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)

The objective of this study was to determine if endothelium-dependent vasodilation is preserved in the spastic segment of the epicardial coronary artery. Segmental responses of the coronary artery to substance P were examined by the use of a quantitative angiographic technique in 21 patients with variant angina. Coronary diameter at the basal state did not differ between the spastic and the nonspastic segments (2.3 +/- 0.2 mm, 2.3 +/- 0.4 mm, p greater than 0.05). Changes in coronary diameter in response to substance P did not differ between segments with ergonovine-induced spasm and nonspastic segments. Maximal dilation averaged 27.1 +/- 9.5% in the spastic segment and 24.4 +/- 9.6% in the nonspastic segment (expressed as a percent increase over the value before drug administration). It appears that both the potential of the endothelium to release endothelium-dependent relaxing factor and the dilating response of the smooth muscle to endothelium-dependent relaxing factor are preserved, even in the spastic segment.
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PMID:Preservation of endothelium-dependent vasodilation in the spastic segment of the human epicardial coronary artery by substance P. 137 Oct 34

Cisternal blood injection in the rat induces a biphasic angiographic vasospasm, with a maximal acute spasm at 10 minutes and a maximal late spasm at 2 days after the subarachnoid hemorrhage (SAH). Depletion of substance P-containing sensory nerves to the cerebral arteries with capsaicin prior to SAH prevents the development of both acute and late spasm. Intrathecal administration of the substance P antagonist spantide 2 hours prior to SAH also prevents the development of vasospasm, while spantide administration 1 hour before SAH only hinders the occurrence of late vasospasm. Intracisternal administration of spantide 2 hours post-SAH prevents the development of late vasospasm. This antagonist per se can induce a short-lasting dose-dependent angiographic vasoconstriction. Substance P-containing nerve fibers on the cerebral arteries could constitute the sensory link in a reflex arc system involved in the development of vasospasm in which the presence of blood in the subarachnoid space stimulates sensory substance P-containing nerve fibers on the cerebral arteries inducing a centripetal impulse to the A2-nucleus tractus solitarius setting into motion the events in the brain stem leading to acute and late vasospasm.
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PMID:Prevention of cerebral vasospasm in the rat by depletion or inhibition of substance P in conducting vessels. 169 85

The influence of nociceptive peripheral input on the response characteristics of spinal interneurons may result in long-term alterations of interneuronal excitability and modify their responses to subsequent stimuli. Such neuromodulation has been found to result in physiological changes including hyperalgesia, lowering of pain thresholds, expansion of receptive fields and changes in response behaviors of muscles. These types of alterations may contribute to clinically significant findings including muscle spasm, hypomobility, edema, chronic pain, recurrences in areas of previous injury and resistance to treatment. This article reviews studies concerning plasticity of response behaviors of interneurons including habituation, spinal learning, spinal fixation, neuromodulation and the effects of substance P. Potential clinical and chiropractic application are discussed and a brief review of clinically relevant studies of chiropractic adjustments are cited.
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PMID:Spinal learning: central modulation of pain processing and long-term alteration of interneuronal excitability as a result of nociceptive peripheral input. 169 16

Pain related to fibromyalgia may consist of a complex interaction of nociceptive, neuropathic, dysregulatory central nervous system and psychosomatic mechanisms. Nociceptor pain is based on the excitation of nervous sensors specialized to signal potentially harmful stimuli, i.e., the nociceptors. Metabolic deficiencies in muscle and neurogenic inflammation induced by the release of substance P and other neuropeptides from the peripheral nerve endings may result in chemical sensitization of nociceptors and an ensuing hyperalgesia particularly present in tender points. Neuropathic pain is due to pathological mechanisms within nerve cells and fibers in the peripheral and central nervous system. Pathophysiology may be related to compression (such as in the carpal tunnel syndrome or a vertebral disk herniation) or regeneration of nerves, resulting in ectopic impulse discharges and disturbances of axonal transport. The ensuing neuronal hyperexcitability and trophic changes induced by a disturbed axonal transport system may be major factors of pain in fibromyalgia. Dysregulatory pain denotes pain maintained by dysfunction of efferent control loops. Thus, if spinal motoneuron output results in excessive tension of postural muscle, nociceptors in muscles, tendons and joints might become more excited. Persistent abnormal spinal reflex transmission due to, e.g., peripheral trauma or inappropriate postural habits may result in a vicious circle between muscle hypertension and pain. Similarly, a defective sympathetic control may result in disturbed microcirculation and nociceptor excitation (e.g., in sympathetic algodystrophy). Many symptoms of pain in fibromyalgia (trigger points, pain referral, pain associated with muscle spasm or neurogenic joint immobilization) can be attributed to abnormal control mechanisms in a complex cybernetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological mechanisms of fibromyalgia. 181 May 27

