Nociception attenuates parasympathetic but not sympathetic baroreflex via NK1 receptors in the XXXX nucleus tractus solitarii.

@entity10133 @entity11714 @entity11359 @entity591 @entity6372 @entity1017 @entity35
Somatic noxious stimulation can evoke profound cardiovascular responses by altering activity in the autonomic nervous system. This noxious stimulation attenuates the cardiac vagal baroreflex, a key cardiovascular homeostatic reflex. This attenuation is mediated via NK1 receptors expressed on GABAergic interneurones within the nucleus of the solitary tract (NTS). We have investigated the effect of noxious stimulation and exogenous substance @entity10133 ) on the sympathetic component of the baroreflex. We recorded from the sympathetic chain in a decerebrate, artificially perfused @entity35 preparation. Noxious hindlimb pinch was without effect on the sympathetic baroreflex although the cardiac @entity1017 was decreased (56 %, P < 0.01). Bilateral NTS microinjection of SP (500 fmol) produced a similar selective attenuation of the cardiac @entity1017 (62 %, P < 0.005) without effect on the sympathetic baroreflex. Recordings from the cardiac sympathetic and vagal nerves confirmed the selectivity of the SP inhibition. Control experiments using a GABAA receptor agonist, @entity11359 , indicated that both components of the baroreflex (parasympathetic and sympathetic) could be blocked from the NTS injection site. The NTS microinjection of a NK1 antagonist ( @entity11714 ) in vivo attenuated the @entity6372 . Our data suggest that noxious pinch releases SP within the NTS to selectively attenuate the cardiac vagal, but not the sympathetic, component of the baroreflex. This selective withdrawal of the cardiac vagal baroreflex seems to underlie the pinch-evoked @entity591 seen in vivo. Further, these findings confirm that baroreflex sympathetic and parasympathetic pathways diverge, and can be independently controlled, within the NTS.
