Abstract
With clear dependence of ethanol actions on central NMDAR signaling, studies on the unexplored interaction between ethanol and peripheral cardiovascular NMDAR are warranted. We tested the hypothesis that peripheral vascular effects of ethanol might involve blockade of peripheral NMDAR; activation of the latter causes increases in blood pressure (BP), vascular ROS and NOS‐derived NO generation. Hemodynamic studies were conducted in seven groups (n=5–6) of conscious Sprague Dawley male rats that received: 1) Saline, 2) NMDA (125–1000 μg/kg), 3) Ethanol (1g/kg), 4) Ethanol + NMDA, 5) Saline infusion, 6) NMDA (180 μg/kg/min for 30 min) or 7) Ethanol + NMDA infusion. Ethanol or its vehicle (water) was administered by gavage 30 min prior to either bolus i.v. injections or infusion of NMDA or its vehicle. Ethanol, which had no effect on BP, caused a downward shift in the NMDA dose‐pressor response curve. It was important to evaluate the interaction between ethanol and sustained peripheral NMDAR activation (groups 5–7) because bolus NMDA elicited short lived (approx.1 min) response. Ethanol attenuated the sustained NMDA pressor response during the entire 30 min of NMDA infusion. Further, ethanol abrogated the peripheral NMDAR‐mediated increases in vascular NO and ROS generation. These findings provide new insight into a potential role for peripheral NMDAR in the cardiovascular effects of ethanol [NIH grant AA07839].
Published Version
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