To study the axon reflex as a contributing factor to capsaicin-induced bronchoconstriction in vivo, 30 guinea pigs weighing 325 +/- 7 g were randomly divided into four groups: Group 1, control (n = 6); Group 2, bupivacaine (n = 11); Group 3, tetrodotoxin (TTX, n = 10); and Group 4, tachykinin depletion (n = 3). Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All animals were treated with atropine and phenoxybenzamine, and a ganglionic blocking agent (chlorisondamine) was given to about half of the animals. Capsaicin (16 micrograms/kg) was intravenously injected to induce bronchoconstriction. Immediately upon the capsaicin being induced each animal exhibited a decrease in vital capacity, maximal expiratory flow and respiratory compliance, as well as a more than six-fold increase in residual volume, indicating severe bronchoconstriction. Then, the airway spasm decreased gradually toward the baseline values. The animals in Group 4 indicated a complete abolishment of the capsaicin-induced bronchoconstriction, whereas Group 2 and Group 3 displayed a significantly attenuated constriction at 15 to 20 min after capsaicin injection. Administration of chlorisondamine did not alter the capsaicin-induced bronchospasm. Since it is known that bupivacaine and TTX block nerve conduction, the data suggest that the axon reflex plays a significant role in the late phase of bronchoconstriction, which is apparently mediated via tachykinins.
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PMID:Role of the axon reflex in capsaicin-induced bronchoconstriction in guinea pigs. 202 6

The role of oxygen radicals in capsaicin-induced bronchoconstriction was investigated using scavengers of the radicals. A total of 48 guinea pigs weighing 293 +/- 7 g were employed in this study, which consisted of two phases. In phase 1, 35 anesthetized paralyzed animals were divided into five groups: group 1A, control (n = 6); group 1B, chronic dimethylthiourea (DMTU, n = 12); group 1C, acute DMTU (n = 6); group 1D, superoxide dismutase (n = 4); and group 1E, catalase (n = 7). All animals were injected with capsaicin (16 micrograms/kg iv), and changes in respiratory compliance and maximal expiratory flow rate were used as indicators of bronchoconstriction. The capsaicin injection caused a marked airway spasm that was significantly ameliorated by chronic DMTU pretreatment, but no amelioration was noted with the other treatments. An additional study for group 1C was performed using a double dose of DMTU. Again no amelioration was found. In phase 2, 13 animals were divided into two groups: group 2A, substance P (SP, n = 7) and group 2B, chronic DMTU + SP (n = 6). There was no significant difference in SP-induced bronchoconstriction between animals in these two groups. These data suggest that capsaicin-induced airway constriction is modulated by oxygen radicals which may augment mainly on the biosynthesis and/or axonal transport of tachykinins.
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PMID:Oxygen radicals in capsaicin-induced bronchoconstriction. 210 20

Intimal injury and atherosclerotic change seem to be causative factors linked to spasm of the coronary artery. Intimal thickening was produced by mechanical injury to the endothelium of the canine coronary artery and we investigated the distribution of adrenergic, cholinergic, and peptidergic nerves in the coronary arteries. Although adrenergic and cholinergic nerves were not altered in density, neuron specific enolase positive nerve fibers were increased in number in dogs killed 1 and 3 months after injury. Substance P-containing fibers were also increased at 3 months after the induced injury.
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PMID:Intimal thickening and the distribution of vasomotor nerves in the mechanically injured dog coronary artery. 242 54

