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Cardiovascular Responses to Hemorrhage and Volume Receptor Control of Vasopressin in Rats Exposed to Prenatal Ethanol
Author(s) -
Pole Ginger L.,
Bird Danielle N.,
Lim Jenny M.,
Sato Aileen K.,
Uyehara Catherine F.T.,
Claybaugh John R.
Publication year - 2006
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.20.5.a1444-d
Subject(s) - vasopressin , medicine , endocrinology , blood pressure , blood volume , baroreceptor , heart rate , offspring , ethanol , chemistry , pregnancy , biology , organic chemistry , genetics
Hemorrhage‐induced vasopressin (VP) release is less in prenatal ethanol (PE) than non‐prenatal ethanol (NPE) exposed rats. Altered responses in arterial blood pressure (BP), heart rate (HR) or baroreceptor control of VP may contribute to the decreased response. Rats fed 35% of calories from ethanol on days 7 to 21 (n=54) or 10 to 21 (n=15) of pregnancy produced PE litters; NPE litters were from dams fed an equi‐caloric control diet (n=58). At 12 weeks, offspring were hemorrhaged 10% of their blood volume (BV) two consecutive times. After the normotensive 10 % BV loss, plasma VP was 50% lower in PE than NPE rats, possibly because PE rats have increased initial BV (6%) and plasma volume (8 %) causing increased atrial stretch. VP was also lower in the PE rats following the hypotensive 20% BV loss with no difference in the VP/BP relationship. HR was 32 beats/min faster in PE than NPE rats after 20% BV loss, suggesting a reduced sympathetic withdrawal in the PE rats. Perhaps better filling of the cardiac chambers occurred with delayed onset of low ventricular filling thought to activate vagal C fibers and sympathoinhibition. Supported in part by a Research Centers in Minority Institutions award, P20 RR11091.