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Perinatal exposure to PBDEs elevate systolic blood pressure in response to hyperosmotic stimulation in aged adult rats
Author(s) -
Shah Ashini,
Gaertner Mark,
Coburn Cary,
Kodavanti Prasada Rao,
WatsonSiroboe Abeena,
Shahidizadeh Anoush,
Whitley Rebecca,
Gillard Elizabeth R,
CurrasCollazo Margarita
Publication year - 2008
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.22.1_supplement.738.18
Subject(s) - vasopressin , polybrominated diphenyl ethers , osmotic concentration , medicine , endocrinology , vasoconstriction , blood pressure , chemistry , organic chemistry , pollutant
Polybrominated diphenyl ethers (PBDEs) are flame retardants used widely throughout the US. These chemicals are persistent throughout the environment and accumulate in biota. In previous work we showed that PBDEs and the structurally similar compounds PCBs disrupt the somatodendritic and/or peripheral release of vasopressin from the supraoptic nucleus of the hypothalamus (Coburn et al, 2005; 2007). Vasopressin hormone output into the circulation produces vasoconstriction and antidiuresis. Because of the interaction between PBDEs and VP we hypothesized that there should be measurable effects of PBDEs on blood pressure (BP) regulation. PBDE‐treated rats were exposed perinatally to the PBDE industrial mixture, DE‐71 (mothers given 1.7 or 30.6 mg/kg/d, GD 6‐PND 21 by oral gavage) and then tested as aged adults (14–18 months). BP was measured using tail cuff sphygmometry. First, the rats were tamed until their baseline BP was stable (compared restraint vs anesthesia). Rats were divided into two groups and subjected to an ip injection (0.6cc/100g) of 0.15 M (normosmotic) or 3.5 M NaCl (hyperosmotic). PBDE treatment alone did not change basal BP at 30 min or 3 h. Hyperosmotic PBDE‐treated rats showed a significant increase in systolic BP at 3 h post injection. In comparison, hyperosmotic controls (PBDE‐naïve) showed no significant rise in BP at any timepoint. These results suggest that exposure to environmental PBDEs may permanently disrupt cardiovascular function. Supported by UC Mexus (MC) and American Heart Association (RW), UC Dean's Research Fellowship (AS), MARC program (MG), EPA (PK)