To further examine the role that substance P plays in initiating the observed massive postmortem bronchoconstriction in guinea pig lungs and to explore the role of neural reflex in this airway spasm, six groups of animals were employed: control (n = 6), morphine (n = 6), substance P (n = 5), chronic capsaicin pretreatment + substance P (n = 5), tetrodotoxin (TTX) + acute capsaicin (n = 4), and chlorisondamine + acute capsaicin (n = 5). Pressure-volume curves were performed prior to and following the initiation of artificial pulmonary perfusion with 1% bovine serum albumin and 5% dextran in Tyrode's solution. A decrease in inflation volume (the lung volume between transpulmonary pressure of 0 and 30 cmH2O during inflation) was used as an index of bronchoconstriction. In control animals, inflation volume decreased to 20-30% of the base-line value at 15-30 min of perfusion, indicating massive bronchial constriction during this time period. Morphine (an agent inhibiting substance P release) significantly attenuated the spasm, whereas the presence of substance P in the perfusate markedly enhanced the constriction. Depletion of endogenous substance P by chronic capsaicin pretreatment did not affect exogenous substance P-induced spasm. Acute capsaicin-induced bronchoconstriction was significantly attenuated by TTX but was not affected by the ganglionic blocking agent, chlorisondamine. These data suggest that substance P initiates the massive postmortem bronchoconstriction in guinea pig lungs and that substance P is released by local stimulation of sensory nerve endings via axonal reflex.
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PMID:Substance P-inducing massive postmortem bronchoconstriction in guinea pig lungs. 243 99

A 36 amino acid residue peptide, which contains a substance K sequence at its C-terminus has been isolated from porcine brain extracts. The primary structure of the peptide, designated neuropeptide K (NPK), was found to be: (sequence; see text) This N-terminally extended form of substance K is present in a high concentration in the brain. The peptide is highly biologically active with regard to gallbladder contraction, protein extravasation, hypotension and bronchial smooth muscle spasm and may act as an additional tachykinin neuromessenger.
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PMID:Neuropeptide K: isolation, structure and biological activities of a novel brain tachykinin. 258 73

1. Strips of longitudinal muscle can be obtained from guinea-pig ileum either retaining or free from Auerbach's plexus.2. The denervated strip is unresponsive to electrical stimulation by brief shocks, whether given singly or in trains; it also fails to respond to nicotine or dimethylphenylpiperazinium iodide (DMPP), and eserine causes no spasm.3. Denervated strips neither contain detectable acetylcholine (< 0.4 ng/mg), nor release it spontaneously (< 5 pg/mg/min) or in response to stimulation (< 31 pg/mg/min). The acetylcholine metabolism of the innervated strip is therefore that of the adherent Auerbach's plexus. Innervated strips had a mean acetylcholine content of 28 ng/mg, a mean resting output of 94 pg/mg/min and an output in response to stimulation at 10 c/s of 700-1200 pg/mg/min.4. By comparing the responses of innervated and denervated strips it was concluded that arecoline, methylfurmethide, alpha,beta-ethylal-gamma-tri-methylammonium propanediol iodide (2268 F), muscarine, histamine, tremorine, oxytocin, and substance P, like acetylcholine, act primarily on the smooth muscle directly; and that angiotensin, barium, potassium, m-bromophenyl choline ether and 5-hydroxytryptamine have a progressively increasing proportionate effect on the nerve plexus. Nicotine and DMPP were inactive in the absence of the plexus.5. The longitudinal muscle with its accompanying plexus contains about one quarter of the acetylcholine of the whole ileum, and is responsible for about one fifth of the output to electrical stimulation.6. The volley output of acetylcholine by the innervated strip declines sharply as rate of stimulation increases. Output of acetylcholine was reduced by morphine and by cocaine, particularly when resting or when stimulated at low rates.7. Acetylcholine output by whole ileum from guinea-pig declines in the absence of glucose, but is insulin-independent. Output by strips of ileum from rats made diabetic with alloxan was similar to that from normal rats.8. The similarity in properties of acetylcholine output from innervated strips, where it must come from nervous tissue, to that from whole ileum, and the insulin-independence of output from whole ileum suggest that the whole of the acetylcholine output of intestine is nervous in origin.9. Comparison of the acetylcholine metabolism of the innervated strip with that of the superior cervical ganglion suggests that the typical features of the former (high resting output, high volley output at low rates, low minute output at high rates of stimulation, and sensitivity to morphine) may be linked with the absence of specialized neuro-effector junctions and represent a relatively primitive transmission process.
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PMID:The origin of acetylcholine released from guinea-pig intestine and longitudinal muscle strips. 429 53


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