Arterial baroreﬂex, an important physiological regulatory system for buffering systemic blood pressure, is impaired in obesity.
This study investigated whether the blunted baroreﬂex function in obesity is attributed to the altered nitroxidergic or N-methyl-Daspartate (NMDA) mechanism. Baroreﬂex bradycardia responses, blood pressure and heart rate in 30 lean and 30 obese
anesthetized Zucker rats (8–12 weeks of age) were assessed after injecting phenylephrine with intravenous preadministration of
saline (control), dextromethorphan (DXM, NMDA receptor antagonist, 10 mg kg 1
) or N(G)-nitro-L-arginine methyl ester (L-NAME,
nitric oxide synthase inhibitor, 100 mg kg 1
). Compared with lean rats ( 2.00±0.29 b.p.m. mm Hg 1
), the baroreﬂex sensitivity
(BRS) in obese rats (–0.43±0.05 b.p.m. mm Hg 1) was signiﬁcantly blunted. The BRS was signiﬁcantly suppressed by DXM in
lean rats but not in obese rats. After administration of L-NAME, BRS was signiﬁcantly suppressed in lean Zucker rats but not in
obese Zucker rats. The normal BRS was signiﬁcantly suppressed in lean rats after administration of both DXM and L-NAME, and
the blunted BRS in obesity was signiﬁcantly blocked to nearly no BRS after administration of both DXM and L-NAME. This study
suggests that BRS is blunted in obese rats and that blunted baroreﬂex is, at least in part, attributed to altered nitroxidergic or
NMDA receptor-mediated modulation.