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)

A method of quantitatively measuring tachykinin-induced salivation in conscious, male, Sprague-Dawley rats is described. Salivation is quantified by determining the weight of a preweighed, absorbant foam cube after it has been used to swab the oral cavity of a tachykinin challenged rat. Salivation is induced by intravenous (i.v.) injection of sialogogues (microgram/kg) via the lateral tail vein. Measurements are made immediately after injection. Substance P (Sub.P), Sar9, Met (O2) 11Substance P (Sar9 Sub.P), a selective neurokinin (NK) 1 receptor agonist, Physalaemin and Eledoisin are equipotent sialogogues as determined by this method. Neurokinin A (NKA), the endogenous NK2 receptor agonist, is 0.27 (0.14-0.46) times as potent as Sub. P, while (Suc-[Asp6, MePhe8]Substance P(6-11), (senktide), a selective NK3 receptor agonist, only induced salivation at 300 microgram/kg. Acetylcholine (Ach) is only 0.006 (0.002-0.012) times as potent as Sub.P. Treatment with the neurokinin antagonist [D-Arg1, D-Trp7,9 Leu11]-Substance P (spantide) dose-dependently inhibits Sub. P stimulated salivation. Atropine dose-dependently inhibits Ach induced salivation but is inactive against Sub.P-induced salivation. These data are consistent with literature values and indicate that this method provides a simple, quantitative model, free of any possible anesthetic side effects, for the measurement of neurokinin stimulated salivation and the assessment of potential neurokinin antagonists in vivo.
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PMID:Measurement of tachykinin-induced salivation in conscious rats. 171 93

Tachykinin peptides acting on structures located on the ventral surface of the medulla can increase cholinergic outflow to the tracheal smooth muscles and augment respiratory motor output. In the experiments reported here (performed in anesthetized, paralyzed and artificially ventilated dogs), we examined the effects of tachykinin peptides substance P on secretion from submucosal glands. Changes in secretion were measured in an exposed section of tantalum-coated tracheal epithelium. Substances P was administered intracisternally or applied topically on the intermediate area of the ventral surface of medulla (VMS). Intracisternal infusion and the local medullary administration of tachykinin peptide caused a significant increase in tracheal submucosal gland secretion. Atropine given intravenously prevented the secretory changes induced by central action of tachykinins. In addition, prior application of 2% lidocaine to the medullary surface blocked the responses caused by substance P locally applied on the VMS. These findings suggest that substances P acting centrally can tracheal fluid secretion mainly via cholinergic mechanisms, and that the ventral surface of the medulla is one of the site of these action.
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PMID:Central effects of tachykinin peptide on tracheal secretion. 172 94

The effects of substance P, cholecystokinin and neuropeptide Y were examined on rabbit distal colonic motility. All three agents produced increased contractile activity but the mechanisms responsible differed depending on the agent tested. In the intact animal, peptide effects were measured under basal conditions and following exposure to atropine, tetrodotoxin and the alpha-adrenergic antagonist phentolamine. Administration of all three peptides resulted in a stimulation of colonic motility. Phentolamine did not significantly effect substance P-, cholecystokinin- or neuropeptide Y-induced activity. By contrast, the in vivo activity induced by cholecystokinin and neuropeptide Y, but not substance P, was nearly eliminated by tetrodotoxin. Only the neuropeptide Y response was partially atropine sensitive. In isolated colonic strips, cholecystokinin-induced activity, but not that produced by neuropeptide Y or substance P, was blocked by tetrodotoxin. Atropine did not significantly inhibit any of the hormone-induced contractions.
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PMID:Modulation of colonic motility by substance P, cholecystokinin and neuropeptide Y. 172 96

A possible role of spinal substance P (SP) in the mediation of signals to inhibit gastric acid secretion by central activation of the sympatho-adrenomedullary system was examined in urethane-anesthetized rats. Intrathecal (i.t.) administration of SP (1-10 nmol) inhibited vagally induced acid output. I.t. administration of spantide, a SP receptor antagonist, reduced the inhibitory effect of 3 nmol SP. I.t. administration of spantide (0.1-1 nmol) blocked the inhibition of vagally induced gastric acid output evoked by electrical stimulation of the preoptic area. Atropine, hexamethonium, phentolamine, propranolol, DL-para-chlorophenylalanine (PCPA) and 5,7-dihydroxytryptamine (5,7-DHT) were without effect. Repeated i.t. administration of 10 nmol SP produced desensitization to the SP-induced inhibitory response on gastric acid output. In these animals, electrical stimulation of the preoptic area did not inhibit vagally induced gastric acid output. These results suggest that electrical stimulation of the preoptic area excites SP-containing neurons in the spinal cord, and a resultant sympatho-adrenomedullary system-mediated inhibition of gastric acid secretion occurs.
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PMID:Spinal cord substance P mediates the inhibition of gastric acid secretion induced by electrical stimulation of the preoptic area. 172 67

