Acute reduction of plasma vasopressin levels by rehydration in sheep

1985 ◽  
Vol 248 (1) ◽  
pp. R68-R71 ◽  
Author(s):  
J. R. Blair-West ◽  
A. P. Gibson ◽  
R. L. Woods ◽  
A. H. Brook
Keyword(s):  
Drinking Water ◽  
Plasma Osmolality ◽  
Nacl Solution ◽  
Water Restriction ◽  
Stomach Tube ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Solution Saline ◽  
Voluntary Intake ◽  
Water Administration

Sheep were depleted of water by restricting water intake to 500 ml/day for 7-9 days and were then rehydrated by three treatments: voluntary intake of water, administration of water by tube into the stomach, or voluntary intake of 0.9% NaCl solution (saline). The volumes of fluids drunk within 2-3 min, or administered by tube, were approximately equal to the animal's weight loss. Plasma vasopressin rose from 4.4 +/- 0.6 to 16.8 +/- 1.0 pg/ml during water restriction. After drinking water plasma vasopressin fell from 19.0 +/- 1.9 to 7.5 +/- 0.4 pg/ml (P less than 0.001) in 15 min and gradually fell to 3.2 +/- 0.4 pg/ml over 6 h. Plasma osmolality fell from 302.4 +/- 0.9 to 301.0 +/- 1.1 mosmol/kg (NS) 15 min after water drinking and then gradually fell to subnormal levels. Sheep given water by stomach tube showed a similar decline in plasma osmolality, but the fall in plasma vasopressin was attenuated. The fall in plasma vasopressin in the first 30 min after drinking saline was almost identical with the fall after drinking water, but plasma osmolality was unaltered. Plasma vasopressin fell so rapidly after drinking water or saline as to suggest that the act of drinking caused almost complete inhibition of vasopressin release without a change in plasma osmolality. The results are consistent with earlier evidence that oropharyngeal receptors initiate the inhibition of vasopressin release after drinking.

Osmoregulation of thirst and vasopressin during normal menstrual cycle

1988 ◽  
Vol 254 (4) ◽  
pp. R641-R647 ◽  
Author(s):  
T. J. Vokes ◽  
N. M. Weiss ◽  
J. Schreiber ◽  
M. B. Gaskill ◽  
G. L. Robertson
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Plasma Osmolality ◽  
Free Water ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Normal Menstrual Cycle ◽  
Basal Plasma

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

Increased plasma osmolality stimulates peripheral and central vasopressin release in male and female rats

1994 ◽  
Vol 267 (4) ◽  
pp. R923-R928 ◽  
Author(s):  
M. Ota ◽  
J. T. Crofton ◽  
H. Liu ◽  
G. Festavan ◽  
L. Share
Keyword(s):  
Interstitial Fluid ◽  
Plasma Osmolality ◽  
Female Rats ◽  
Microdialysis Probe ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Male And Female Rats ◽  
Supraoptic Nuclei

It has been demonstrated that the neurohypophysial hormones can be released intrahypothalamically by the paraventricular (PVN) and supraoptic nuclei. The present experiments were undertaken to determine whether a physiological stimulus for vasopressin release, increased plasma osmolality, will stimulate the release of vasopressin by the PVN into the surrounding interstitial fluid, and whether the responses are affected by gender. Intravenous infusion of 2.5 M NaCl for 60 min (0.1 ml.kg-1.min-1) in conscious rats resulted in an increased vasopressin concentration in the dialysate from a microdialysis probe adjacent to the PVN. This response was greater in nonestrous females than in males. On the other hand, the rise in the plasma vasopressin concentration was greater in males than in nonestrous females. Mean arterial blood pressure increased and heart rate decreased, but these responses were not affected by gender. The role of centrally released vasopressin in the control of the peripheral release of vasopressin is conjectural, but both responses may be modulated by the gonadal steroid hormones.

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.

