responses of plasma osmolality, electrolytes and arterial pressure to the osmotic load were not affected significantly by haloperidol injections into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. The iv infusion of isotonic saline (0.15 mol/l) did not change plasma vasopressin and the other variables significantly, and this was also the case when preceded by application of haloperidol into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. Dopamine injection into the anteroventral third ventricular region increased plasma vasopressin 5 min later, without affecting plasma osmolality, electrolytes or arterial pressure. On the basis of these results, we concluded that dopamine receptors responsible for facilitatory roles in osmotically stimulated vasopressin secretion may exist in the anteroventral third ventricular region and ventral tegmental area. ken'ichi Yamaguchi, Department of Physiology, Niigata University School of Medicine, Asahimachi-Dori 1, Niigata City, Niigata 951, Japan

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