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Osmotic Stress Induces Transcriptional Changes in Vasopressin and Vasopressin 1b Receptor Gene Expression

机译:渗透压诱导血管加压素和血管加压素1b受体基因表达的转录变化

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Arginine vasopressin (AVP) plays a critical role in the regulation of mammalian salt and water homeostasis. To further define central nervous system adaptation to osmotic challenges, transcription of AVP and vasopressin 1b receptor (v1bR) genes by magnocellular neurons of the hypothalamus and epithelial cells of the choroid plexus was studied using in situ hybridization. Compared to animals given a single injection of normal saline, animals that received a single injection of hypertonic saline had increases in AVP heteronuclear RNA (hnRNA) after 15 and 30 minutes. Animals given an injection of hypertonic saline followed by a second injection of hypertonic saline (H-H) had an increase in AVP hnRNA levels that were equivalent to the response seen after a single hypertonic saline injection. Levels of AVP hnRNA after H-H were greater than the levels detected in animals given an injection of normal saline followed by a second injection of hypertonic saline (N-H). This is the first study to show repeated exposure to hypertonic saline causes an immediate, robust, and reproducible increase in vasopressin gene transcription. These results suggest there is a correlation between increased neuronal firing rate and vasopressin gene transcription. We also studied long-term adaptation to an osmotic challenge. Compared to rats maintained on tap water, salt-drinking rats had increased levels of AVP and V1bR mRNAs in the supraoptic and paraventricular nuclei, and in the choroid plexus. The increase in AVP and V1bR mRNAs in the SON and PVN as a result of plasma hyperosmolality may indicate the intranuclear release of AVP has a role in the autoregulation of magnocellular neuron activity. The role of AVP in cerebrospinal fluid formation remains to be elucidated. However, the increase of AVP and V1bR mRNA in the choroid plexus suggests the involvement of AVP in the regulation if brain water content and cerebral edema.

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