The effect of social environment on markers of vascular oxidative stress and inflammation in the Watanabe heritable hyperlipidemic rabbit.
OBJECTIVE
Previous research demonstrated that social environment can influence progression of atherosclerosis in the Watanabe Heritable Hyperlipidemic (WHHL) rabbit. This study examined the effect of social environment on markers of oxidative stress and inflammation to clarify the physiological pathways potentially responsible for the influence of social environment on disease.


RESULTS
WHHL rabbits were assigned to 1 of 3 social groups: an unstable group, in which unfamiliar rabbits were paired daily, with the pairing switched each week; a stable group, in which littermates were paired daily; and an individually-caged group. The stable group engaged in more affiliative social behavior than the unstable group. The unstable group showed more agonistic behavior compared with the stable group and higher C-reactive protein levels than the individually caged group. The individually caged group was behaviorally sedentary, had higher 24-hour urinary catecholamine levels than the other groups, and exhibited higher NAD(P)H-oxidase activity in the aortic arch relative to the stable group.


CONCLUSIONS
The results suggest that social environment creates distinct behavioral contexts that can affect markers of inflammation and oxidative stress early in the development of atherosclerosis. Specifically, physical inactivity associated with individual caging affects indices of oxidative stress and inflammation. These pathophysiological markers may help to explain behaviorally related differences in the extent of atherosclerosis observed in prior studies.
Nation
Daniel A
DA
Department of Psychology, University of Miami, P.O. Box 248185, 5665 Ponce De Leon, Blvd., Coral Gables, FL 33124, USA.
Gonzales
Julie A
JA
Mendez
Armando J
AJ
Zaias
Julia
J
Szeto
Angela
A
Brooks
Larry G
LG
Paredes
Jamespaul
J
D'Angola
Alyssa
A
Schneiderman
Neil
N
McCabe
Philip M
PM
D000378:Agonistic Behavior / Q000502:physiology; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D001143:Arousal / Q000502:physiology; D050197:Atherosclerosis / Q000235:genetics* / Q000473:pathology / Q000523:psychology; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004837:Epinephrine / Q000652:urine; D006949:Hyperlipidemias / Q000235:genetics* / Q000473:pathology / Q000523:psychology; D018836:Inflammation Mediators / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D019255:NADPH Oxidases / Q000097:blood; D009638:Norepinephrine / Q000652:urine; D018384:Oxidative Stress / Q000502:physiology*; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000097:blood; D044140:Receptor, Angiotensin, Type 1 / Q000097:blood; D012931:Social Environment; D012934:Social Isolation; D013315:Stress, Psychological / Q000150:complications*
D018836:Inflammation Mediators; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D017382:Reactive Oxygen Species; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D002097:C-Reactive Protein; D002784:Cholesterol; D019255:NADPH Oxidases; D007703:Peptidyl-Dipeptidase A; D009638:Norepinephrine; D004837:Epinephrine