Inhibition of the neuronal nitric oxide synthase (nNOS) reduces cardiovascular responses elicited by acetylcholine (Ach) microinjection within the Nucleus of the Solitary Tract (NTS) of conscious rats

Ach seems to participate in baroreflex transmission modulating L‐glutamate release in the NTS. Centrally released nitric oxide (NO) is involved in cardiovascular transmission within the NTS. We investigated whether inhibition of nNOS could affect cardiovascular responses elicited by Ach into the NTS of conscious Male Wistar rats. Five days before the experiments rats were anesthetized with Ketamin (50mg/kg) and Xylazin 2% and guide cannulae aiming at the NTS were implanted bilaterally. One day before the experiments, femoral artery was cannulated to record mean arterial pressure (MAP, mmHg) and heart rate (HR, bpm). Control unilateral microinjection of Ach (500pmol/100nl) elicited hypotension (Δ MAP: −50±6 mmHg) and bradycardia (Δ HR: −100±26 bpm). Ach responses were reduced 10 and 20 min after NOS blockade into the NTS (L‐NAME, 10 nmol/100 nl):Δ MAP 10 min: −9±4 mmHg, and Δ MAP 20 min: − 6±4mmHg; Δ HR 10 min: −20±10 bpm, and Δ HR 20 min: −24± 9 bpm; p< .05; n=8. NTS microinjection of the selective nNOS inhibitor (TRIM 10 nmol/60 nl) also reduced Ach elicited hypotension (Δ MAP control: −42±4 mmHg vs after TRIM: Δ MAP 10 min: −26±7 mmHg; p< .05; n=7) and bradycardia (ΔHR control: −104±17 bpm vs after TRIM: Δ HR 10 min: −73±19 bpm). L‐NAME and TRIM did not alter baseline MAP and HR, all responses were back to control 30–45 min after treatment. Ach responses were not affected after D‐NAME or saline. We suggest that NO may modulate baroreflex transmission within the NTS through Ach release. Supported by Fapesp, CNPq‐PIBIC, CNPq/PRONEX. ± Δ