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Effect of water deprivation on ACE binding and AT1 angiotensin receptor expression in regions of the brain that regulate hemodynamics
Author(s) -
Bourassa Erick A,
Speth Robert C
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.958.2
Subject(s) - subfornical organ , rostral ventrolateral medulla , lamina terminalis , medicine , endocrinology , angiotensin ii , circumventricular organs , hypothalamus , median preoptic nucleus , angiotensin ii receptor type 1 , lateral parabrachial nucleus , renin–angiotensin system , supraoptic nucleus , solitary tract , blood pressure , area postrema , vasopressin , angiotensin receptor , choroid plexus , chemistry , central nervous system , medulla oblongata , biology , parabrachial nucleus
The rostral ventrolateral medulla (RVLM) is a brainstem region critical to the maintenance of blood pressure. A period of water deprivation leads to increased sensitivity of the RVLM and paraventricular nucleus of the hypothalamus (PVH) to angiotensin II (Ang II). This Ang II helps sustain blood pressure. It has been proposed that peripheral Ang II can influence the RVLM via an angiotensinergic neural connection involving circumventricular organs and the PVH. We studied the differences in angiotensin type 1 (AT 1 ) receptor and angiotensin converting enzyme (ACE) expression in these and other brain regions involved in blood pressure regulation and water intake following a 48 hr period of water‐deprivation. Brains were sectioned and used for quantitative AT 1 receptor and ACE autoradiography. AT 1 receptor expression was increased in the subfornical organ and periventricular nucleus of the hypothalamus, but not in other brain regions measured. ACE expression was increased in the RVLM, PVH, choroid plexus, median preoptic nucleus, and organosum vasculosum of the lamina terminalis. These findings suggest that increased brain‐derived Ang II production, but not increased receptor expression or sensitivity is the mechanism by which Ang II in the brain helps to sustain systemic blood pressure during water‐deprivation. Supported by the Peptide Radioiodination Service Center of the University of Mississippi.