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)

1. A modified continuous assay of alpha-amylase is detailed and its usefulness in measuring amylase secretion from rat parotid salivary gland described. 2. The alpha-amylase secretion from the rat parotid gland can be evoked by acetylcholine, substance P and isoprenaline. 3. The secretion of amylase was greatest following isoprenaline stimulation and was of a slower time course than with the other two agonists.
Gen Pharmacol 1987
PMID:Description of an automated assay for measurement of alpha-amylase in vitro from rat parotid gland slices. 244 21

1. A possible role of substance P-containing nerves in the contractile response to nicotine was investigated in isolated rabbit bronchial smooth muscle preparation. 2. Nicotine caused a contraction which was attributed to the release of acetylcholine in the rabbit bronchus. The response was reduced by capsaicin (10(-5) M) and a substance P antagonist, [D-Arg1, D-Pro2, D-Trp7.9, Leu11] substance P (10(-5) M). 3. Substance P (10(-7) M)-induced contraction was reduced by atropine (10(-6) M) and potentiated by physostigmine (10(-6) M). Furthermore, substance P (10-7 M) enhanced the release of tritium or acetylcholine from the [3H]choline labelled bronchi. 4. Results suggest that substance P-like tachykinin accelerates the nicotine-evoked prejunctional endogenous neural release of acetylcholine on the nervous cells in the rabbit bronchial preparation.
Gen Pharmacol 1988
PMID:Substance P-containing nerves mediate nicotine-induced contractions of rabbit bronchial smooth muscle. 245 Aug 7

1. A new method was developed for quantitative studies on defecation reflex in urethane-anesthetized rats which involves the continuous infusion of saline (0.1 ml/min) to distend a balloon placed in the rectum. At threshold values, the balloon was expelled during an active rectal contraction. 2. Balloon expulsion was greatly delayed or even abolished by i.v. hexamethonium. Cord transection at the upper cervical level increased defecation threshold but a functional, hexamethonium-sensitive response was still elicited in spinal rats. 3. Various parameters of the defecation response were modulated by drugs (phentolamine, picrotoxin, naloxone) expected to interfere (either centrally or peripherally), with neural pathways controlling the autonomic outflow for the reflex response. 4. In capsaicin-pretreated rats (50 mg/kg s.c. on 2nd day of life, experiments performed at 2 months), daily fecal production was unchanged as compared to vehicle-treated, age-matched controls. However, under urethane-anesthesia, defecation threshold was increased at higher-than-normal values by capsaicin-pretreatment. 5. In in vitro experiments, capsaicin (1 microM) induced a transient inhibition of field stimulation-induced contractions of the rat isolated rectum. This effect was mimicked by application of calcitonin gene-related peptide (CGRP) (0.1 microM) while Substance P (0.1 microM) had an opposite effect. In preparations desensitized to exogenous CGRP, the inhibitory effect of capsaicin was almost abolished. 6. These findings indicate that in rats, reflex defecation is mainly organized at spinal level, although the participation of supraspinal centers may modify the functional response. Capsaicin-sensitive afferents may be involved in the initiation of certain forms of reflex defecation, although capsaicin-resistant mechanisms are capable of activating the normal excretory function.
Gen Pharmacol 1988
PMID:Neural pathways and pharmacological modulation of defecation reflex in rats. 245 37

The relationship between receptor-mediated increases in the intracellular free calcium concentration [( Ca]i) and the stimulation of ion fluxes involved in fluid secretion was examined in the rat parotid acinar cell. Agonist-induced increases in [Ca]i caused the rapid net loss of up to 50-60% of the total content of intracellular chloride (Cli) and potassium (Ki), which is consistent with the activation of calcium-sensitive chloride and potassium channels. These ion movements were accompanied by a 25% reduction in the intracellular volume. The relative magnitudes of the losses of Ki and the net potassium fluxes promoted by carbachol (a muscarinic agonist), phenylephrine (an alpha-adrenergic agonist), and substance P were very similar to their characteristic effects on elevating [Ca]i. Carbachol stimulated the loss of Ki through multiple efflux pathways, including the large-conductance Ca-activated K channel. Carbachol and substance P increased the levels of intracellular sodium (Nai) to more than 2.5 times the normal level by stimulating the net uptake of sodium through multiple pathways; Na-K-2Cl cotransport accounted for greater than 50% of the influx, and approximately 20% was via Na-H exchange, which led to a net alkalinization of the cells. Ionomycin stimulated similar fluxes through these two pathways, but also promoted sodium influx through an additional pathway which was nearly equivalent in magnitude to the combined uptake through the other two pathways. The carbachol-induced increase in Nai and decrease in Ki stimulated the activity of the sodium pump, measured by the ouabain-sensitive rate of oxygen consumption, to nearly maximal levels. In the absence of extracellular calcium or in cells loaded with the calcium chelator BAPTA (bis[o-aminophenoxy]ethane-N,N,N',N'-tetraacetic acid) the magnitudes of agonist- or ionomycin-stimulated ion fluxes were greatly reduced. The parotid cells displayed a marked desensitization to substance P; within 10 min the elevation of [Ca]i and alterations in Ki, Nai, and cell volume spontaneously returned to near baseline levels. In addition to quantitating the activation of various ion flux pathways in the rat parotid acinar cell, these results demonstrate that the activation of ion transport systems responsible for fluid secretion in this tissue is closely linked to the elevation of [Ca]i.
J Gen Physiol 1989 Feb
PMID:Effects of muscarinic, alpha-adrenergic, and substance P agonists and ionomycin on ion transport mechanisms in the rat parotid acinar cell. The dependence of ion transport on intracellular calcium. 246 62

