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1 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Zablocki Department of Veterans Affairs Medical Center, Milwaukee, WI, USA
2 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: jseagard{at}mcw.edu.
Cannabinoids have been shown to modulate central autonomic regulation and baroreflex control of blood pressure (BP). The presence of cannabinoid CB1 receptors on fibers in the NTS suggests that some presynaptic modulation of transmitter release could occur in this region which receives direct afferent projections from arterial baroreceptors and cardiac mechanoreceptors. This study, therefore, was performed to determine the mechanism(s) of effects of microinjection of an endocannabinoid, arachidonylethanolamide (anandamide, AEA), into the NTS on baroreflex sympathetic nerve responses produced by phenylephrin (PE)-induced pressure changes in anesthetized rats. AEA was found to prolong reflex inhibition of renal sympathetic nerve activity (RSNA), suggesting an increase in baroreflex sensitivity. This effect of AEA was blocked by prior microinjection of SR141716 to block cannabinoid CB1 receptors. To determine if this baroreflex enhancement by AEA involved a GABAA mechanism, the baroreflex response to AEA was tested after prior blockade of postsynaptic GABAA receptors by bicuculline (BIC), which would eliminate any effects due to modulation of GABA activity. Following BIC, which alone prolonged the baroreflex inhibition of RSNA, AEA shortened the duration of RSNA inhibition, suggesting a possible presynaptic inhibition of glutamate release previously obscured by a more dominant GABAA effect. To support a possible physiological role for AEA, the concentration of AEA in the NTS was measured after a PE-induced increase in BP. AEA content in the NTS was increased significantly over normotensive animals. These results support the hypothesis that AEA content is increased by brief periods of hypertension and suggest that AEA can modulate the baroreflex through activation of CB1 receptors within the NTS, possibly modulating effectiveness of GABA and/or glutamate neurotransmission.
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