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Activator of G‐protein Signaling 3 null mice: unexpected alterations in metabolic and cardiovascular function
Author(s) -
Blumer Joe B.,
Lord Kevin,
Saunders Thomas L.,
Black Cory,
Lazartigues Eric,
Varner Kurt J.,
Gettys Thomas W.,
Lanier Stephen M.
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.908.1
Subject(s) - endocrinology , medicine , biology , activator (genetics) , in vivo , sodium nitroprusside , microbiology and biotechnology , nitric oxide , receptor
Activator of G‐protein Signaling (AGS) 3 and AGS5/LGN, via regulation of G‐protein signaling, play central functional roles in cell division, synaptic plasticity, addictive behavior and/or neuronal development. As part of a broad effort to define the extent of functional diversity of AGS regulated‐events in vivo , we present this report on AGS3 null mice. Surprisingly, AGS3 null adult mice exhibited unexpected alterations in cardiovascular and metabolic functions, without any obvious changes in basic behavioral traits or gross brain morphology. Despite higher food consumption AGS3 −/− mice deposited significantly less fat than wild type mice, primarily due to higher rates of nocturnal energy expenditure. Conscious, unrestrained AGS 3−/− mice exhibited significantly lower arterial pressures and reduced diurnal variations in arterial pressure that are associated with increased baroreceptor reflex sensitivity and a failure to adequately compensate to the decrease in arterial pressure elicited by the vasodilator sodium nitroprusside. These studies expand the functional repertoire for AGS3 and other GPR proteins providing unexpected venues for the development of therapeutic agents to influence obesity and cardiovascular regulation.