Effect of TRH on Plasma Arginine Vasopressin

Jawadi, Husain; Ho, Lydia; DeJong, David C.

doi:10.1159/000179872

Cited by 13 publications

(5 citation statements)

References 11 publications

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“…In addition, the plasma EAP levels showed significant correlation with free T4 and AVP levels. The lower basal AVP levels in our hypothyroid patients are different from previous reports (17,18); however, the reason for the discrepancy may be due to patient selection in which patients with severe hypothyroidism were studied in contrast to our group of hypothyroid patients.…”

Section: Discussioncontrasting

confidence: 99%

Arginine-vasopressin and endothelium-associated proteins in thyroid disease

Awidi²,

Am³

et al. 1992

Acta Endocrinologica

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endothelium-associated proteins in thyroid disease. Acta Endocrinol 1992;126:399-403. Plasma concentrations of endothelium-derived proteins (fibronectin and von Willebrand factor), liver synthesized proteins (haptoglobin, transferrin, ceruloplasmin, \g=a\1-antitrypsin, antithrombin III and factor VIII-coagulant) and plasma arginine-vasopressin (AVP) were measured in 12 hyperthyroid, 9 hypothyroid and 1 5 age-and sex-matched normal controls. In hyperthyroid patients the plasma concentrations of AVP and endothelium-associated proteins (EAP) were significantly higher than in the control group (p <0.05 and p <0.01 respectively). Rendering hyperthyroid patients into the euthyroid state significantly lowered AVP (p<0.01), fibronectin (p<0.05) and von Willebrand factor (p<0.01) compared with pretreatment levels. Hypothyroid patients were studied at diagnosis and after replacement therapy with levothyroxine. Compared with pretreatment values, significant increases were noted in plasma concentrations of von Willebrand factor, fibronectin and AVP (p<0.01). With the exception of factor VIII-coagulant, the concentrations of hepatic synthesized proteins did not deviate from normal values in hyperthyroid and hypothyroid patients. Significant correlations were found beween serum-free thyroxine on the one hand and the plasma concentrations of fibronectin (p<0.005), von Willebrand factor (p<0.001) and AVP (p<0.0001). Similarly, there was significant correlation between the plasma concentrations of AVP on the one hand and fibronectin (p <0.002) and von Willebrand factor (p<0.01). The results demonstrate elevated plasma levels of AVP in hyperthyroid patients and an increase during levothyroxine treatment of hypothyroid patients. The increase in EAP (fibronectin and von Willebrand factor) was dependent on thyroid hormone, and correlated with the increase in the plasma AVP concentrations. The mechanism(s) underlying the interrelation between AVP, EAP and thyroid hormones is (are) yet to be defined.Endothelial cells are metabolically active tissue (1, 2) known to synthesize and release a variety of proteins, such as tissue-plasminogen activator, fibronectin and von Willebrand factor, which are involved in blood coagulation and the fibrinolytic process. Alterations in components of both the fibrinolytic enzyme system and the coagulation mechanism have been reported in both hyper-and hypothyroidism, and include in hyperthyroid patients a rise in von Willebrand factor (3), fibronectin (1,4) and tissue-plasminogen activator (1, 5).The mechanism responsible for the hyperthyroidismassociated increase in endothelially synthesized proteins, i.e. endothelium-associated proteins (EAP) including fibronectin and von Willebrand factor, remains unknown. A jS-adrenergic mechanism has been pro¬ posed as a mediator for the increase of EAP in hyperthyroidism. However, the increase of EAP was not prevented by ß-blocker agents, suggesting that a mechanism(s) other than the ß-adrenergic system is respon¬ sible for the elevation of EAP in hyperthyroidism ...