The purpose of the present investigation was to elucidate the influence and mechanism of the action of substance P (SP) upon intraluminal pressure in proximal porcine colon. In 9 pigs, SP was infused intra-arterially in varying doses from 0.5 to 160 ng/kg/min. Mean baseline colonic pressure was 8.9 mm Hg increasing in a dose-dependent manner to 34.6 mm Hg at an SP dose of 40 ng/kg/min. Hereafter, the colonic pressure remained constant. In other series, SP infusion (5-80 ng/kg) was preceded by infusion of hexamethonium (0.5 mg/kg/min, continuous i.v.; n = 7), atropine (0.01 mg/kg/30 min, i.v.; n = 6), by naloxone (0.01 mg/kg/15 min, i.a.; n = 5) or tetrodotoxin (1 microgram/kg/h, i.a.; n = 7). Atropine significantly inhibited the effect of SP on colonic pressure, whereas the other blockers were without influence on the SP-induced colonic pressure. It is concluded that SP has a potent dose-dependent stimulatory effect upon right colonic intraluminal activity of the pig, mediated partly by atropine-sensitive receptors.
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PMID:Effect of substance P on right colonic pressure: a dose response study in pigs. 172 44

The innervation of the heart of the snake Elaphe obsoleta was examined with peptide immunohistochemistry, glyoxylic acid-induced catecholamine fluorescence, and in vitro physiological preparations. Snakes were anesthetized with Nembutal. Many somatostatin (SOM)-like immunoreactive (LI) axons were observed in the sinus venosus, atria, and ventricle. Cell bodies with SOM-LI were found in the intracardiac nerve trunks of the sinus venosus, the interatrial septum, and the atrioventricular region. The SOM-LI axons and cell bodies were not affected by 6-hydroxy-dopamine and capsaicin. They are probably intrinsic parasympathetic neurons. Adrenergic, neuropeptide Y-LI, substance P-LI, and calcitonin gene-related peptide-LI axons were found in the sinus venosus, atria, and ventricle. In spontaneously beating sinoatrial or electrically driven atrial preparations, applied SOM (6 x 10(-9) M and 6 x 10(-8) M) decreased the force of atrial contraction and/or the rate of beating. The effects of SOM were tachyphylactic. SOM had no effect on the force of contraction of the driven ventricle. Stimulation of the left and right vagus nerves elicited negative chronotropic and inotropic responses followed by poststimulus positive inotropic and chronotropic responses. Atropine abolished the inhibition, and bretylium abolished the excitation. After cholinergic and adrenergic blockade, high-frequency vagal nerve stimulation had no effect on heart rate and the force of contraction. Thus, although there is an extensive distribution of intrinsic SOM-LI neurons in the heart and although applied SOM is a potent inhibitor of rate and force, SOM in the vagal neurons does not appear to act as a direct inhibitory transmitter to the cardiac muscle or pacemaker cells.
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PMID:Somatostatin and innervation of the heart of the snake Elaphe obsoleta. 197 Apr 54

Clonidine, noradrenaline and adrenaline (in the presence of propranolol), but not phenylephrine and methoxamine, stimulated an increase in the oxygen consumption of these slices that was blocked by yohimbine but not by prazosin. The stimulation was inhibited by ouabain and required the presence of Ca2+ in the incubation medium. The calcium ionophore A 23187 stimulated oxygen consumption in the tissue slices and enhanced the respiratory effect of clonidine. Atropine and (D-Pro2, D-Trp7.9)-substance P failed to block the respiratory response to clonidine in concentrations that inhibited the respiratory effects of carbachol and substance P, respectively. Release of acetylcholine from the unstimulated gland slices was reduced by clonidine or Ca2+ omission. Yohimbine prevented the clonidine effect and stimulated acetylcholine resting release. Nifedipine did not affect either the release of acetylcholine or the clonidine-induced reduction of acetylcholine release but blocked the oxygen uptake due to clonidine or to release acetylcholine.
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PMID:Differentiation of alpha adrenoceptors mediating increase of oxygen consumption in rat submandibular salivary gland slices. 217 72

