Angiotensin II receptors in the arcuate nucleus mediate stress-induced reduction of prolactin secretion in steroid-primed ovariectomized and lactating rats
Angiotensin II (Ang II) is a peptide that exerts an inhibitory effect upon pituitary prolactin (PRL) release through the hypothalamic arcuate nucleus (ARC). Since both PRL and Ang II are known to be affected by stress, the experiments reported here were conducted to investigate the possible particip...
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Published in | Brain research Vol. 1006; no. 1; pp. 59 - 65 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Elsevier B.V
23.04.2004
Amsterdam Elsevier New York, NY |
Subjects | |
Online Access | Get full text |
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Summary: | Angiotensin II (Ang II) is a peptide that exerts an inhibitory effect upon pituitary prolactin (PRL) release through the hypothalamic arcuate nucleus (ARC). Since both PRL and Ang II are known to be affected by stress, the experiments reported here were conducted to investigate the possible participation of Ang II in the stress-induced response of PRL in situations in which pre-stress PRL levels are high, as during the PRL surge induced by estradiol (E
2) and progesterone (P) in ovariectomized rats (OVXE
2P) and lactating females on day 7 post-partum. Adult female rats were stereotactically implanted with bilateral guide-cannulae in the ARC; 3 days later, they were microinjected with saline or losartan and, after a 15-min interval, they were submitted to stress by ether inhalation during 1 min. Five minutes after stress, trunk blood samples were collected. Plasma PRL was measured by radioimmunoassay (RIA). In OVXE
2P and lactating rats, a significant reduction in PRL levels was detected after stress compared to non-stressed animals. The microinjection of losartan in the ARC before stress blocked the reduction of PRL in both OVXE
2P and lactating females. In conclusion, the stress-induced reduction of plasma PRL in OVXE
2P and lactating rats is mediated by Ang II through AT
1 receptors in the ARC. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0006-8993 1872-6240 |
DOI: | 10.1016/j.brainres.2004.01.052 |