An inhibitor of leukotriene synthesis affects vasopressin secretion following osmotic stimulus in rats

1. The release of arginine vasopressin (AVP) after an osmotic stimulus and head-up tilt was assessed in diabetic subjects with and without autonomic neuropathy 2. Six diabetic subjects with (DAN +ve) and five without (DAN − ve) evidence of autonomic neuropathy and five normal subjects were infused with 5% (w/v) NaCl at a rate of 0.05 ml min−1 kg−1 body weight for 120 min. Blood pressure, heart rate and plasma AVP were measured over this period 3. Seven DAN +ve, six DAN −ve and six normal subjects were tilted head-up to 45° for 120 min. Blood pressure, heart rate and plasma AVP were measured during the study 4. Infusion of 5% (w/v) NaCl produced appropriate rises in plasma osmolality and plasma AVP levels which did not differ between the three groups, confirming the normal osmotic release of AVP in the diabetic subjects 5. During head-up tilt, there were no differences in AVP responses between the three groups, despite a major hypotensive stimulus in the DAN + ve group 6. We conclude that osmotic release of AVP is normal in diabetes, but that cardiovascular release of AVP is impaired in diabetic subjects with cardiovascular reflex evidence of autonomic neuropathy, reflecting an afferent defect.

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Regulation of drinking and vasopressin secretion: role of organum vasculosum laminae terminalis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.253.1.r108 ◽

1987 ◽

Vol 253 (1) ◽

pp. R108-R120 ◽

Cited By ~ 19

Author(s):

T. N. Thrasher ◽

L. C. Keil

Keyword(s):

Conscious Dogs ◽

Ang Ii ◽

Cellular Dehydration ◽

Organum Vasculosum Laminae Terminalis ◽

Before And After ◽

Electrolytic Ablation ◽

Vasopressin Secretion ◽

Osmotic Stimulus ◽

Organum Vasculosum

We have proposed that the organum vasculosum laminae terminalis (OVLT) contains osmoreceptors involved in the regulation of drinking and secretion of arginine vasopressin (AVP) in the dog. By use of the technique of electrolytic ablation, conscious dogs were evaluated for their responses to acute peripheral challenges of hypertonic NaCl and angiotensin II (ANG II) and hemorrhage (20 ml/kg) before and after destruction of the OVLT (n = 7) or adjacent tissue (n = 9) as a control. Lesions confined to the tip of the optic recess and destroying greater than 90% of the OVLT caused a dramatic increase in the threshold to drink and increase plasma AVP levels and a significant (P less than 0.01) reduction in the magnitude of these responses to an osmotic stimulus. Drinking and secretion of AVP in response to ANG II, but not the rise in peripheral corticosteroids, were also blocked (P less than 0.01) by ablation of the OVLT. In contrast responses to hemorrhage were not affected by the lesion. These results support the hypothesis that the OVLT contains osmoreceptors involved in physiological responses to cellular dehydration and suggest involvement in drinking and secretion of AVP in response to ANG II. The results also indicate that forebrain mechanisms which depend on the OVLT are independent of mechanisms responding to hemorrhage in conscious dogs.

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Adaptive resetting of the volume control of vasopressin secretion during sustained hypovolemia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.268.2.r349 ◽

1995 ◽

Vol 268 (2) ◽

pp. R349-R357 ◽

Cited By ~ 3

Author(s):

Y. Iwasaki ◽

M. B. Gaskill ◽

G. L. Robertson

Keyword(s):

