The effects of isatin indole-2, 3-dione on pituitary adenylate cyclase-activating polypeptide-induced hyperthermia in ratsReportar como inadecuado




The effects of isatin indole-2, 3-dione on pituitary adenylate cyclase-activating polypeptide-induced hyperthermia in rats - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

BMC Neuroscience

, 3:2

First Online: 20 February 2002Received: 01 December 2001Accepted: 20 February 2002

Abstract

BackgroundPrevious studies have demonstrated that centrally administered natriuretic peptides and pituitary adenylate cyclase-activating polypeptide-38 PACAP-38 have hyperthermic properties. Isatin indole-2, 3-dione is an endogenous indole that has previously been found to inhibit hyperthermic effects of natriuretic peptides. In this study the aim was to investigate the effects of isatin on thermoregulatory actions of PACAP-38, in rats.

ResultsOne μg intracerebroventricular icv. injection of PACAP-38 had hyperthermic effect in male, Wistar rats, with an onset of the effect at 2 h and a decline by the 6 h after administration. Intraperitoneal ip. injection of different doses of isatin 25-50 mg-kg significantly decreased the hyperthermic effect of 1 μg PACAP-38 icv., whereas 12.5 mg-kg isatin ip. had no inhibiting effect. Isatin alone did not modify the body temperature of the animals.

ConclusionThe mechanisms that participate in the mediation of the PACAP-38-induced hyperthermia may be modified by isatin. The capability of isatin to antagonize the hyperthermia induced by all members of the natriuretic peptide family and by PACAP-38 makes it unlikely to be acting directly on receptors for natriuretic peptides or on those for PACAP in these hyperthermic processes.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2202-3-2 contains supplementary material, which is available to authorized users.

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Autor: Imre Pataki - Ágnes Adamik - Vivette Glover - Gábor Tóth - Gyula Telegdy

Fuente: https://link.springer.com/







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