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Role of the OVLT in the Development of DOCA‐salt Hypertension
Author(s) -
Collister John P,
Nahey David B,
Banek Christopher T,
Osborn John W
Publication year - 2017
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.31.1_supplement.868.4
Subject(s) - lamina terminalis , third ventricle , medicine , endocrinology , subfornical organ , efferent , median preoptic nucleus , limiting , mineralocorticoid , blood pressure , afferent , renin–angiotensin system , aldosterone , central nervous system , mechanical engineering , engineering
Lesions of the anteroventral third ventricle (AV3V region) are known to prevent many forms of experimental hypertension, including mineralocorticoid (DOCA‐salt) hypertension in the rat. However, AV3V lesions include the organum vasculosum of the lamina terminalis (OVLT) and portions of the median preoptic nucleus, as well as efferent fibers from the subfornical organ (SFO), thereby limiting the ability to define the individual contribution of these structures to the prevention of experimental hypertension. Having previously reported that the SFO does not play a significant role in the development of DOCA‐salt hypertension, the present study was designed to test the hypothesis that the OVLT is necessary for DOCA‐salt hypertension in the rat. In uninephrectomized OVLT lesioned (OVLTx; n = 4) and SHAM (n = 3) Sprague‐Dawley rats consuming a 2% NaCl diet and 0.9% NaCl drinking solution, 24‐hour mean arterial pressure (MAP) was recorded telemetrically 5 days before and 21 days after DOCA implantation (100 mg/rat; SQ). No differences in control MAP were observed between groups. The chronic pressor response to DOCA was attenuated in OVLTx rats such that MAP increased to 132±4 mmHg in SHAM rats by Day 21 of DOCA compared to 123±4 mmHg in OVLTx rats. These results support the hypothesis that the OVLT is an important brain site of action for the pathogenesis of DOCA‐salt hypertension in the rat. Support or Funding Information University of Minnesota Academic Health Center Grant 15.05