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 effect of octreotide (OCT), a stable somatostatin analog, (OCT) on changes in short-circuit current (Isc) induced by vasoactive intestinal peptide (VIP), aminophylline, serotonin (5-HT) and substance P. OCT significantly decreased basal Isc at a concentration of 10(-9) M; the maximum decrease in Isc was observed at 10(-6) M. OCT (10(-7) M) significantly inhibited the intestinal secretory response to all the secretagogues studied. The maximum Isc response was reduced when tissues were stimulated with VIP (184.9 +/- 18.0 vs. 119.7 +/- 14.1, P less than 0.05), 5-HT (135.1 +/- 14.4 vs. 79.5 +/- 13.4, P less than 0.05) and substance P (156.0 +/- 19.2 vs. 30.7 +/- 5.4, P less than 0.01). In the case of aminophylline, the concentration-response curve was shifted to the right but the maximum response was not reduced. Because VIP and aminophylline increase cAMP while 5-HT and substance P stimulate intestinal secretion principally by a calcium linked mechanism, we conclude that OCT inhibits Isc in rat colon by more than one mechanism.
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PMID:Octreotide inhibits increases in short-circuit current induced in rat colon by VIP, substance P, serotonin and aminophylline. 169 51

Rats were fed a liquid diet with the aim of decreasing nervous reflex activity in the parotid glands. In rats killed after 21 days on this diet the glands were atrophied and the total amounts of the neuropeptides, substance P, vasoactive intestinal peptide and calcitonin gene-related peptide, were lower than in control glands.
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PMID:Neuropeptides and disuse of the rat parotid gland. 169 60

Substance P produced a dose-dependent, long-lasting hyperpolarization of the membrane of the Schwann cells of the giant nerve fibre of the tropical squid. A survey of the effectiveness of a range of other naturally occurring tachykinin agonists suggested that the receptors present on the squid Schwann cell belong to the subtype SP-P or NK1, for which substance P is the preferred agonist. A survey of the effectiveness of a range of substance P fragments indicated that the direct hyperpolarizing effects of the substance P molecule were mediated by peptides with an intact amidated C-terminal. However, a second subset of receptors that can be activated by N-terminal fragments and analogues lacking an amidated C-terminal was also present in this preparation. The non-subtype-specific antagonist D-Arg1,D-Trp7,9,Leu11 substance P (spantide) was a potent blocker of the effects of substance P in this preparation. Activation of the substance P receptors did not interact with the effects induced by activation of either the nicotinic cholinergic receptors or octopaminergic receptors present in this preparation. However, it did potentiate the effects of activation of the receptors for vasoactive intestinal peptide (VIP), either in response to bath application of the peptide or due to their activation by the release of an endogenous VIP-like peptide after stimulation of the giant axon.
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PMID:Substance P modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre. 169 92

1. Whole-cell patch-clamp recordings were made from pairs of neurones in cell cultures of rat myenteric neurones. In some pairs, action potentials evoked in the first neurone evoked a slow excitatory postsynaptic potential (EPSP) in the second neurone. 2. Action potentials at a frequency of at least 5 Hz were required to evoked slow EPSPs. In one group of cells, the slow EPSP followed a series of nicotinic fast EPSPs; in another group, fast EPSPs did not precede the slow EPSP. 3. The slow EPSPs were 2-16 mV in amplitude and were accompanied by decreased resting potassium conductance. 4. Most (17/28) neurones in which action potentials evoked only slow EPSPs in a follower cell contained substance P (SP)-like immunoreactivity; they were not immunoreactive for 5-hydroxytryptamine (0/15) or vasoactive intestinal peptide (0/22). 5. Postsynaptic responses to SP, neurokinin A and a synthetic tachykinin [( pGlu6, Pro9]SP6-11) mimicked the slow EPSPs. The non-tachykinin peptide vasoactive intestinal polypeptide (VIP), which was not found in neurones that evoked only slow EPSPs, also mimicked the slow EPSPs. Responsiveness to SP decreased significantly during slow EPSPs. 6. Desensitization to either SP or VIP reduced or prevented the slow EPSPs and also responses to each other. Two proposed antagonists of SP receptors, [D-Arg1, D-Pro2,D-Trp7,9,Leu11]substance P and [D-Arg1,D-Trp7,9,Leu11]substance P, did not affect the slow EPSPs significantly. 7. Antisera against SP reversibly blocked or reduced slow EPSPs evoked by eight of thirteen presynaptic neurones that evoked slow EPSPs without evoking fast EPSPs. All eight of the presynaptic neurones that evoked anti-SP-sensitive slow EPSPs contained SP-like immunoreactivity. None of the presynaptic neurones that evoked anti-SP-insensitive slow EPSPs contained detectable SP-like immunoreactivity. Normal sera and anti-VIP antisera did not alter the slow EPSPs detectably. 8. It is concluded that subsets of myenteric neurones release an SP-like transmitter to evoke slow EPSPs. These neurones appear to lack a 'classical' neurotransmitter that evokes fast EPSPs.
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PMID:Substance P mediates synaptic transmission between rat myenteric neurones in cell culture. 170 Jan 7