Control Mechanism ◽

Diuretic Therapy ◽

Volume Control ◽

Plasma Sodium ◽

Plasma Vasopressin ◽

Plasma Electrolytes ◽

Vasopressin Secretion ◽

Osmotic Stimulus ◽

Relationship Of ◽

The Relationship

To determine the effect of sustained hypovolemia on vasopressin secretion, we studied rats after 1-32 h of diuretic therapy. We found that an injection of furosemide (10 mg/kg) produced a transient marked increase in urine output, a moderate 7-10% reduction in blood volume, and a three- to fourfold rise in plasma vasopressin from 1.6 +/- 0.2 to 5.6 +/- 1.0 pmol/l. When the hypovolemia was maintained by repeated injections of the diuretic, plasma vasopressin remained elevated for > or = 8 h but returned almost to normal by 32 h, even though plasma electrolytes, blood pressure, hematocrit, and the other measures of hypovolemia were unchanged. At this time, pituitary vasopressin was undiminished, and plasma vasopressin rose normally or even supranormally when an acute hypovolemic or osmotic stimulus (intraperitoneal polyethylene glycol or hypertonic saline) was superimposed. However, the lines describing the relationship of log plasma vasopressin to plasma volume and plasma sodium in the rats treated with furosemide for 32 h lay to the left of the same relationships in the rats treated for 8 h or the sham-treated controls. We conclude that, in rats, the vasopressin response to sustained hypovolemia persists for > or = 8 h but is markedly diminished by 32 h. The decline in plasma vasopressin during this interval appears to be due to adaptive resetting of the volume control mechanism.

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Central indomethacin enhances volume-dependent vasopressin release

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1984.247.6.r1017 ◽

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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LESIONS OF THE ORGANUM VASCULOSUM OF THE LAMINA TERMINALIS (OVLT) ATTENUATE OSMOTICALLY-INDUCED DRINKING AND VASOPRESSIN SECRETION IN THE DOG

Endocrinology ◽

10.1210/endo-110-5-1837 ◽

1982 ◽

Vol 110 (5) ◽

pp. 1837-1839 ◽

Cited By ~ 177

Author(s):

TERRY N. THRASHER ◽

LANNY C. KEIL ◽

DAVID J. RAMSAY

Keyword(s):

Lamina Terminalis ◽

Vasopressin Secretion ◽

Organum Vasculosum

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Norepinephrine regulates arginine vasopressin secretion in hypothalamic paraventricular nucleus relating with pain modulation

Neuropeptides ◽

10.1016/j.npep.2009.06.003 ◽

2009 ◽

Vol 43 (4) ◽

pp. 259-265 ◽

Cited By ~ 5

Author(s):

Jun Yang ◽

Hui-Feng Yuan ◽

Wen-Yan Liu ◽

Xiao-Xia Zhang ◽

Jian-Peng Feng ◽

...

Keyword(s):

Paraventricular Nucleus ◽

Arginine Vasopressin ◽

Pain Modulation ◽

Hypothalamic Paraventricular Nucleus ◽

Vasopressin Secretion

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Reproducibility of osmotic and nonosmotic tests of vasopressin secretion in men

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.260.3.r533 ◽

1991 ◽

Vol 260 (3) ◽

pp. R533-R539 ◽

Cited By ~ 5

Author(s):

C. J. Thompson ◽

P. Selby ◽

P. H. Baylis

Keyword(s):

Blood Glucose ◽

Linear Regression ◽

Hypertonic Saline ◽

Linear Regression Analysis ◽

Plasma Osmolality ◽

Saline Infusion ◽

Intraindividual Variation ◽

Insulin Tolerance ◽

Vasopressin Secretion ◽

Hypertonic Saline Infusion

We have studied the reproducibility of the thirst and arginine vasopressin (AVP) responses to osmotic and hypoglycemic stimulation in healthy volunteers undergoing repeat hypertonic (855 mmol/l) saline infusion and insulin tolerance tests (ITTs). Hypertonic saline infusion caused similar mean rises in plasma osmolality, AVP, and thirst on each occasion. Linear-regression analysis defined close relationships between the slopes (r = +0.72, P less than 0.05) and the abscissal intercepts (r = +0.89, P less than 0.001) of the regression lines relating plasma osmolality (Posmol) and plasma AVP (PAVP), and the group intraindividual component of the variance for the slopes and intercepts was 7 and 0.6%, respectively. There were close correlations between the slopes (r = +0.79, P less than 0.02) and the intercepts (r = +0.84, P less than 0.01) of the regression lines relating Posmol and thirst, and group intraindividual component of the variance was 14 and 0.7%, respectively. Hypertonic saline infusion was infused on four occasions in four subjects, and the results showed that the linear regression lines relating PAVP and Posmol and thirst and Posmol were reproducible within an individual. There were similar falls in blood glucose and elevations in PAVP in both ITTs. No relationship was defined between the fall in blood glucose and either the rise in PAVP or the area under the AVP curve (AUC). The intraindividual component of the variance for the rise in AVP and the AUC was 77 and 22.5%, respectively. The AVP and thirst responses to osmotic stimulation are highly reproducible, but there is considerable intraindividual variation in the AVP response to hypoglycemia.

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