Nitric oxide modulates cardiovascular function in the rat by activating adenosine A2A receptors and inhibiting acetylcholine release in the rostral ventrolateral medulla

摘要: Summary 1. Nitric oxide (NO), a gas transmitter, modulates many physiological processes, including the central regulation of cardiovascular activity. However, mechanisms underlying activity remain relatively unexplored. In present study, we hypothesized that NO-dependent sympathetic inhibition is mediated by activation adenosine A2A receptors (A2AR) and acetylcholine (ACh) release in rostral ventrolateral medulla (RVLM). 2. l-Arginine (l-Arg; an NO donor; 100 nmol/100 nL) was microinjected into RVLM male Sprague–Dawley rats heart rate variability (HRV) assessed as index cardiac sympathovagal balance. Following microinjection l-Arg, decreases were seen mean arterial pressure (MAP), (HR) ratio low- to high-frequency components (LF/HF) HRV. Pretreatment with SCH58261 (40 pmol/60 nL RVLM), competitive antagonist A2AR, attenuated these effects. 3. Western blot analysis ELISA revealed A2AR levels increased following l-Arg microinjection, whereas ACh muscarinic M1 receptor decreased significantly, parallel responses microinjection. The decrease abolished pretreatment. 4. Microinjection NG-nitro-l-arginine methyl ester (a non-selective inhibitor synthase; 15 nmol/100 nL) significantly MAP, HR activity, evidenced HRV (LF, HF LF/HF all increased). 5. results indicate NO/NO synthase system may modulate activating which subsequently inhibits receptor.