In order to study the effects of peptides on intrinsic cardiac neurons, substance P, bradykinin, oxytocin, calcitonin gene related peptide, atrial natriuretic peptide and vasoactive intestinal peptide were administered into canine atrial or ventricular ganglionated plexi. When substance P was injected into right atrial or cranial medial ventricular ganglionated plexi heart rate, atrial force and ventricular intramyocardial pressures were augmented. No cardiac changes occurred when similar volumes of saline (i.e., peptide vehicle) were injected into these ganglionated plexi. When bradykinin was injected into atrial or ventricular ganglionated plexi heart rate, atrial force and ventricular force were augmented in approximately 50% and depressor responses were elicited in approximately 50% of these animals. When oxytocin was injected into right atrial ventral ganglionated plexi heart rate and atrial forces were reduced in five of ten dogs studied. No cardiac changes occurred when oxytocin was injected into left atrial or ventricular ganglionated plexi. No responses were elicited when calcitonin gene related peptide, atrial natriuretic peptide or vasoactive intestinal peptide was administered into atrial or ventricular ganglionated plexi. Following acute decentralization of the heart, no significant responses were elicited by repeat administrations of substance P, bradykinin or oxytocin, implying that connectivity with central nervous system neurons was necessary for consistent responses to be elicited. It is concluded that substance P, bradykinin and oxytocin can affect neurons on the heart such that cardiodynamics are modified, these different peptides eliciting different cardiac responses.
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PMID:Cardiac responses elicited by peptides administered to canine intrinsic cardiac neurons. 170 Mar 99

An in vivo model for the simultaneous study of the motility of the gallbladder, sphincter of Oddi and duodenal wall in the anesthetized cat was developed. Changes in gallbladder volume were recorded as well as changes in the outflow from the sphincter of Oddi and from a vein graft inserted through the duodenal wall during perfusion at constant pressure. The distribution of three peptide hormones (substance P-SP, vasoactive intestinal peptide-VIP and cholecystokinin-CCK) within the feline extrahepatic biliary tree was studied immunocytochemically. Nerve terminals with SP-like immunoreactivity (LI) were distributed to the smooth muscle layers and also to acetylcholinesterase-positive ganglions cells in the intrinsic plexa. SP-LI was further demonstrated in cell bodies of the intrinsic plexa as well as in vagal axons. VIP-LI had a similar distribution. An especially rich VIP-ergic innervation was observed within the circular muscle layer of the sphincter of Oddi. SP-LI or VIP-LI did not occur in mucosal endocrine cells. On the other hand, CCK-LI was not demonstrated in nerves but occurred regularly in endocrine cells of the duodenal mucosa. Regional administration of SP elicited dose-dependent contractile motor effects on the biliary tree, which were not dependent on muscarinic or nicotinic cholinoceptors, but were inhibited by infusion of an antagonistic SP analogue indicating a direct effect on the smooth muscle cell. Efferent electrical vagal nerve stimulation elicited contractile motor responses, which were blocked by either atropine or infusion of the SP-analogue, indicating activation of a postganglionic cholinergic neuron via intrinsic or extrinsic SP neurons. These observation correlate well with the presence of SP nerve terminals on acetylcholinesterase-positive ganglion cells of the intrinsic plexa and SP axons within the vagus. An afferent mechanism cannot be excluded; antidromic activation of SP-containing axon collaterals from vagal afferents might act on intrinsic cholinergic neurons. The cellbodies of such afferents may be present in intrinsic plexa or within the sensory vagal nodose ganglion. VIP elicited relaxatory motor responses from the extrahepatic biliary tree, not influenced by blockade of cholinoceptors or beta-adrenoceptors. Stimulation of beta-adrenoceptors, or selective stimulation of beta 2-adrenoceptors caused dose-dependent relaxatory motor responses, which were antagonized by specific blockade. Stimulation of beta-adrenoceptors following selective blockade of beta 2-adrenoceptors resulted in relaxation, most probably mediated by beta 1-adrenoceptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The vagal nerves and peptides in the control of extrahepatic biliary motility. An experimental study in the cat. 170 May 77