Hypothalamic thermal stimulation modulates vasopressin release in hyperosmotically stimulated rabbits

1994 ◽  
Vol 267 (4) ◽  
pp. R1089-R1097 ◽  
Author(s):  
R. Keil ◽  
R. Gerstberger ◽  
E. Simon
Keyword(s):  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Significant Rise ◽  
Hypertonic Solution ◽  
Temperature Plasma ◽  
Evaporative Water ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Hypothalamic Control ◽  
Hypertonic Stimulation

Under thermoneutral conditions conscious rabbits received systemic infusions of NaCl as hypertonic solution (90 mueq.min-1.kg body wt-1), which raised their plasma osmolality from 283 to 312 mosmol/kgH2O. Rabbits receiving isotonic saline served as controls. Hypertonic stimulation induced a 60% reduction of both respiratory frequency and evaporative water loss. Rectal temperature rose by 0.4 degrees C despite enhanced peripheral vasodilation as indicated by increased ear skin temperature. Plasma vasopressin (AVP), aldosterone (ALDO), and corticosterone (COR) were significantly elevated from 6 to 16 pg/ml, 90 to 180 pg/ml, and 17 to 40 ng/ml, respectively. To elucidate the importance of central temperature for AVP and adrenal corticosteroid release, hypothalamic thermal stimulations (20 min) were superimposed during established iso- and hyperosmotic steady-state conditions. Different from isosmotic controls, hyperosmotic animals responded to hypothalamic cooling (37 degrees C) with a significant decrease in plasma AVP from 16 to 13 pg/ml and to hypothalamic warming (41 degrees C) with a significant rise from 16 to 19 pg/ml. A weak temperature effect on COR release was also disclosed, especially of hypothalamic cooling, which significantly lowered plasma COR from 42 to 34 ng/ml. These results provide evidence for positive local temperature coefficients of hypothalamic control of AVP release and suggest a similar property also for the control of COR release by the hypothalamo-adenohypophysial axis.

Cardiomegaly and Vasoactive Hormones in Rats with Chronic Myocardial Infarction: Long-Term Effects of Chlorothiazide

1996 ◽  
Vol 90 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Masahiro Kohzuki ◽  
Masayuki Kanazawa ◽  
Kazunori Yoshida ◽  
Eikatsu Tsutsumi ◽  
Minoru Yasujima ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Drinking Water ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Chronic Myocardial Infarction ◽  
Plasma Vasopressin ◽  
Body Sodium ◽  
Vasoactive Hormones ◽  
Sodium Plasma

1. The effects of prolonged chlorothiazide treatment of left ventricular failure on cardiac hypertrophy, circulating vasoactive hormones and exchangeable body sodium were examined in rats with chronic myocardial infarction induced by left coronary artery ligation. Chlorothiazide therapy commenced either immediately or 2 weeks after infarction. For 4 weeks, the rats were given either chlorothiazide (50 mg day−1 kg−1) in their drinking water or drinking water alone. 2. Cardiac weight increased in untreated rats with infarction in comparison with sham-operated controls, indicating the presence of chronic left ventricular dysfunction, although exchangeable body sodium, plasma renin activity, plasma vasopressin and plasma osmolality remained unchanged. 3. Chlorothiazide raised haematocrit and plasma renin activity equally in rats with and without infarction, although exchangeable body sodium, plasma vasopressin and plasma osmolality were not changed by the treatment. Plasma atrial natriuretic peptide was 2-fold higher in rats with infarction and this response was not affected by chlorothiazide treatment. Chlorothiazide therapy did not prevent or reverse cardiac hypertrophy. 4. Chronic diuretic therapy in this experimental model of heart failure did not reduce extracellular sodium, plasma vasopressin or the extent of ventricular hypertrophy, possibly because the condition was associated with activation of the renin—angiotensin system.