Light microscopic double immunocytochemical stainings, performed on sea bass hypothalamo-hypophysial sections, revealed the projection of different neuropeptide-immunoreactive neurons innervating the hormone-producing cell populations in the pituitary gland. In the rostral pars distalis (PD) the ACTH cells were found in close proximity to fibers immunoreactive for somatostatin (SRIF), growth hormone-releasing hormone (GRF), corticotropin-releasing hormone (CRF), vasotocin (VT), isotocin (IT), substance P (SP), neurotensin, and galanin (GAL), while the PRL cell zone seemed only innervated by nerve fibers immunopositive for GAL. In the proximal PD, fibers immunoreactive for SRIF, GRF, VT, IT, cholecystokinin, SP, neuropeptide Y, and GAL formed a close relationship with the growth hormone cells. The gonadotrophs were observed near nerve fibers immunostained for gonadotropin-releasing hormone, IT, and less obviously GRF and VT, while fibers positive for GRF, CRF, VT, IT, SP, and GAL penetrated between and formed a close association with the thyrotrophs. In the pars intermedia the MSH cells and the PAS-positive (PAS+) cells seemed both innervated by separate nerve fibers immunoreactive for GRF, CRF, melanin concentrating hormone, VT, IT, and SP. All these results suggest a functional role of the neuropeptides in the adenohypophysis of the sea bass, possibly in the synthesis and/or release of hypophysial hormones from the different cell types.
Gen Comp Endocrinol 1989 Feb
PMID:Immunocytochemical demonstration of close relationships between neuropeptidergic nerve fibers and hormone-producing cell types in the adenohypophysis of the sea bass (Dicentrarchus labrax). 246 54

1. Capsaicin produced a prompt release of substance P-like immunoreactivity (SP-LI) from superfused mucosa-free muscle strips excised from the guinea-pig urinary bladder. A second application of capsaicin had no further effect, indicating desensitization. 2. Neither tetrodotoxin (1 microM) or nifedipine (10 microM) had any inhibitory effect on SP-LI release by capsaicin nor influenced the establishment of the desensitized state. Nifedipine produced per se some SP-LI release. 3. SP-LI release by capsaicin was abolished by incubation in a Calcium(Ca)-free medium containing EDTA (1.0 mM) which also afforded a partial protection toward desensitization. A lower EDTA concentration (0.1 mM) did not suppress SP-LI release by capsaicin but still inhibited desensitization. 4. When the concentration of CaCl2 in the medium was lowered to 1/10-1/100 of that present in normal Krebs solution, capsaicin still evoked a marked SP-LI release and desensitization occurred. In a nominally Ca free medium (maximal Ca concentration due to impurities was 6.7 microM) SP-LI release was still observed and desensitization was incomplete. 5. In a nominally Ca free medium, removal of Mg ions enhanced the SP-LI release induced by capsaicin and enhanced desensitization. 6. In functional studies, nifedipine greatly reduced or abolished the capsaicin- or SP-induced contraction of the rat or guinea-pig isolated bladder but did not prevent desensitization. Likewise, SP-LI depletion in the rat bladder following systemic capsaicin desensitization was not prevented by nifedipine pretreatment. On the other hand, the protective action of Ca free media (containing EDTA) was confirmed in organ bath studies (guinea-pig bladder). 7. These findings indicate that: (a) the requirements of extracellular calcium for activation of neuropeptide release from sensory nerves by capsaicin are very low; (b) both excitation of sensory fibers (SP-LI release) and desensitization are dependent upon the presence of extracellular calcium and (c) L-type voltage-sensitive Ca channels are not likely to be involved in the actions of capsaicin on sensory nerve terminals.
Gen Pharmacol 1989
PMID:The effect of calcium free medium and nifedipine on the release of substance P-like immunoreactivity and contractions induced by capsaicin in the isolated guinea-pig and rat bladder. 247 39