Gastrin-releasing peptide (GRP) and bombesin can stimulate pepsinogen release by both gastrin-dependent and -independent mechanisms. Using isolated guinea pig gastric chief cells, we determined that GRP can act directly on the guinea pig chief cell to cause pepsinogen release. GRP and bombesin stimulated a 2.5- to 3-fold increase in pepsinogen release above basal release. Substance P also stimulated a small but significant increase in pepsinogen release. No gastrin immunoreactivity was detected in the supernatants of cells stimulated with up to 1 microM GRP or bombesin or 1 mM carbachol. GRP-stimulated pepsinogen release was completely inhibited by GRP/bombesin receptor agonists as well as substance P receptor antagonist but not by antagonists to receptors for gastrin, the octapeptide of cholecystokinin (CCK-8), secretin, vasoactive intestinal peptide (VIP), or muscarinic agents. Substance P-stimulated pepsinogen release was completely inhibited by substance P receptor antagonist but not by GRP/bombesin receptor antagonists. An additive effect on pepsinogen release was seen when GRP was combined with maximally effective concentrations of adenosine 3',5'-cyclic monophosphate (cAMP)-mediated agents (VIP, secretin, 8-BrcAMP) but not with calcium-mediated agents (carbachol, CCK-8, gastrin). These results indicate that GRP can directly stimulate pepsinogen release from guinea pig chief cells by a specific GRP receptor that mobilizes intracellular calcium.
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PMID:Gastrin-releasing peptide directly releases pepsinogen from guinea pig chief cells. 170 Jun 25

The effects of the tachykinin antagonist Spantide II (D-Nic-Lys1,3-Pal3,D-Cl2Phe5,Asn6,D-Trp7,9,Nl e11)-substance P (SP) and the vasoactive intestinal peptide (VIP) antagonist (Ac-Tyr1,D-Phe2)-GRF(1-29)-NH2 on the excitability of the spinal nociceptive flexor reflex to intrathecally (i.t.) applied SP and VIP, respectively, as well as the facilitation evoked by activation of cutaneous C-afferent was examined. Both antagonists blocked the effects of the respective neuropeptides in rats with both intact and sectioned sciatic nerves. Spantide II antagonised C-afferent induced reflex facilitation in rats with intact nerves, but the degree of antagonism declined after axotomy. In contrast, the VIP antagonist did not block C-afferent induced facilitation in rats with intact nerves, but did so after axotomy. The results indicate that the role of tachykinins in mediating C-afferent-induced reflex facilitation is taken over by VIP after axotomy.
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PMID:Plasticity of the peptidergic mediation of spinal reflex facilitation after peripheral nerve section in the rat. 170 Aug 43

Both carotid bodies from 26 patients coming to necropsy were fixed in 10% neutral buffered formalin and sections 4 microns thick were stained for various peptides by use of the immunogold technique. The results show that the human carotid body contains met- and leu-enkephalin, substance P, vasoactive intestinal peptide (VIP), neurotensin and bombesin. The distribution of these six peptides within the carotid body differs. Thus met- and leu-enkephalin are both present predominantly within glomic chief cells but with a marked tendency to favour the dark variant of these cells. Substance P and VIP both show a weak immunoreactivity in comparison to the enkephalins and are present in all three variants of chief cell. Neurotensin shows the weakest immunoreactivity of all and is restricted to a few glomic chief cells in a minority of cases. Bombesin also shows a weak immunoreactivity in glomic chief cells but a strong reaction in glomic arteries and arterioles. In these vessels bombesin appears to be confined to smooth muscle cells in the media but we cannot say whether it is secreted by them or merely bound to receptor sites on their membranes. These findings are related to quantitative data on the concentration of peptides in the human carotid body from a previous paper with which we were associated.
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PMID:The occurrence and distribution of certain polypeptides within the human carotid body. 170 Sep 31

Release of [3H]acetylcholine ([3H]ACh) was examined in a submucous plexus preparation obtained from the guinea pig small intestine in vitro. Constant-current field stimulation evoked ACh output; this output was dependent on the stimulus frequency applied. Maximal release was observed at 10 Hz; this release was blocked by tetrodotoxin (1 x 10(-6) M) or in Ca2(+)-free buffer. Serotonin [5-hydroxytryptamine (5-HT)] stimulated the release of ACh dose dependently, with an ED50 of 5 x 10(-7) M. Substance P was ineffective, while vasoactive intestinal peptide weakly stimulated ACh secretion. Several neuropeptides were tested on their ability to modulate 5-HT-evoked ACh release. Dynorphin A inhibited 5-HT-stimulated ACh release, while Met-enkephalin was without any effect. Both somatostatin and galanin were effective modulators, with an inhibitory effect in the submicromolar range and an excitatory effect at higher concentrations. The response characteristics of the cholinergic neurons of submucosal plexus differ markedly from those of the myenteric plexus. These distinct features form an important framework for future functional studies on submucous plexus neurons.
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PMID:Modulation of submucosal cholinergic neurons by 5-hydroxytryptamine and neuropeptides. 170 72


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