Effect of ovariectomy and treatment with ovarian steroids on vasopressin release and fluid balance in the rat

1990 ◽  
Vol 124 (2) ◽  
pp. 277-284 ◽  
Author(s):  
K. Peysner ◽  
M. L. Forsling
Keyword(s):  
Water Intake ◽  
Fluid Balance ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Control Group ◽  
Oestrogen Treatment ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Progesterone Treatment ◽  
Food And Water Intake

ABSTRACT Plasma vasopressin concentrations have previously been shown to vary during the oestrous cycle of the rat, being highest on the morning of pro-oestrus and lowest on dioestrus day 1. To determine the effect of gonadal steroids on vasopressin secretion and fluid balance, mature rats were ovariectomized and given oestrogen, progesterone or vehicle alone s.c. for periods of up to 16 days. Plasma vasopressin concentrations fell after ovariectomy and this was reflected in an increase in 24-h urine volume. The normal increase in plasma vasopressin concentrations seen over daylight hours was also suppressed. The change in vasopressin concentrations observed on steroid treatment depended upon both the dose and the duration. High doses of oestrogen were associated with a fall in plasma vasopressin, probably as a result of fluid retention. Thus, of an initial group of rats given silicone elastomer implants containing 50, 500 or 1000 μg oestradiol in oil, plasma vasopressin concentrations were reduced after 7 days treatment with 1000 μg oestradiol implants in association with reduced plasma sodium concentrations. Daily s.c. injections of 100 μg oestradiol benzoate/100 g body weight produced an immediate small increase in plasma vasopressin concentrations, but by 14 days the plasma concentrations of 0·7 ± 0·16 pmol/l (mean ± s.e.m.) had fallen significantly and were less than those in the vehicle-treated group (1·2± 0·26 pmol/l). However, after treatment for 14 days with implants containing only 50 μg oestradiol, plasma vasopressin concentations were higher compared with the group receiving vehicle alone, despite the fact that the plasma osmolality was lower in the latter group, suggesting a long term resetting of the osmoreceptors. Progesterone treatment with two implants containing 17·5 mg progesterone in oil was associated with an initial suppression of plasma vasopressin concentrations, but 16 days after the implant the plasma concentrations were higher than in the control group. Neither oestrogen nor progesterone restored the vasopressin concentrations to those seen in the intact animal. Oestrogen treatment resulted in a reduction in food and water intake, whereas progesterone treatment produced an initial increase in food and water intake, and a fall in plasma osmolality which could account for the reduced plasma vasopressin. This was followed by an increase in urine flow over days 6 to 15. Thus ovariectomy had a marked effect on circulating vasopressin concentrations, probably as a result of complex changes since administration of either oestrogen or progesterone in doses giving normal circulating concentrations had little effect. Journal of Endocrinology (1990) 124, 277–284

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.

Osmoregulation of thirst and vasopressin secretion in insulin-dependent diabetes mellitus

1988 ◽  
Vol 74 (6) ◽  
pp. 599-606 ◽  
Author(s):  
C. J. Thompson ◽  
S. N. Davis ◽  
P. C. Butler ◽  
J. A. Charlton ◽  
P. H. Baylis
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Sodium Chloride ◽  
Plasma Osmolality ◽  
Glucose Infusion ◽  
Diabetic Patients ◽  
Healthy Controls ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion

1. Osmotically stimulated thirst and vasopressin release were studied during infusions of hypertonic sodium chloride and hypertonic d-glucose in euglycaemic clamped diabetic patients and healthy controls. 2. Infusion of hypertonic sodium chloride caused similar elevations of plasma osmolality in diabetic patients (288.0 ± 1.0 to 304.1 ± 1.6 mosmol/kg, mean ± sem, P < 0.001) and controls (288.6 ± 0.9 to 305.7 ± 0.6 mosmol/kg, P < 0.001), accompanied by progressive increases in plasma vasopressin (diabetic patients, 0.9 ± 0.3 to 7.7 ± 1.5 pmol/l, P < 0.001; controls 0.5 ± 0.1 to 6.5 ± 1.0 pmol/l, P < 0.001) and thirst ratings (diabetic patients 1.0 ± 0.2 to 7.1 ± 0.5 cm, P < 0.001; controls 1.8 ± 0.4 to 8.0 ± 0.5 cm, P < 0.001) in both groups. 3. Drinking rapidly abolished thirst and vasopressin secretion before major changes in plasma osmolality occurred in both diabetic patients and healthy controls. 4. There were close and significant correlations between plasma vasopressin and plasma osmolality (diabetic patients, r = + 0.89, controls r = + 0.93) and between thirst and plasma osmolality (diabetic patients r = +0.95, controls r = +0.97) in both diabetic patients and healthy controls during hypertonic saline infusion. 5. Hypertonic d-glucose infusion caused similar elevations in blood glucose in diabetic patients (4.0 ± 0.2 to 20.1 ± 1.2 mmol/l, P < 0.001) and healthy controls (4.3 ± 0.1 to 19.3 ± 1.2 mmol/l, P < 0.001) but did not change plasma vasopressin or thirst ratings. There was no correlation between plasma osmolality and either thirst or plasma vasopressin during hypertonic d-glucose infusion. 6. The characteristics of osmoregulated thirst and vasopressin release are similar in health and diabetes mellitus. As hyperglycaemia was not dipsogenic, however, the thirst of poorly controlled diabetes mellitus may be due to hypovolaemia secondary to polyuria rather than hyperosmolality due to elevated blood glucose concentrations.