Isometric tension was recorded from strips of bovine tracheal smooth muscle in which the tone had been artificially raised by agonist drugs such as histamine and carbachol. Application of exogenous acetylcholine produced a biphasic response consisting of an initial contraction followed by a more prolonged relaxation before tone was restored to normal. Atropine blocked both components of the biphasic response to exogenous acetylcholine. Tetrodotoxin blocked neither phase of the response to exogenous acetylcholine even though a similar biphasic response to electrical stimulation was severely disrupted. Application of exogenous substance P produced a biphasic response of similar magnitude and form to that produced by acetylcholine. Application of exogenous histamine (tone raised by carbachol) also produced a biphasic response although higher concentrations were required to produce a relaxation of equal magnitude to that produced by acetylcholine. It is concluded that the inhibitory component of the biphasic response to exogenous acetylcholine occurs as a non-specific sequel to contraction.
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PMID:Relaxation following contraction in tonically contracted smooth muscle from the bovine trachea. 241 66

The present study explores whether a peptide, such as substance P (SP), has some role subserving the atropine-resistant component of electrically-evoked contractions, in isolated rat urinary bladders. The electric field stimulation (EFS) employed herein, consisted in square wave pulses of 5 Hz, 50 ms duration and supramaximal voltage (40 V), applied for 10 sec, every 3 min and conducted to the tissue via a pair of platinum ring electrodes, surrounding the isolated preparations. In order to assess whether electric stimuli, induced urinary bladder inotropism through the activation of nerve structures, degeneration of intramural nerve elements was attempted by cooling the tissue (48 h at 4-5 degrees C). After such procedure, 80-90% inhibition of responses to EFS, was detected. Moreover, tetrodotoxin, at 10(-6) M, evoked similar effects than cooling. Atropine, at 10(-6) M, failed to produce a significant decrement of contractile responses, whereas at 10(-5) M, the electrically-induced inotropism declined around 40%, in comparison with controls. In another set of experiments, atropinized urinary bladders (atropine at 10(-5) M) were exposed to capsaicin (5 X 10(-6) M) and this coincided with decreased (-43%) responses to EFS. Next, SP, at 10(-9) M, was added to the medium containing capsaicin and complete restoration of full contractile responses to EFS, was observed. Inasmuch as it has been proposed that capsaicin releases SP from sensory nerve fibers and since our experiments show that SP restored the inotropism elicited by electric stimuli on capsaicin-exposed preparations, it is suggested that SP could be involved, at least in part, in the non-cholinergic, EFS-evoked, contractile responses of isolated rat urinary bladders.
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PMID:Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P. 241 26

Cholinergic influences on intestinal propulsion were determined in vivo in fasted rats by measuring the movement of a nonabsorbable radioactive marker along the intestine following treatment with cholinergic drugs. The marker was instilled directly into the intestine via a previously implanted cannula. The direct effects of cholinergic drugs on intestinal contractions were determined in vitro using isolated segments of duodenum and jejunum. Neostigmine (0.1 mg/kg) produced a marked increase in intestinal transit that was blocked by atropine pretreatment (1.0 mg/kg) but not hexamethonium pretreatment (20 mg/kg). Atropine pretreatment alone significantly delayed transit while hexamethonium treatment alone did not affect intestinal transit. Neostigmine produced a concentration-dependent (0.3-30 microM) increase in contractions in both duodenal and jejunal segments in vitro. Prior incubation of the tissues with atropine (10(-7) M) blocked the neostigmine-induced contractions while prior incubation with hexamethonium (10(-6) M) did not. Contractions produced by substance P were not affected by atropine or hexamethonium. These data indicate that enhancement of cholinergic neurotransmission by neostigmine treatment increased intestinal propulsion and that this effect was mediated at muscarinic cholinergic receptors. Furthermore, inhibition of ongoing cholinergic transmission by atropine treatment reduced intestinal propulsion. The increase in transit produced by neostigmine may result from a stimulation of intestinal contractions. Cholinergic neurons are important mediators of intestinal propulsion in the rat as in other species.
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PMID:Cholinergic neurons mediate intestinal propulsion in the rat. 242 41


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