The influence of reproductive status on vasopressin release in the rat

1991 ◽  
Vol 130 (3) ◽  
pp. 387-393 ◽  
Author(s):  
M. L. Forsling ◽  
H. Kelestimur ◽  
R. Windle
Keyword(s):  
Polyethylene Glycol ◽  
Fluid Balance ◽  
Ovarian Function ◽  
Extracellular Fluid ◽  
Hormone Release ◽  
Vasopressin Release ◽  
Ovarian Steroids ◽  
Plasma Vasopressin ◽  
Long Acting ◽  
Lh Releasing Hormone

ABSTRACT It has been shown that surgical ovariectomy of the rat results in a fall in plasma vasopressin concentrations suggesting that ovarian steroids may influence hormone release. To determine whether a similar fall is found on suppression of the oestrous cycle, vasopressin concentrations were monitored after treatment with the antioestrogen preparation tamoxifen or a long-acting analogue of LH-releasing hormone (LHRH) which suppresses ovarian function. Treatment with either agent was found to result in a fall in circulating vasopressin concentrations, with little effect on fluid balance. To determine whether the ovary could influence the vasopressin release in response to known stimuli, hormone concentrations were measured in ovariectomized animals during extracellular fluid hypertonicity produced by an i.p. injection of hypertonic saline and hypovolaemia produced by an i.p. injection of polyethylene glycol. It was found that after ovariectomy or treatment with tamoxifen, the response to hypertonicity was unaffected but that to hypovolaemia was attenuated. Treatment with LHRH affected the response to both hypovolaemia and hypertonicity. Journal of Endocrinology (1991) 130, 387–393

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

Effect of ovarian steroids on vasopressin secretion

1982 ◽  
Vol 95 (1) ◽  
pp. 147-151 ◽  
Author(s):  
Mary L. Forsling ◽  
P. Strömberg ◽  
M. Åkerlund
Keyword(s):  
Postmenopausal Women ◽  
Vasopressin Release ◽  
Ovarian Steroids ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Menstruating Women ◽  
Plasma Oestradiol

In normally menstruating women plasma vasopressin concentrations vary with the stage of the cycle and are highest at the time of ovulation and lowest at the onset of menstruation. To determine whether this is the result of changes in the circulating concentrations of ovarian steroids, vasopressin concentrations were determined in six postmenopausal women given oestrogen and progestogen. An increase in plasma oestradiol concentrations to 299 ± 97·8 pmol/l augmented vasopressin release. Administration of medroxyprogesterone did not influence vasopressin concentrations but when given in combination with oestrogen a fall was observed. Thus it appears that ovarian steroids can modulate vasopressin release.

A comparison of the vasopressin response of rats to intraperitoneal and intravenous administration of hypertonic saline, and the effect of opioid and aminergic antagonists

1988 ◽  
Vol 116 (2) ◽  
pp. 217-224 ◽  
Author(s):  
M. L. Forsling ◽  
C. Matziari ◽  
L. Aziz
Keyword(s):  
Sodium Chloride ◽  
Hypertonic Saline ◽  
Intravenous Administration ◽  
Opioid Peptides ◽  
Plasma Osmolality ◽  
Inhibitory Effect ◽  
Hormone Release ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Osmotic Response

ABSTRACT The vasopressin response of rats to i.p. injection of hypertonic sodium chloride (1·5 mol/l) was compared with that following i.v. infusion of 1·05 mol sodium chloride/l. The two regimes produced a similar vasopressin response in terms of the osmotic threshold, although the slopes of the plot of plasma vasopressin levels against plasma osmolality were not identical. Pretreatment with naloxone and levallorphan increased the resting vasopressin levels and effectively potentiated vasopressin release in response to hypertonic saline by reducing the osmotic threshold for hormone release. Thus, opioid peptides appear to exert an inhibitory effect on vasopressin release under resting and stimulated conditions. The adrenoreceptor antagonists propanolol, phenyoxybenzamine and phentolamine produced a fall in resting vasopressin concentrations while propanolol and phenoxybenzamine potentiated the osmotic release of vasopressin in association with a fall in the osmotic threshold. This would suggest that noradrenergic pathways are excitatory at rest while having an inhibitory effect on the osmotic response. Metoclopramide also produced a fall in resting plasma vasopressin concentrations while increasing the osmotic response. In contrast haloperidol did not affect the vasopressin response. J. Endocr. (1988) 116, 217–224

scholarly journals Vasopressin at Central Levels and Consequences of Dehydration

2016 ◽  
Vol 68 (Suppl. 2) ◽  
pp. 19-23 ◽  
Author(s):  
Daniel G. Bichet
Keyword(s):  
Animal Studies ◽  
Transient Receptor Potential ◽  
Animal Experiments ◽  
Extracellular Fluid ◽  
Receptor Potential ◽  
Circumventricular Organ ◽  
Thermal Perception ◽  
Trpv1 Channel ◽  
Vasopressin Release ◽  
Transient Receptor

