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.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Ventricular receptors stimulate vasopressin release during hemorrhage

1988 ◽  
Vol 254 (2) ◽  
pp. R204-R211 ◽  
Author(s):  
B. C. Wang ◽  
G. Flora-Ginter ◽  
R. J. Leadley ◽  
K. L. Goetz
Keyword(s):  
Left Atrial ◽  
Heart Rate Response ◽  
Venous Pressure ◽  
Control Level ◽  
Conscious Dogs ◽  
Central Venous ◽  
Vasopressin Release ◽  
Cardiac Denervation ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.

Effect of blood glucose concentration on osmoregulation in diabetes mellitus

1989 ◽  
Vol 256 (3) ◽  
pp. R597-R604 ◽  
Author(s):  
C. J. Thompson ◽  
S. N. Davis ◽  
P. H. Baylis
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Blood Glucose Concentration ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Plasma Sodium ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Insulin Dependent ◽  
Vasopressin Secretion

Poorly controlled insulin-dependent diabetes mellitus is associated with considerable elevations of plasma vasopressin concentrations, although well-controlled diabetics have normal osmoregulated thirst and vasopressin release. We studied the effect of blood glucose concentration on osmoregulated thirst and vasopressin secretion in insulin-dependent diabetes mellitus. Blood glucose was maintained overnight, and for the duration of the study, in either the euglycemic (4-5 mmol/l) or hyperglycemic (10-12 mmol/l) range, and patients underwent infusion of hypertonic (855 mmol/l) sodium chloride solution. Plasma sodium was lower during the hyperglycemic study, but elevation in plasma sodium concentration by infusion of saline caused progressive linear increases in both thirst and plasma vasopressin concentrations in both studies. Linear regression analysis defined lowered plasma sodium thresholds for both thirst appreciation and vasopressin release during the hyperglycemic study, although the sensitivity of the osmoreceptors remained unchanged. Analysis of the data in terms of plasma osmolality, corrected for the increase in blood glucose in the hyperglycemic study, revealed no differences in the osmotic thresholds for thirst or vasopressin release; sensitivity of the osmoreceptors also remained the same. Drinking abolished thirst and lowered plasma vasopressin concentrations before major changes in plasma sodium were observed. These results show that insulin-dependent diabetic patients osmoregulate appropriately when moderately hyperglycemic but that the threshold plasma sodium for vasopressin secretion and thirst appreciation is lowered by an unknown mechanism.

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

Central cholinergic control of vasopressin release in conscious rats

1986 ◽  
Vol 251 (2) ◽  
pp. E146-E150 ◽  
Author(s):  
K. Iitake ◽  
L. Share ◽  
Y. Ouchi ◽  
J. T. Crofton ◽  
D. P. Brooks
Keyword(s):  
Blood Pressure ◽  
Muscarinic Receptors ◽  
Dependent Manner ◽  
Conscious Rat ◽  
Vasopressin Release ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Dose Dependent ◽  
Stimulation Of

Intracerebroventricular (icv) administration of carbachol into conscious rats evoked a substantial increase in vasopressin secretion and blood pressure in a dose-dependent manner. These effects were blocked by pretreatment with the muscarinic blocker, atropine (10 micrograms icv), but not by the nicotinic blocker, hexamethonium (10 micrograms icv). Hexamethonium did, however, block the increase in blood pressure, the decrease in heart rate, and the very small elevation in the plasma vasopressin concentration induced by nicotine (10 micrograms icv). These results indicate that stimulation of either central nicotinic or muscarinic receptors can affect the cardiovascular system and suggest that the cholinergic stimulation of vasopressin secretion may involve primarily muscarinic receptors in the conscious rat.

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.

Angiotensin II-induced thirst and vasopressin release in man

1985 ◽  
Vol 68 (6) ◽  
pp. 669-674 ◽  
Author(s):  
P. A. Phillips ◽  
B. J. Rolls ◽  
J. G. G. Ledingham ◽  
J. J. Morton ◽  
M. L. Forsling
Keyword(s):  
Angiotensin Ii ◽  
Water Deprivation ◽  
Vasopressin Release ◽  
Physiological Conditions ◽  
Physiological Range ◽  
Pathological Conditions ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin ◽  
Vasopressin Secretion ◽  
Single Blind

1. The thirst and plasma vasopressin responses to single-blind controlled intravenous angiotensin II infusions (2-16 ng min−1 kg−1) were investigated in ten healthy young men. 2. Thirst and vasopressin secretion were stimulated in four out of ten subjects. These effects occurred at plasma angiotensin concentrations well above those measured under physiological conditions associated with thirst and vasopressin secretion such as water deprivation. 3. Further studies are needed to define why only certain individuals respond to intravenous angiotensin II infusions and to determine whether potentiation of angiotensin-induced thirst and vasopressin secretion by other stimuli (e.g. hypovolaemia and hypertonicity) might occur in man, in particular under pathological conditions when plasma angiotensin levels are above the physiological range.

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.

scholarly journals Plasma Vasopressin Response to Hypertonic Saline Infusion to Assess Posterior Pituitary Function

1980 ◽  
Vol 73 (4) ◽  
pp. 255-260 ◽  
Author(s):  
P H Baylis ◽  
G L Robertson
Keyword(s):  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Strong Positive Correlation ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Plasma Arginine ◽  
Cranial Diabetes Insipidus ◽  
Hypertonic Saline Infusion

Hypertonic saline was infused into 11 volunteers to osmotically stimulate vasopressin secretion. A strong positive correlation between plasma arginine vasopressin (PAVP) and plasma osmolality (Pos) was obtained, defined by the function PAVP = 0.63 (Pos – 284), r = +0.80, P < 0.001. The sensitivity of vasopressin secretion to osmotic stimulation was represented by the slope of the expression and the theoretical threshold of vasopressin release by the abscissal intercept. Plasma osmolality at the onset of thirst was 298.5 ± 1.1 mmol/kg. Application of hypertonic saline infusion to 10 polyuric patients clearly separated those with normal osmoregulation of vasopressin secretion from those with cranial diabetes insipidus.

Central indomethacin enhances volume-dependent vasopressin release

1984 ◽  
Vol 247 (6) ◽  
pp. R1017-R1021
Author(s):  
D. P. Brooks ◽  
L. Share ◽  
J. T. Crofton ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E2 ◽  
Mean Arterial Blood Pressure ◽  
Inhibitory Effect ◽  
Volume Depletion ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Severe Hemorrhage ◽  
Vasopressin Secretion

The effect of centrally administered indomethacin on hemorrhage-induced vasopressin release was studied in the morphine-sedated, urethan/chloralose-anesthetized dog. Ventriculocisternal perfusion of indomethacin 1) significantly reduced the amount of prostaglandin E2 in the effluent from the cisterna magna, 2) significantly enhanced the vasopressin response to volume depletion, and led to a greater fall in mean arterial blood pressure during severe hemorrhage. The results suggest that central prostaglandins may have an inhibitory effect on vasopressin secretion during volume depletion.

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