Acetylcholine injected into the intermediate nucleus of the solitary tract reduced sympathetic nerve activity (-54% vs -5% for vehicle; P<0.001) and phrenic nerve activity in male juvenile rats.
Cholinergic mechanisms, primarily via nicotinic receptors, differentially modulate sympathetic and respiratory activities depending on their location within the nucleus of the solitary tract.
Absolute Event Rate: -54% vs -5%
p-value: p=<0.001
New Findings What is the central question of this study? Is sympathorespiratory activity affected in a different manner by cholinergic mechanisms in the intermediate (iNTS) and commissural nucleus of the solitary tract (cNTS) and are cholinergic mechanisms involved in baro‐ and chemoreflexes? What is the main finding and its importance? Acetylcholine (ACh) injected into the iNTS promotes sympatho‐inhibition and reduces the phrenic frequency, whereas ACh injected into the cNTS increases phrenic frequency and affects sympathetic–respiratory coupling, without changing the sympathetic activity. These responses are abolished by mecamylamine (nicotinic antagonist) in the NTS. Mecamylamine in the cNTS also reduces peripheral chemoreflex‐induced tachypnoea. The contribution of cholinergic mechanisms of the nucleus of the solitary tract (NTS) to cardiorespiratory control is not completely clear. In the present study, we investigated the involvement of the cholinergic mechanisms in the intermediate NTS (iNTS) and commissural NTS (cNTS) on the control of sympathetic (SNA) and phrenic nerve activity (PNA). Decorticated, arterially perfused in situ preparations of male juvenile rats (60–100 g) were used. Acetylcholine (10 m m , 60 nl) injected into the iNTS reduced SNA (−54 ± 4%, versus vehicle −5 ± 3%; P < 0.001) and PNA (−30 ± 4%, versus vehicle −5 ± 6%; P < 0.001), whereas injections of ACh into the cNTS increased PNA (30 ± 6%, versus vehicle 5 ± 3%; P < 0.001), without changing SNA. Pretreatment with mecamylamine (nicotinic antagonist; 5 m m ) abolished all the effects of ACh injected into the iNTS or the cNTS, whereas atropine (muscarinic antagonist; 5 m m ) reduced only the effects of ACh injected into the cNTS. Mecamylamine injected into the cNTS also reduced the tachypnoea in response to peripheral chemoreflex activation. The baroreflex was unaltered by injections of atropine or mecamylamine into the NTS. The results suggest that ACh and mainly nicotinic receptors in the NTS are involved in the modulation of SNA and PNA, with distinct functions between the iNTS and the cNTS. An involvement of the nicotinic receptors in the cNTS in the tachypnoea in response to peripheral chemoreflex activation is also suggested.
Furuya et al. (Sat,) reported a other. Acetylcholine (ACh) injected into the iNTS vs. Vehicle was evaluated on Sympathetic nerve activity (SNA) (p=<0.001). Acetylcholine injected into the intermediate nucleus of the solitary tract reduced sympathetic nerve activity (-54% vs -5% for vehicle; P<0.001) and phrenic nerve activity in male juvenile rats.
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