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1 Hypertension and Stroke Research Laboratory, Department of Physiology, University of Sydney, Sydney, NSW, Australia; Department of Neurosurgery, Royal North Shore Hospital, Sydney, NSW, Australia
* To whom correspondence should be addressed. E-mail: pilowsky{at}med.usyd.edu.au.
The effects of activation and blockade of the neurokinin 1 (NK1) receptor in the rostral ventrolateral medulla (RVLM) on arterial blood pressure, splanchnic sympathetic nerve activity (sSNA), phrenic nerve activity, the somato-sympathetic reflex, baroreflex and chemoreflex were studied in urethane anaesthetized, and artificially ventilated Sprague-Dawley rats. Bilateral microinjection of either the stable substance P analogue (pGlu5, MePhe8, Sar9)-SP(5-11)(DiMe-SP) or the highly selective NK1 agonist [Sar9, Met(O2)11]-substance P into the RVLM resulted in an increase in arterial blood pressure, sSNA, and heart rate and an abolition of phrenic nerve activity. The effects of [Sar9, Met(O2)11]-substance P were blocked by the selective non-peptide NK1 receptor antagonist WIN 51708. NK1 receptor activation also dramatically attenuated the somato-sympathetic reflex elicited by tibial nerve stimulation whilst leaving the baroreflex and chemoreflex unaffected. This effect was again blocked by WIN 51708. NK1 receptor antagonism in the RVLM with WIN 51708 significantly attenuated the sympathoexcitatory response to hypoxia, but had no effect on baseline respiratory function. Our findings suggest that substance P and the NK1 receptor play a significant role in the cardiorespiratory reflexes integrated within the RVLM.
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