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Trait Aggression (TA) Correlates with Increased Blood Pressure in the Wistar‐Kyoto Rat
Author(s) -
Rana Samir,
Stringfellow Sara,
Pugh Phyllis,
White Roger,
Stauss Harald,
Wyss J. Michael,
Kerman Ilan
Publication year - 2015
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.29.1_supplement.lb610
Subject(s) - blood pressure , medicine , endocrinology , norepinephrine , sympathetic nervous system , dopamine
Classical studies have implicated specific personality traits as predictive of adverse cardiovascular function, yet biological mechanisms that contribute to such associations remain elusive. We investigated potential impact of early‐life experience on the emergence of TA and cardiovascular function. Male Wistar‐Kyoto rats that experienced either maternal separation or neonatal handling during postnatal days 1‐14 were instrumented for continuous blood pressure (BP) recording as adults. They were then single‐housed and scored on aggressive behavior in response to a 10‐min. exposure to a conspecific male. Rats were then sacrificed and thoracic aortas were harvested for functional and structural studies, along with plasma and end organs. Half of the animals regardless of their early‐life experience demonstrated TA (scored as clinch attack). TA rats exhibited significant elevations of mean and systolic (SBP) blood pressures along with increased low‐frequency power of SBP variability, an index of sympathetic modulation of vascular tone. Hearts from TA rats had a greater norepinephrine content, and their aortas exhibited a significantly lower EC 50 to phenylephrine‐induced contractions along with an increased wall‐to‐lumen ratios. Taken together these data indicate that TA may be an inborn emotionality trait that develops independently of early‐life experience in rats. Furthermore, it correlates with alterations in vascular structure and function that lead to increased BP, and which may be mediated by alterations in the activity of the sympathetic nervous system. Support: R00MH081927 (IAK), 13PRE16940050 (SR), P30NS47466 (UAB core)