Disorders of water balance are a common feature of clinical practice. An understanding of the physiology and pathophysiology of central vasopressin release and perception of thirst is the key to diagnosis and management of these disorders. Mammals are osmoregulators; they have evolved mechanisms that maintain extracellular fluid osmolality near a stable value, and, in animal studies, osmoregulatory neurons express a truncated delta-N variant of the transient receptor potential vannilloid (TRPV1) channel involved in hypertonicity and thermal perception while systemic hypotonicity might be perceived by TRPV4 channels. Recent cellular and optogenetic animal experiments demonstrate that, in addition to the multifactorial process of excretion, circumventricular organ sensors reacting to osmotic pressure and angiotensin II, subserve genesis of thirst, volume regulation and behavioral effects of thirst avoidance.

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.

Electrolytes and Fluid balance

2011 ◽  
pp. 153-163
Keyword(s):  
Adult Male ◽  
Fluid Balance ◽  
Extracellular Fluid ◽  
Intracellular Fluid ◽  
Total Body

Electrolytes: introduction 154 Sodium 154 Potassium 158 Chloride 161 Fluid balance 162 The monovalent electrolytes are Sodium (Na), Chlorine (Cl), and Potassium (K). An adult male (70 kg) has total body Na of 4 mol (92 g); 2000 mmol is in extracellular fluid (ECF), 1500 mmol in bone, and 500 mmol in intracellular fluid (ICF)....

ACTH-elicited sodium appetite in sheep

1980 ◽  
Vol 239 (1) ◽  
pp. E45-E50 ◽  
Author(s):  
R. S. Weisinger ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
J. S. Fan ◽  
S. Hatzikostas ◽  
...  
Keyword(s):  
Steroid Hormones ◽  
Steroid Hormone ◽  
Extracellular Fluid ◽  
Blood Levels ◽  
Adrenal Steroid ◽  
Sodium Appetite ◽  
Intramuscular Injections ◽  
Acth Treatment ◽  
Long Acting

Intramuscular injections of long-acting synthetic ACTH (45 U twice daily for 5 days) caused a large increase in the intake of 0.5 M NaCl in sheep. Mean Na intake of the sheep on the last 3 days of treatment approximated 50% of their total extracellular fluid Na. The mineral appetite was specific for NaCl. Intakes of 0.5 M KCl or 0.25 M CaCl2 were not significantly altered. The enhanced appetite for Na induced by ACTH appeared to precede any increase in urinary Na excretion. ACTH treatment was ineffective in adrenalectomized sheep. However, an infusion into adrenalectomized sheep of a combination of adrenal steroid hormones (including aldosterone, deoxycorticosterone, 11-deoxycortisol, cortisol, and corticosterone) that contrived blood levels similar to those, obtained with ACTH treatment in normal sheep did induce Na appetite. Thus, ACTH induces a specific, adrenal-steroid hormone-dependent Na appetite in sheep.

Anti-calmodulin agents affect osmotic and angiotensin II-induced vasopressin release

1989 ◽  
Vol 256 (4) ◽  
pp. E516-E523 ◽  
Author(s):  
N. F. Rossi ◽  
R. W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Calcium Ions ◽  
Calcium Influx ◽  
Alternative Mechanism ◽  
Hormone Release ◽  
Ang Ii ◽  
Vasopressin Release ◽  
Blocking Effects ◽  
Osmotic Stimulation ◽  
Crucial Part

Calcium ions and particularly calcium influx play a crucial part in initiating the intracellular events that result in arginine vasopressin (AVP) release to both osmotic and nonosmotic stimuli. Calmodulin appears to modulate the effects of calcium on synaptic transmission and hormone release in other systems. This study tested the effects of three distinct classes of anti-calmodulin agents on the release of AVP to either a rise in osmolality of 20 mosmol/kg water or to 1 X 10(-5) angiotensin II (ANG II) in cultured hypothalamo-neurohypophysical complexes. Micromolar concentrations of R 24571, the active naphthalenesulfonamides, W 7 and W 13, and trifluoperazine (TFP) inhibited AVP release to osmotic stimulation. In contrast, W 5, a severalfold less active anti-calmodulin agent, had no effect on osmotically stimulated AVP release. The active naphthalenesulfonamides, but not R 24571 or TFP, blocked release of AVP to ANG II. In contrast, neither R 24571 nor TFP inhibited AVP release to ANG II stimulation. Collectively, the data demonstrated a dissociation between inhibition of AVP release and the anti-calmodulin properties of the drugs, thereby suggesting that nonspecific actions masked the calmodulin-blocking effects of the drugs or that the inhibition occurred by some alternative mechanism(s).

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