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Analysis of the Role of Angiotensin II in Mediation of Adrenocorticotropin Secretion^*

P.M. PLOTSKY, S.W. SUTTON, T.O. BRUHN and A.V. FERGUSON

The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute La Jolla, California 92037
the Department of Physiology, Queen’s University (A.V.F.) Kingston, Ontario, Canada K7L 3N6

Address requests for reprints to: Dr. Paul M. Plotsky, Laboratory for Peptide Biology, The Salk Institute, P.O. Box 85800, San Diego, California 92138.

Abstract

It has been suggested that ACTH secretion in response to selected stimuli may be modulated by angiotensin II (All) via direct action at the level of the corticotrope or through central actions to facilitate CRF secretion into the hypophysialportal circulation. These hypotheses were evaluated in the present series of experiments. Our failure to observe a significant portal to peripheral plasma immunoreactive (ir) All gradient suggested that All does not act as a physiologically significant ACTH secretagogue at the level of the corticotrope. Central administration of synthetic All evoked a modest dose-related stimulation of hypothalamic irCRF secretion into the portal circulation, which was reversed by the All receptor antagonist saralasin. Activation of a known All-positive neuronal pathway projecting from the subfornical organ (SFO) to the hypothalamic paraventricular nuclei resulted in an elevation of hypophysialportal plasma irCRF levels and increased circulating ACTH. Pretreatment with saralasin prevented SFO stimulation-induced irCRF secretion. These observations suggest that central Allcontaining pathways may participate in mediation of ACTH secretion in response to hypovolemia or hyperosmolality by facilitating irCRF secretion. Involvement of the SFO, a circumventricular organ, in this circuit is intriguing as it provides a means of monitoring peripheral irAII concentration and then converting this humoral signal into a neural signal distributed to regions regulating drinking behavior, neurohypophysial AVP secretion, and activation of the hypothalamic-pituitary-adrenal axis (Endocrinology 122: 538–545, 1988)

Footnotes

^* This work was supported by NIH Grant AM-33093 (to P.M.P.), the Medical Research Council of Canada (to A.V.F.). Research was conducted in part by the Clayton Foundation for Research, California Division.

Clayton Foundation Investigator.

Present address: Division of Endocrinology, Rhode Island Hospital, Providence, Rhode Island 02093.

Received June 9, 1987.

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