Vasopressin Analogue DDAVP in Diabetes Insipidus: Clinical and Laboratory Studies

Edwards, C. R. W.; Kitau, M. J.; Chard, Tim; Besser, G. M.

doi:10.1136/bmj.3.5876.375

Cited by 131 publications

(44 citation statements)

References 11 publications

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“…The results of the present study are consistent with earlier observations that a single intranasal administration of DDAVP resulted in a prompt and persistent antidiuresis in patients with diabetes insipidus (Vavra et al, 1969;Anderson and Amer, 1972;Edwards et al, 1973;Robinson, 1976;Seif et al, 1978). The effect appeared within the first hr and lasted for at least 6 hr in all of the patients studied.…”

Section: Discussionsupporting

confidence: 93%

“…Previous studies have shown that intranasal administration of this analogue possesses several advantages over other types of therapies (Vavra et al, 1969 ;Anderson and Arner, 1972 ;Edwards et al, 1973 ;Robinson, 1976 ;Seif et al, 1978). These include its convenience, a longer duration of action and less pressor activity (Anderson and Arner, 1972) compared with any other commercial preparation of vasopressin.…”

Section: Ddavpmentioning

confidence: 99%

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Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): Correlation to its plasma levels and nephrogenous cyclic AMP production.

Katayama¹,

Itabashi²,

Yamaji³

1980

Endocrinol Japon

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Section: Discussionsupporting

confidence: 93%

Section: Ddavpmentioning

confidence: 99%

Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): Correlation to its plasma levels and nephrogenous cyclic AMP production.

Katayama¹,

Itabashi²,

Yamaji³

1980

Endocrinol Japon

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“…In the first experiment, we administered desmopressin (dDAVP), a longacting analog of AVP (13), to the FNDI mouse model to decrease AVP synthesis, and examined possible changes in the phenotype. In the second experiment, we examined whether the excess in Na intake might accelerate the phenotype in the FNDI mice model, as it was demonstrated that the Na intake stimulated AVP release (12,42).…”

mentioning

confidence: 99%

Activation of vasopressin neurons leads to phenotype progression in a mouse model for familial neurohypophysial diabetes insipidus

Hiroi

Morishita

Hayashi

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Familial neurohypophysial diabetes insipidus (FNDI) is a rare disease that is inherited in an autosomal dominant manner. In a previous study, we made a mouse model for FNDI, which showed progressive polyuria accompanied by inclusion bodies in the arginine vasopressin (AVP) neurons formed by aggregates in the endoplasmic reticulum. The present study was conducted to determine whether the activities of AVP neurons are related to the phenotype progression in the FNDI model. In the first experiment, female heterozygous mice were administered either desmopressin (dDAVP) or a vehicle (control) subcutaneously with osmotic minipumps for 30 days. The dDAVP treatment significantly decreased the urine volume, AVP mRNA expression, and inclusion bodies in the AVP neurons. Urine volume in the dDAVP group remained significantly less than the control for 14 days even after the minipumps were removed. In the second experiment, the males were fed either a 0.2% Na or 2.0% Na diet for 6 mo. Urine AVP excretion was significantly increased in the 2.0% Na group compared with the 0.2% Na group for the first 2 mo but gradually decreased thereafter. Throughout the experiments, urine volume increased progressively in the 2.0% Na group but not in the 0.2% Na group. Immunohistochemical analyses revealed that inclusion bodies in the AVP cells had significantly increased in the 2.0% Na compared with the 0.2% Na group. These data demonstrated that activation of AVP neurons could accelerate the aggregate formation as well as the progression of the polyuria in the FNDI model mice.hereditary disease; aggregates ARGININE VASOPRESSIN (AVP), an antidiuretic hormone, is synthesized in the magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus of the hypothalamus (2, 36). The synthesis, as well as the release of AVP, is stimulated by increases in plasma osmolality and decreases in blood volume (blood pressure) (2, 36). The process from synthesis to release includes transcription, translation of the mRNA, folding of the precursor within the endoplasmic reticulum (ER), cleavage of the precursors during axonal transport, and release of AVP into the circulation (6).AVP plays a pivotal role in the homeostasis of water balance, and a deficiency of AVP leads to diabetes insipidus (DI) characterized by polyuria (22). Familial neurohypophysial DI (FNDI) is a rare autosomal dominant disorder (23). More than 50 point mutations in FNDI have been reported in the AVP gene so far, with most mutations existing in the domain of neurophysin II (NPII) (11), which functions as a carrier protein of AVP (36). While mechanisms underlying progressive polyuria in FNDI have not yet been fully elucidated, we demonstrated recently (15) that aggregates had progressively accumulated in the ER of AVP neurons in parallel with the progressive polyuria in mice possessing a point mutation (Cys98stop) in the NPII gene, which causes FNDI in humans (26). These data suggest that the accumulations of aggregates in ER that were probably derived from AVP precursors ...

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“…Of the synthetic preparations, LVP administered as a nasal spray is now in widespread use. More recently, synthetic analogues of vasopressin with prolonged action have been described ; these include tri-glycyl vasopressin (TGLVP) (Kyncl & Rudinger, 1970;Pliska et al, 1973) and l-desamino-8-Darginine vasopressin (DDAVP) (Vavra et al, 1968;Edwards et al, 1973). The latter has a prolonged half-life in the circulation (see Fig.…”

Section: Diabetes Insipidusmentioning

confidence: 99%

The Posterior Pituitary Gland

Chard

1975

Clinical Endocrinology

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Vasopressin Analogue DDAVP in Diabetes Insipidus: Clinical and Laboratory Studies

Cited by 131 publications

References 11 publications

Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): Correlation to its plasma levels and nephrogenous cyclic AMP production.

Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): Correlation to its plasma levels and nephrogenous cyclic AMP production.

Activation of vasopressin neurons leads to phenotype progression in a mouse model for familial neurohypophysial diabetes insipidus

The Posterior Pituitary Gland

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