The periaqueductal grey appears to mediate the reduction in baroreflex sensitivity following injury, but not the associated baroreflex resetting or pressor responses.
Answers are grounded in this paper and cite their sources.
Animal data implicate PAG in ischaemia-induced baroreflex desensitization; leaves open its role in human injury responses.
Cell bodies within the periaqueductal grey (PAG) of the midbrain of the propofol-anaesthetized rat were stimulated using the excitotoxin kainic acid. This resulted in a rise in arterial blood pressure and a tachycardia, together with a reduction in the sensitivity and a rightward resetting of the baroreflex. These changes mimicked the cardiovascular effect of bilateral hindlimb ischaemia in the rat. Further experiments in conscious rats indicated that electrolytic lesions in the PAG prevented the reduction in baroreflex sensitivity induced by limb ischaemia, but did not abolish the rightward resetting of the reflex or the pressor response and tachycardia when compared with sham-lesioned controls. It is postulated that the PAG, a site of importance both in the integration of the defence reaction and the processing of afferent nociceptive information, may form part of a pathway involved in the reduction of the sensitivity of the baroreflex following injury. This pathway is suggested to be separate from a second, as yet undefined, pathway mediating the baroreflex resetting and pressor responses associated with injury.
No takes yet. Share an insight, caveat, or question.
Jones et al. (1990) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: