A compression neuropathy model that produces pain-related behaviour in rats was used to investigate changes in skin vascular reactivity in the innervated area. Neuropathy was produced by 4 ligatures tied loosely around the common sciatic nerve. Vascular reactivity was assessed via perfusion of the neuropeptide substance P (SP) over the base of a blister raised on the rat foot pad. Compared to sham-operated rats, experimental rats exhibited a decrease in their vasodilatation response to SP 2-5 weeks after ligatures were tied. A bilateral decrease in vasodilatation to sodium nitroprusside perfusion in treated rats suggested part of the altered SP response was due to diminished vascular reactivity. Plasma extravasation in response to SP was also decreased on the operated side of ligatured rats, significant 4 and 6 weeks after the operation. The results support studies that suggest neurogenic inflammation is altered in chronic neuropathic pain states.

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Among the mammalian tachykinins, substance P (SP) has been shown to be the most potent at modulating the response due to nicotinic acetylcholine receptor stimulation of bovine adrenal chromaffin cells. SP-like immunoreactivity has been detected in nerve terminals innervating the adrenal medulla; however, little is known of the presence of other tachykinins in this tissue. In this study, reverse-phase HPLC was used to fractionate peptides in bovine adrenal medullary extracts, and the fractions were analyzed by radioimmunoassay using antisera to SP or neurokinin A (NKA). The results show that both NKA- and SP-like immunoreactivities are present in the adrenal medulla. The presence of neurokinin B is also indicated. The presence of multiple tachykinins in this tissue raises questions as to their functions in the adrenal medulla.