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)

To clarify whether various neuropeptides found in the hypothalamus act directly on a pituitary adenoma causing Nelson's syndrome, we examined the influence of these peptides on the secretion of immunoreactive ACTH, beta-endorphin, and melanotropins, the proopiomelanocortin (POMC)-derived peptides, by the cultured pituitary adenoma from a patient with Nelson's syndrome. Results showed that somatostatin-14 and somatostatin-28 suppressed the secretion of POMC-derived peptides by the adenoma and that somatostatin-28 was as potent as somatostatin-14. Other neuropeptides such as arginine vasopressin, vasoactive intestinal polypeptide, and oxytocin stimulate the secretion of POMC-derived peptides. Substance P, TRF, Met-enkephalin and Leu-enkephalin were also found to modulate the secretion of POMC-derived peptides. This suggests that the adenoma may have multiple receptors to various neuropeptides.
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PMID:Effects of various neuropeptides on the secretion of proopiomelanocortin-derived peptides by a cultured pituitary adenoma causing Nelson's syndrome. 612 87

Specific binding sites for somatostatin have been characterized in cytosolic fraction of rat intestinal mucosa by using 125I-labelled Tyr11-somatostatin and a variety of physicochemical conditions. The binding depended on time, temperature and pH, and was reversible, saturable and specific. At apparent equilibrium, the specific binding of 125I-Tyr11-somatostatin was competitively inhibited by native somatostatin in the 1 nM-4 microM concentration range. Binding studies suggested the presence of two classes of binding sites: a class with high affinity (Kd = 0.07 microM) and low capacity (4.6 pmol/mg protein) and a class with low affinity (Kd = 1.05 microM) and high capacity (277 pmol/mg protein) at 25 degrees C. Somatostatin exhibited competitive inhibition of tracer binding, while neuropeptides such as neurotensin, substance P, Leu-enkephalin, and vasoactive intestinal peptide were ineffective. The presence of somatostatin binding sites in cytosolic fraction of intestinal mucosa, together with the known occurrence of somatostatin in D-cells and nerve endings in the small intestine, strongly suggest that this peptide may be involved in the physiology and physiopathology of intestinal epithelium.
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PMID:Characterization of somatostatin binding sites in cytosolic fraction of rat intestinal mucosa. 614 67

The carotid body type I cell contains amines and has features, both morphological and cytochemical, which indicate that it may also produce a peptide. Many regulatory peptides are now known to be present in both central and peripheral tissues. In the periphery these neuropeptides occur in both classical endocrine (APUD) cells and the neurones of the autonomic nervous system. We have now investigated the possible presence of neuropeptides in the cat carotid body using both immunocytochemistry and radioimmunoassay. Met- and Leu-enkephalin-like material occurred in considerable quantities in carotid body extracts and enkephalin-like immunoreactivity was localised in type I cells. Both vasoactive intestinal polypeptide (VIP)- and substance P-like immunoreactivity was also present but was localised in nerve fibres distributed throughout the organ. These active neuropeptides are widely distributed in mammalian tissues, forming a diffuse regulatory system which now seems to include the carotid body.
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PMID:Enkephalin-, VIP- and substance P-like immunoreactivity in the carotid body. 615 60

The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulus-evoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic gamma-aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.
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PMID:Regulation of neuropeptide release. 615 55

Neonatal administration of capsaicin on the days 2, 10 or 20 leads to a long-lasting loss of substance P immunoreactive material in fibers of primary sensory neurons in the spinal cord and medulla oblongata. The degree of depletion examined 6 months after treatment was related to the day of injection. Injections on the second day produced dramatic losses of substance P in fibers of the substantia gelatinosa and the marginal layer of the spinal cord and the spinal nucleus of the trigeminal nerve, although these losses were never complete. The observed depletion of substance P immunoreactive material was homogenous throughout the superficial layers of the dorsal horn and the spinal nucleus of the trigeminal nerve. No changes were observed for the immunoreactivity of Leu-enkephalin in the substantia gelatinosa and the marginal layer of the spinal cord in consecutive sections from the same treated animals. In the medulla oblongata a reduction of substance P immunofluorescent fibers was found in the nucleus tractus solitarii and the spinal nucleus of the trigeminal nerve. Other areas of the central nervous system with a rich innervation of substance P immunoreactive fibers were not affected by capsaicin treatment.
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PMID:Substance P immunoreactive neurons following neonatal administration of capsaicin. 616 95

