The healing power of vasopressin

Istvan Berczi, Andres Quintanar, Egina C. Villalobos-Hernández, Rafael Campos, Kalman Kovacs

Resultado de la investigación: Contribución a una revistaArtículo

13 Citas (Scopus)

Resumen

Hypothalamus-Pituitary-Adrenal, (HPA) axis activation and prolactin (PRL) release was studied in rats having chronic experimental autoimmune encephalitis (EAE). Corticotropin releasing hormone (CRH) did not respond to the inflammatory stimulus, but vasopressin (VP), glucocorticoids (GC) and PRL responded at 15 or 29 days of disease. The responses of corticosterone (COS) and of PRL to inflammation were mediated by VP. VP also controlled cytokine release in rats with adjuvant arthritis (AA). The VP agonist, desmopressin (DP), released GC, PRL and restored EAE reactivity in neurointermediate hypohysectomy (NIL) rats. Thus VP regulates the chronic inflammatory process, which eventually leads to healing and recovery from acute febrile illness. After healing VP remains in control of homeostasis in the host. The effects of anterior-, posterior-and total pituitary hormones were examined on cytokine (interleukins-IL-1,-2,-6,-10, -12 and interferon (IFN)-gamma) release during AA of rats. Hormones amplified or inhibited cytokines, which indicated their biological function in immunoregulation.

Idioma originalInglés
Páginas (desde-hasta)217-224
Número de páginas8
PublicaciónAdvances in Neuroimmune Biology
Volumen3
N.º2
DOI
EstadoPublicada - 22 oct 2012

Huella dactilar

Vasopressins
Prolactin
Experimental Arthritis
Cytokines
Interleukin-1
Glucocorticoids
Posterior Pituitary Hormones
Deamino Arginine Vasopressin
Corticotropin-Releasing Hormone
Corticosterone
Hypothalamus
Interferon-gamma
Interleukin-2
Homeostasis
Fever
Hormones
Inflammation

Citar esto

Berczi, I., Quintanar, A., Villalobos-Hernández, E. C., Campos, R., & Kovacs, K. (2012). The healing power of vasopressin. Advances in Neuroimmune Biology, 3(2), 217-224. https://doi.org/10.3233/NIB-2012-012047
Berczi, Istvan ; Quintanar, Andres ; Villalobos-Hernández, Egina C. ; Campos, Rafael ; Kovacs, Kalman. / The healing power of vasopressin. En: Advances in Neuroimmune Biology. 2012 ; Vol. 3, N.º 2. pp. 217-224.
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Berczi, I, Quintanar, A, Villalobos-Hernández, EC, Campos, R & Kovacs, K 2012, 'The healing power of vasopressin', Advances in Neuroimmune Biology, vol. 3, n.º 2, pp. 217-224. https://doi.org/10.3233/NIB-2012-012047

The healing power of vasopressin. / Berczi, Istvan; Quintanar, Andres; Villalobos-Hernández, Egina C.; Campos, Rafael; Kovacs, Kalman.

En: Advances in Neuroimmune Biology, Vol. 3, N.º 2, 22.10.2012, p. 217-224.

Resultado de la investigación: Contribución a una revistaArtículo

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AU - Berczi, Istvan

AU - Quintanar, Andres

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AU - Campos, Rafael

AU - Kovacs, Kalman

PY - 2012/10/22

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N2 - Hypothalamus-Pituitary-Adrenal, (HPA) axis activation and prolactin (PRL) release was studied in rats having chronic experimental autoimmune encephalitis (EAE). Corticotropin releasing hormone (CRH) did not respond to the inflammatory stimulus, but vasopressin (VP), glucocorticoids (GC) and PRL responded at 15 or 29 days of disease. The responses of corticosterone (COS) and of PRL to inflammation were mediated by VP. VP also controlled cytokine release in rats with adjuvant arthritis (AA). The VP agonist, desmopressin (DP), released GC, PRL and restored EAE reactivity in neurointermediate hypohysectomy (NIL) rats. Thus VP regulates the chronic inflammatory process, which eventually leads to healing and recovery from acute febrile illness. After healing VP remains in control of homeostasis in the host. The effects of anterior-, posterior-and total pituitary hormones were examined on cytokine (interleukins-IL-1,-2,-6,-10, -12 and interferon (IFN)-gamma) release during AA of rats. Hormones amplified or inhibited cytokines, which indicated their biological function in immunoregulation.

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Berczi I, Quintanar A, Villalobos-Hernández EC, Campos R, Kovacs K. The healing power of vasopressin. Advances in Neuroimmune Biology. 2012 oct 22;3(2):217-224. https://doi.org/10.3233/NIB-2012-012047