It is shown that the isolated oviduct as well as the proctodeum of the cockroach Periplaneta americana are sensitive to substance P application. In contrast, the hyperneural muscle and the dilator muscle of the antennal heart were insensitive to this neuropeptide. The entire substance P amino acid sequence is necessary for the effects. This provides evidence for a pharmacological effect of substance P in insects.
Gen Comp Endocrinol 1989 Jul
PMID:Evidence for a myotropic effect of substance P in Periplaneta americana L. 247 85

1. Neurotensin binding to synaptosomes isolated from the rat cerebral cortex and corpus striatum reached saturation after 4 min of incubation. 2. The rates of binding were found to be higher in the corpus striatum than in the cerebral cortex. 3. Concentration study revealed the presence of two different and independent classes of neurotensin binding sites with a negative cooperative interaction within each class of binding sites. 4. At saturation levels, the low affinity binding component was found to have a flat regional difference, while the high affinity binding component showed regional differences in terms of maximal binding capacity, suggesting a higher number of high affinity binding sites in the striatum than in the cortex. 5. In the competition related experiments, dopamine was found to displace around 70% of neurotensin binding sites in the corpus striatum and the cerebral cortex. 5. Substance P displaced around 50% of [3H]neurotensin in the cerebral cortex. Whereas, 50% and 70% displacement were observed in the striatum at high and low affinity binding sites, respectively. 6. These results show the overlap in the binding sites of neurotensin, dopamine and substance P.
Gen Pharmacol 1989
PMID:Characteristics and displaceability of neurotensin binding sites in the rat cerebral cortex and corpus striatum. 248 Feb 61

Concentrations of regulatory peptides in an extract of the intestine of the cyclostome, Myxine glutinosa (Atlantic hagfish), were measured by radioimmunoassay using 12 antisera of defined regional specificity that were raised against mammalian gastrointestinal peptides. The hagfish gut contained somatostatin-, cholecystokinin/gastrin-, C-terminal substance P-, and neurokinin A-like immunoreactivity in concentrations that were 10 to 100 times less than the corresponding concentrations in the rat intestine. The hagfish gut also contained glucagon-like immunoreactivity, measured with both C- and N-terminally directed antisera, but the immunoreactivity did not dilute in parallel with the porcine glucagon standard in radio-immunoassay. No immunoreactivity was detected using antisera to calcitonin gene-related peptide, gastrin-releasing peptide, neuromedin U, neurotensin, N-terminal substance P, and vasoactive intestinal polypeptide. The somatostatin-like immunoreactivity in the hagfish gut was resolved by HPLC into components with the retention times of somatostatin-34 and somatostatin-14, previously isolated from the hagfish islet organ (relative abundance 2:1). The retention times of hagfish glucagon and of the multiple molecular forms of the tachykinin-like peptides were appreciably different from the retention times of the corresponding mammalian peptides.
Gen Comp Endocrinol 1989 Nov
PMID:Neurohormonal peptides in the gut of the Atlantic hagfish (Myxine glutinosa) detected using antisera raised against mammalian regulatory peptides. 248 Feb 67

1. Muscle strips from the dome of the human urinary bladder responded to field stimulation with contractions which were atropine- (3 microM) and tetrodotoxin- (1 microM) sensitive. These contractions were sensitive to omega conotoxin (CTX, 0.1 microM). The atropine- and tetrodotoxin-resistant contractions produced by field stimulation were totally unaffected by CTX. 2. DMPP (30-100 microM), a nicotinic agonist, produced transient bladder contractions which were hexamethonium- and atropine-sensitive. 3. Tachykinins produced a contraction of the human bladder. Among several synthetic tachykinin analogs only those having activity at the NK-2 receptor produced a consistent contractile response. 4. Either capsaicin (1 microM) or calcitonin gene-related peptide (10 nM-0.1 microM) had no motor effect. At 10 microM, capsaicin exerted a depressant effect on nerve-mediated contractions but this effect did not exhibit desensitization. 5. These findings provide evidence that NK-2 receptors are the main if not the sole mediators of the contractile response of the muscle from the dome of the human isolated bladder to tachykinins. 6. No evidence was found for a tachykininergic component in the excitatory response to field stimulation nor for motor responses mediated by capsaicin-sensitive nerves. 7. CTX-sensitive calcium channels are probably present on cholinergic nerve terminals in the human bladder muscle.
Gen Pharmacol 1989
PMID:Further studies on the motor response of the human isolated urinary bladder to tachykinins, capsaicin and electrical field stimulation. 248 3


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