Modern Approach in Treatment of Diabetes Insipidus

Kapić, Elvedina; Bečić, Fahir; Todić, Maida

doi:10.17305/bjbms.2005.3282

Cited by 3 publications

(3 citation statements)

References 16 publications

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“…The possible expression and function of putative VRs variants have not been clarified here, nevertheless, in the present study, we report that HCT8 cells express functional V1a and V2 receptors which are sensitive to the action of dDAVP. dDAVP is a stable analog of vasopressin and it is widely applied clinically to treat bleeding disorders, nocturnal polyuria, and central diabetes insipidus due to the antidiuretic properties mediated by the V2R (Mannucci, 1997;Kapić et al, 2005;Weiss and Everaert, 2019). However, affinity binding assays showed that dDAVP exhibits differences in the affinity binding across species (Chini and Manning, 2007).…”

Section: Discussionmentioning

confidence: 99%

dDAVP Downregulates the AQP3-Mediated Glycerol Transport via V1aR in Human Colon HCT8 Cells

Centrone

D’Agostino

Ranieri

et al. 2022

Front. Cell Dev. Biol.

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Vasopressin (AVP) plays a key function in controlling body water and salt balance through the activation of the vasopressin receptors V1aR and V2R. Abnormal secretion of AVP can cause the syndrome of inappropriate antidiuresis that leads to hyponatremia, which is an electrolyte disorder often observed in the elderly hospitalized and oncologic patients. Beyond kidneys, the colonic epithelium modulates water and salt homeostasis. The water channel AQP3, expressed in villus epithelial cells is implicated in water absorption across human colonic surface cells. Here, the action of dDAVP, a stable vasopressin analog, was evaluated on the AQP3 expression and function using human colon HCT8 cells as an experimental model. Confocal and Western Blotting analysis revealed that HCT8 cells express both V1aR and V2R. Long-term (72 h) treatment with dDAVP reduced glycerol uptake and cell viability. These effects were prevented by SR49059, a synthetic antagonist of V1aR, but not by tolvaptan, a specific V2R antagonist. Of note, the SR49059 action was impaired by DFP00173, a selective inhibitor of AQP3. Interestingly, compared to the normal colonic mucosa, in the colon of patients with adenocarcinoma, the expression of V1aR was significantly decreased. These findings were confirmed by gene expression analysis with RNA-Seq data. Overall, data suggest that dDAVP, through the V1aR dependent pathway, reduces AQP3 mediated glycerol uptake, a process that is reversed in adenocarcinoma, suggesting that the AVP-dependent AQP3 pathway may represent a novel target in colon diseases associated with abnormal cell growth.

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Section: Discussionmentioning

confidence: 99%

dDAVP Downregulates the AQP3-Mediated Glycerol Transport via V1aR in Human Colon HCT8 Cells

Centrone

D’Agostino

Ranieri

et al. 2022

Front. Cell Dev. Biol.

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“…Either of these agents is effective in treating patients with DI. In the acute intensive care unit setting, aqueous vasopressin may be preferred due to its short duration of effect (2–8 hours) compared with that of desmopressin (6–18 hours) as DI may be a transient clinical situation 109 , 110 . Vasopressin can be given subcutaneously in doses of 4–10 units every 6 hours as needed for urine output exceeding 200 mL 34 .…”

Section: Electrolyte Abnormalitiesmentioning

confidence: 99%

“…DDAVP is a synthetic form of vasopressin that has less potent (2000‐ to 3000‐fold) vasopressor effects than vasopressin. It has a much longer duration of effect and is the preferred therapy for permanent or slowly resolving DI 110 . It is available as intranasal, oral, or IV forms.…”

Section: Electrolyte Abnormalitiesmentioning

confidence: 99%

Considerations in Fluids and Electrolytes After Traumatic Brain Injury

Rhoney

Parker

2006

Nut in Clin Prac

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Appropriate fluid management of patients with traumatic brain injury (TBI) presents a challenge for many clinicians. Many of these patients may receive osmotic diuretics for the treatment of increased intracranial pressure or develop sodium disturbances, which act to alter fluid balance. However, establishment of fluid balance is extremely important for improving patient outcomes after neurologic injury. The use of hyperosmolar fluids, such as hypertonic saline, has gained significant interest because they are devoid of dehydrating properties and may have other beneficial properties for patients with TBI. Electrolyte derangements are also common after neurologic injury, with many having neurologic manifestations. In addition, the role of electrolyte abnormalities in the secondary neurologic injury cascade is being delineated and may offer a potential future therapeutic intervention.

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