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Angiotensin II Increases the Corticotropin-Releasing Factor Messenger Ribonucleic Acid Level in the Rat Hypothalamus^*

Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women’s Medical College Tokyo 162
Laboratory of Genetics (M. Y.), National Children’s Medical Research Center Tokyo 154, Japan

Address all correspondence and requests for reprints to: Dr. Toshihiro Suda, Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women’s Medical College, 8–1 Kawada-cho, Shinjuku-ku, Tokyo 162, Japan.

Abstract

Angiotensin II (All) has an important role in the regulation of CRF release. In the present study, the effect of centrally administered All on CRF messenger RNA (mRNA) levels in the rat hypothalamus was examined. Administration of 0.1 nmol and 1 nmol All into the lateral ventricle increased the levels of plasma ACTH 20 min and 45 min after administration and those of proopiomelanocortin mRNA in the anterior pituitary (AP) and CRF mRNA in the hypothalamus 2 h after administration. On the other hand, ACTH levels in AP and CRF levels in the median eminence temporarily decreased 45 min after the administration of 1 nmol All, but it returned to the control level at 90 min. Administration of 10 nmol saralacin, an All antagonist, blocked 1 nmol All-induced increase in the levels of plasma ACTH, proopiomelanocortin mRNA in AP, and CRF mRNA in the hypothalamus. These results indicate that central administration of All increases the CRF mRNA level in the hypothalamus in a receptor-specific manner and also increases CRF release. Therefore, All seems to have an important role in the regulation of the release and synthesis of CRF in the hypothalamus. (Endocrinology 128: 2248–2252, 1991)

Footnotes

^* This work was supported in part by a Grant-in-Aid for General Scientific Research from the Japanese Ministry of Education, Science, and Culture.

Received November 20, 1990.

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