Osmoregulation and control of vasopressin secretion in healthy humans

1987 ◽  
Vol 253 (5) ◽  
pp. R671-R678 ◽  
Author(s):  
P. H. Baylis
Keyword(s):  
Luteal Phase ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Functional Characteristics ◽  
Vasopressin Release ◽  
Healthy Humans ◽  
Plasma Vasopressin ◽  
Individual Variations ◽  
Vasopressin Secretion ◽  
And Control

The functional characteristics of osmoregulated vasopressin secretion can be defined in terms of an osmotic threshold for its release and a sensitivity of the osmoreceptor and vasopressin-secreting unit. Osmotically stimulated thirst has features similar to osmoregulated vasopressin. There are wide individual variations in the functional characteristics of both thirst and vasopressin release in healthy humans, probably genetic in origin. The influence of aging appears to enhance the sensitivity of vasopressin secretion but blunt thirst appreciation. Yet in many physiological situations changes in osmoregulated vasopressin release and thirst occur in parallel. The fall in plasma osmolality associated with human pregnancy is accounted for entirely by a lowering of the osmotic thresholds for thirst and vasopressin release. Similar but less marked alterations accompany the ovulatory luteal phase of the menstrual cycle. A major nonosmotic stimulus to vasopressin secretion is hypotension and/or hypovolemia, mediated by high- (carotid sinus) and low- (left atrial) pressure receptors. Circulating catecholamines influence the release of vasopressin by alpha- and beta-adrenergic pathways. Drinking by hypertonic humans provides immediate reduction in thirst and vasopressin secretion probably mediated by pathways from the oropharynx. The modest but variable rise in plasma vasopressin in response to hypoglycemia appears to be due to cellular neuroglycopenia and is independent of parasympathetic pathways. Although osmotic and hemodynamic stimuli to vasopressin release do not act independently of each other, the precise subtle interactions between them and other nonosmotic stimuli remain to be clarified.

Fever alters osmosensitivity of hypothalamic–vasopressin system in the rat

1993 ◽  
Vol 71 (3-4) ◽  
pp. 222-226 ◽  
Author(s):  
Ruth A. Cridland ◽  
Norman W. Kasting
Keyword(s):  
Data Analysis ◽  
Linear Relationship ◽  
Hypertonic Saline ◽  
Urine Output ◽  
Bolus Injection ◽  
Plasma Osmolality ◽  
Lower Plasma ◽  
Vasopressin Release ◽  
Regression Slope ◽  
Plasma Vasopressin

The osmosensitivity of peripheral vasopressin release was studied during healthy thermoregulation and endotoxin-induced fever. There was an increase in osmosensitivity following bolus injection of saline in febrile rats. These animals displayed a steeper slope in the linear relationship between plasma osmolality and plasma vasopressin levels compared with afebrile animals. The change in regression slope was due to a significantly lower plasma osmolality in febrile rats. The plasma osmolality of animals infused with hypertonic saline was similarly decreased, but data analysis failed to show a significant change in the regression slope. Osmotic thresholds were not altered in either group. There was an increased urine output in febrile rats, and consequently these animals excreted greater amounts of salts than afebrile rats. This could account for the lower plasma osmolality observed in the febrile rat.Key words: endotoxin, fever, osmolality, vasopressin.

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