The existence of a neuronal pathway containing Leu-enkephalin and connecting the neostriatum with the globus pallidus has been confirmed combining immunohistochemistry with microinjections of neurotoxic agents (kainic acid, colchicine) and discrete knife lesions. The presence of substance P in nerve terminals of the substantia nigra was demonstrated by the application of a monoclonal antibody against this peptide. Electron microscopic studies revealed immunoreactive sites for substance P in nerve terminals establishing symmetric and asymmetric synapses, mainly over dendritic profiles. The possible peptide-containing neuronal pathways in the nigro-striatal system are discussed.
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PMID:Neuropeptides in striato-nigral pathways. 616 72

Spinal cords of rats, cats and monkeys were transected; the animals were perfused at varying times. Other rats were injected with morphine and perfused 10 days later. Immunocytochemistry shows substance P (SP) present in control animals primarily in the substantia gelatinosa (SG) of the dorsal horn of the spinal cord. Slight SP immunoreactivity is found in the ventral horn and near the central canal. Starting a few days after transection, there is a buildup of reaction product in the dorsal horn, in sections cut from below the lesion; staining above remains the same. With time, after chordotomy, SP immunoreactivity appears in fibers in lamina V, only in sections below the lesion. Leu-enkephalin (LE) is also found in the SG, however, it is also present in quantity in the ventral horn and central canal areas. Chordotomy has no effect on its distribution indicating LE is intrinsic in the cord and probably contained within interneurons. Morphine increases SP immunoreactivity in the SG, laminae I, IV and V, and in the ventral horn, suggesting morphine analgesia is due to inhibition of intraneuronal SP release in regions specifically associated with pain--SG and lamina V.
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PMID:Substance P and leucine-enkephalin changes after chordotomy and morphine treatment. 616 70

To test the hypothesis that enkephalins, substance P, bradykinin and angiotensin II could act as neurohumoral modulators of hypothalamic function, these peptides (0.01-20 microgram) were injected into the general circulation of anesthetized rats, and changes in hypothalamo-neurohypophysial activity were determined by continuously monitoring the amplitude of antidromic compound action potentials (CAP) in the hypothalamo-hypophysial tract. A decrease of CAP amplitude was taken to indicate an increase of orthodromic impulse traffic. All peptides elicited a CAP decrease. On a molar basis when injected i.v., the enkephalin analog FK 33-824 was the most effective substance, followed by substance P, Leu-enkephalin and angiotensin II. Enkephalins and substance P injected through the internal carotid artery, were 2-5 times more effective than when injected i.v., whereas bradykinin was most effective when it reached the brain through a vertebral route. Angiotensin II produced the same CAP decrease irrespective of the route of administration and, in contradistinction to the other peptides, its effect was not abolished by stalk section. Tachyphylaxis and reversibility with naloxone was observed only for the enkephalins. The data suggest that sites of action are the hypothalamus for enkephalins and substance P, the neurohypophysis for angiotensin II, and the hindbrain for bradykinin.
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PMID:Enkephalins, substance P, bradykinin and angiotensin II: differential sites of action on the hypothalamo-neurohypophysial system. 616 30

Repetitive stimulation of the midbrain reticular formation with electrical stimuli causes extinction of the hippocampal theta rhythm. This phenomenon was used as an indicator of the effect of intracerebroventricular administration of the C-terminal hexapeptide substance P fragment (SP6-11), Leu- and Met-enkephalin on hippocampal electrical activity in the experiments performed on rabbits. Intracerebroventricular administration of SP6-11 caused an increase in the number of trains of pulses required to produce the extinction of the theta rhythm. Both of the enkephalins had opposite effects, the effect of Met-enkephalin being more than twice as strong as Leu-enkephalin. Control administration of C-terminal pentapeptide substance P fragment (SP7-11) and 0.9% NaCl solution had no significant effect on the tested phenomenon.
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PMID:Extinction of hippocampal theta rhythm evoked by mid-brain stimulation after intracerebroventricular administration of substance P fragment and enkephalin administration in rabbits. 617 Mar 89

Angiotensin-converting enzyme was solubilized with papain from a particulate fraction of rat brain and purified to apparent homogeneity by a procedure including DEAE-cellulose, hydroxylapatite, Sephadex G-200, Cys(Bzl)-Pro-Sepharose, and ricin-Sepharose chromatography. Bradykinin potentiators, SQ 14,225, and Arg-Pro-Pro strongly inhibited the activity of the purified enzyme, whereas Phe-Ala, phosphoramidon, and pentobarbital exerted little inhibitory effect on the activity. Among neuropeptides investigated, substance P, bradykinin, and Leu-enkephalin (Arg6) exerted strong inhibitory actions on the enzyme. Furthermore, the latter two peptides were shown to be good substrates for the enzyme. Thus, angiotensin-converting enzyme of rat brain is distinct from endogenous enkephalinase and may interact with various neuropeptides located in the brain.
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PMID:Purification and inhibition by neuropeptides of angiotensin-converting enzyme from rat brain. 619 11


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