Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the influence of four substances on the excitability of lumbar motoneurons. These substances, three of which coexist in the same bulbospinal descending pathways that end, for the most part, around motoneurons (MNS), are: 5-hydroxytryptamine (5-HT), substance P (SP) and thyrotropin-releasing hormone (TRH). We also studied the effects of clonidine, an alpha 2 noradrenergic (NA) agonist. This study was carried out in rats spinalized at T5 and treated three weeks earlier with 5-7 dihydroxytryptamine (5-7 DHT). Under these conditions, the following responses were observed: 5-HTP (5-HT precursor) intraperitoneally (I.P.), 5-HT intrathecally (I.T.), TRH (I.P. or I.T.) and substance P (I.T.) all elicited strong excitation of MNS as measured by integrated EMG of the hindlimb muscles; substance P reduced by almost half the response to 5-HTP given one hour and 24 hours later; TRH given acutely did not modify the response to 5-HTP, but given chronically for 21 days markedly increased the response to this substance. Clonidine by itself decreased the excitability of MNS and antagonized the excitatory effects of 5-HTP and TRH. In two separate pilot trials, cyproheptadine, a 5-HTP antagonist, decreased the manifestations of spasticity in a patient with a partial spinal lesion. It would appear that clonidine may have potential use in the management of spasticity.
J Spinal Cord Med 1995 Jan
PMID:Action of 5-hydroxytryptamine, substance P, thyrotropin releasing hormone and clonidine on spinal neuron excitability. 754 99

Autonomic dysreflexia (AD) is a clinical phenomenon that affects patients with spinal cord injury (SCI) above the major sympathetic outflow tract. The lesion is most often at or above the T-6 level. Any noxious stimuli below this level initiate reflex sympathetic activity resulting in life threatening hypertension uncontrollable by the feedback parasympathetic activity. The episodes of hypertension generally persist until the offending stimulus is removed. Absence of higher control over reflex sympathetic activity due to transection of the cord is an anatomical explanation of the phenomenon. Current evidence suggests additional factors such as supersensitivity and possibly increased numbers of spinal alpha adrenoreceptors and peripheral microvascular adrenoreceptors as well as accumulation of substance P below the lesion. It has been suggested that substance P acts as a modulator, initiating the sympathetic event to produce a strong, slow and prolonged excitatory action. Autonomic dysreflexia is further accentuated by the absence of gamma amino benzoic acid (GABA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT) below the lesion. GABA is an inhibitory neurotransmitter. It has been suggested that either NE or 5-HT may also act as an inhibitory neurotransmitter. Resetting of the baroreceptors at a lower level also plays an important role. The anatomical transection at or above T-6 then helps in maintaining and accentuating the biochemical changes that develop in patients with high spinal cord lesions. The current article reviews the pathophysiology and management of this potentially life threatening, yet easily treatable, phenomenon.
J Spinal Cord Med 1995 Apr
PMID:Autonomic dysreflexia revisited. 764 Sep 77

This article reviews the innervation of the arterial system of the lower extremity, lumbar sympathectomy in vascular surgery, lumbar sympathectomy for digital gangrene and in the prevention of major amputation of the lower extremity and substance P's role in neurogenic inflammatory modulation. Long-term results of lumbar sympathectomy and direct arterial bypass surgery have also been reviewed. In addition to the pilomotor, sudomotor and vasomotor actions of the sympathetic nervous system via its neurotransmitters, the molecular basis of the chronic neurogenic inflammatory reaction have been addressed with special attention to the discovery of substance P in the lumbar sympathetic chain and ganglia of human beings.
J Spinal Cord Med 1996 Jan
PMID:Surgery of the sympathetic nervous system. 867 10

A quantitative analysis was performed of substance P-like immunoreactivity (SPLI) and of beta-endorphin-like immunoreactivity (beta-ENDLI), in the cerebrospinal fluid (CSF) in various diseases. The results reported to date have not been consistent. The purpose of this study was to investigate whether or not the concentration of SPLI or that of beta-ENDLI in CSF demonstrated any potential for assessing the degree of subjective pain in various spinal diseases. SPLI in CSF was measured by radioimmunoassay in 158 patients with a spinal disease; involving 57 patients with a lumbar disc herniation (LDH), 38 with lumbar canal stenosis (LCS), 46 with cervical myelopathy (CM) and 17 with cervical radiculopathy (CR), and also in 20 healthy controls. beta-ENDLI in CSF was measured in 25 of these same patients; involving 12 with LDH, seven with LCS and six with CM, and also five of the same controls. The concentration of serum SPLI was also measured in 50 of these 158. The severity of pain was self-evaluated by each patient using a linear visual analogue scale (VAS). Their Japanese Orthopaedic Association (JOA) score was also calculated objectively using the clinical findings. Correlations were investigated among the concentrations of SPLI and beta-ENDLI in the CSF and the VAS and JOA clinical assessments of these patients. The concentration of SPLI in CSF was significantly higher in various spinal diseases than in control (P < 0.05), and was correlated with the severity on the VAS and with the JOA score. However, beta-ENDLI was not correlated with either the VAS or the JOA score. We conclude that the measurement of the SPLI concentration in CSF has the potential for assessing objectively the severity of pain associated with various spinal diseases.
Spinal Cord 1997 Nov
PMID:Objective evaluation of pain in various spinal diseases: neuropeptide immunoreactivity in the cerebrospinal fluid. 939 47