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The pressor response to activation of the central command pathway is attenuated by stimulation of peripheral sensory afferents in normotensive but not hypertensive rats
Author(s) -
Liang Nan,
Mizuno Masaki,
Downey Ryan M,
Iwamoto Gary A,
Mitchell Jere H,
Smith Scott A
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.943.5
Subject(s) - stimulation , peripheral , endocrinology , sensory system , inhibitory postsynaptic potential , medicine , neuroscience , sciatic nerve , chemistry , psychology
Recent evidence suggests that central command (CC; a neural drive originating in higher brain centers) partially mediates the exaggerated BP response to exercise in hypertension. The mechanisms underlying this CC overactivity remain unclear. It has been suggested that CC is modulated by input from peripheral sensory afferents (PSA). A change in this modulatory relationship could potentially play a role in the generation CC overactivity in hypertension. To address this issue, the BP response to activation of the CC pathway before and during concurrent stimulation of PSA was examined in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Rats were decerebrated and paralyzed. Activation of the CC pathway was evoked by electrical stimulation of the mesencephalic locomotor region (MLR; 20–50 μA in 10‐μA steps). Electrical stimulation of the sciatic nerve (3, 5 and 10 × motor threshold; MT) was used to activate PSA. The BP response to MLR activation was significantly attenuated by sciatic nerve stimulation at 5 and 10 × MT in WKY but not in SHR. This finding suggests that PSA input maintains the potential to inhibit CC activity in normal rats. The data further indicate that this inhibitory influence is reduced in hypertension. This change in the modulatory capacity of PSA may contribute, in part, to the development of CC overactivity in this disease. Support: NIH HL‐088422