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Section: Discussioncontrasting

confidence: 99%

Arginine-vasopressin and endothelium-associated proteins in thyroid disease

Awidi²,

Am³

et al. 1992

Acta Endocrinologica

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“…The release ofTSH by AVP provides an explanation for the observation that TRH can stimulate AVP release in vivo in humans (24) and rabbits (25) and in vitro from hypothalamic tissue (26) by suggesting that endogenous TRH not only produces TSH release by direct pituitary action, but also by stimulation of AVP secretion to achieve TSH release. In addition, AVP is normally present in hy-SCIENCE, VOL.…”

Section: Utes Perifused Cells Werementioning

confidence: 99%

“…19 27. Note that water reabsorption in the rat initial collecting duct and connecting segment is driven by extremely large transepithelial osmotic gradicnts (24) and that the ratio o basolateral to apica surface areas in principal and connecting cels of these segments ranges between 10 Although hypothyroidism (with concomitant increased levels of thyroid-stimulating hormone) has been associated with elevated plasma vasopressin, the role that vasopressin plays in controlling thyroid-stimulating hormone secretion from the adenohypophysis is not understood. In two in vitro pituitary cell systems, vasopressin caused a specific and dose-related release of thyroid-stimulating hormone from cells that was equal in potency to that elicited by thyrotropin-releasing hormone, the primary acknowledged regulator of thyroid-stimulating hormone release.…”

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confidence: 99%

Arginine Vasopressin as a Thyrotropin-Releasing Hormone

Lumpkin

Samson

McCann

1987

Science

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Although hypothyroidism (with concomitant increased levels of thyroid-stimulating hormone) has been associated with elevated plasma vasopressin, the role that vasopressin plays in controlling thyroid-stimulating hormone secretion from the adenohypophysis is not understood. In two in vitro pituitary cell systems, vasopressin caused a specific and dose-related release of thyroid-stimulating hormone from cells that was equal in potency to that elicited by thyrotropin-releasing hormone, the primary acknowledged regulator of thyroid-stimulating hormone release. When injected into the hypothalamus, however, vasopressin specifically inhibited the release of thyroid-stimulating hormone. Thus, vasopressin may exert differential regulatory effects on thyroid-stimulating hormone secretion in the hypothalamus and pituitary gland.

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“…The administration of thyrotropin-releasing hormone (TRH) reportedly stimulates the release of vasopressin in hypothyroid subjects [24], though another study failed to confirm this finding [22]. A high plasma level of TRH in hypothyroidism may play a role in disturbing the regulation of vasopressin secretion.…”

Section: Discussionmentioning

confidence: 99%

Impaired Water Excretion in a Hyponatremic Patient following Thyroidectomy: Causal Role of Glucocorticoid Deficiency

Yonemura

Furuya²,

Osuga³

et al. 1998

Mineral Electrolyte Metab

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We evaluated the causal role of glucocorticoid deficiency in the hyponatremia that developed in a 57-year-old Japanese man with hypothyroidism following the performance of a total thyroidectomy for laryngeal cancer. The plasma concentration of vasopressin (1.78 pg/ml) was not suppressed in the presence of hyponatremia (125 mEq/l). The urinary excretion of sodium was increased, and the plasma renin activity and plasma aldosterone concentration were suppressed. The infusion of hypertonic saline increased the plasma osmolality, but not the plasma concentration of vasopressin. An oral water load (20 ml/kg of body weight) did not suppress the plasma vasopressin level or induce diuresis. Pretreatment with hydrocortisone normalized the response of plasma vasopressin to the water load was well as the diuretic response during the hypothyroid state. The urinary exretion of 17-hydroxycorticosteroids was below normal in the hypothyroid state in the face of normal serum cortisol concentration. The correction of the hypothyroidism returned these abnormalities to normal. A disturbed metabolism of glucocorticoid may have been responsible for the hyponatremia and disturbance in plasma vasopressin regulation observed in this hypothyroid patient.

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Effect of TRH on Plasma Arginine Vasopressin

Cited by 13 publications

References 11 publications

Arginine-vasopressin and endothelium-associated proteins in thyroid disease

Arginine-vasopressin and endothelium-associated proteins in thyroid disease

Arginine Vasopressin as a Thyrotropin-Releasing Hormone

Impaired Water Excretion in a Hyponatremic Patient following Thyroidectomy: Causal Role of Glucocorticoid Deficiency

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