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)

In muscularis mucosae from the opossum distal colon, both tone and spontaneous contractions were highly dependent on the available oxygen. Acetylcholine and histamine caused, respectively, atropine- and pyrilamine-sensitive contractions. Norepinephrine relaxed the tissue, an effect abolished by propranolol. Under these conditions norepinephrine failed to elicit contractions and at higher concentrations again caused relaxations. The tissue gave concentration-dependent relaxations to ATP but not to ADP, AMP, or adenosine. Electrical field stimulation (20-30 Hz, 1-2 ms, 120 mA) revealed a cholinergic excitatory innervation and a nonadrenergic, noncholinergic neural inhibition. Cholecystokinin, gastrin, substance P, and vasoactive intestinal polypeptide were without effect on this tissue. In these respects, colonic muscularis mucosae differs considerably from that of other gastrointestinal viscera.
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PMID:Pharmacological characterization of opossum distal colonic muscularis mucosae in vitro. 394 17

Vasodepression was found ex vivo in the isolated perfused hind legs of rats, mice and guinea-pigs with paw inflammation using maximum pressure amplitude, EAm, pD2-value and intrinsic sensitivity (i.s.) as the test parameters of dose-response curves of vasopressor substances (noradrenaline, lys- and arg-vasopressin, angiotensin II, substance P, Na2-ATP). Vasodepression is strong in the anaphylactic and dextran paw edema, moderate in the carrageenin paw edema and adjuvant arthritis, but weak in the pertussis vaccine and kaolin paw edema. It is partly long-lasting, does not closely correlate with edema strength and can also be shown in the contralateral non-inflamed leg. Thus, a vasoreactivity depressing factor(s) must be liberated from the site of inflammation and reach the general circulation. Here, the method is described using the adjuvant arthritis as an example.
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PMID:Determination of reactivity of resistance blood vessels in the isolated perfused legs of animals with inflammation as exemplified in adjuvant arthritis. 396 85

This study describes effects of various peptides, neurotransmitters and cyclic nucleotides on brain polyphosphoinositide metabolism in vitro. The interconversion of the polyanionic inositol phospholipids was studied by incubation of a lysed crude mitochondrial/synaptosomal fraction with [gamma-32P]-ATP. The reference peptide ACTH1-24 stimulated the formation of radiolabelled phosphatidylinositol 4,5-diphosphate (TPI) and inhibited that of phosphatidic acid (PA). Substance P inhibited both TPI and PA labelling, whereas beta-endorphin inhibited that of PA without any effect on TPI. Morphine had no effect at any concentration tested, whereas high concentrations of naloxone inhibited the labelling of both PA and TPI. Naloxone did not counteract the effects of ACTH1-24. The other peptides tested (lysine 8-vasopressin and angiotensin II) were without any effect. Under the conditions used, adrenaline, noradrenaline and acetylcholine did not affect the labelling of the (poly)phosphoinositides. Both dopamine and serotonin, however, dose-dependently inhibited the formation of radiolabelled TPI and PA. Low concentrations of cAMP stimulated TPI, but higher concentrations had an overall inhibitory effect on the labelling of TPI, PA and especially phosphatidylinositol 4-phosphate (DPI). The cyclic nucleotide did not mediate or counteract the effects of ACTH, and cGMP was without any effect. These results are discussed in the light of current ideas on the mechanism of action of neuropeptides.
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PMID:Polyphosphoinositide metabolism in rat brain: effects of neuropeptides, neurotransmitters and cyclic nucleotides. 612 17

Electrical field stimulation of the isolated pig bladder neck preparation initiated rapid non-adrenergic, non-cholinergic nerve-mediated relaxations. A wide range of substances were examined as possible candidates for the neurotransmitter involved. Of these, only 5-hydroxytryptamine, vasoactive intestinal polypeptide, adenosine and adenosine 5'-triphosphate produced relaxations. Noradrenaline, acetylcholine, substance P, bradykinin and angiotensin II caused contraction, while neurotensin, somatostatin, bombesin and gamma-amino butyric acid were without effect. The nerve response was not blocked by methysergide, ketanserin, chymotrypsin, apamin or 8-phenyltheophylline, although methysergide antagonised the responses to 5-hydroxytryptamine, chymotrypsin blocked the responses to VIP, and 8-phenyltheophylline antagonised the responses to adenosine and ATP.
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PMID:A novel non-adrenergic, non-cholinergic nerve-mediated relaxation of the pig bladder neck: an examination of possible neurotransmitter candidates. 614 1

Rabbit bladder body was stimulated to contract by a number of agonists, of which bradykinin was the most potent, and ATP one of the least potent substances tested. The atropine-resistant component of the neurogenic response was unaffected by 2 X 10(-5) M chlorpheniramine or 10(-6) M methysergide, doses which suppressed responses to histamine or 5HT. Indomethacin 10(-5) M, or 10(-5) M capsaicin both reduced the atropine-resistant component. Following treatment with 10(-6) M atropine and 10(-5) M prazosin, 10(-4) M ANAPP3 produced a further suppression of the response, but did not antagonize the response to ATP. In the bladder body, the transmitter(s) responsible for the neurogenic response may be acetylcholine and prostaglandins and possibly ATP and substance P.
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PMID:A study of the atropine-resistant component of the neurogenic response of the rabbit urinary bladder. 614 2

Vasoactive intestinal polypeptide (VIP) is a powerful vasodilator agent in the submandibular gland of the cat, and its effect can be reduced by avian pancreatic polypeptide (APP), or by desensitization of the gland's blood vessels to VIP. However, the vasodilatation caused by parasympathetic nerve stimulation is not reduced by either of these means. We conclude, therefore, that VIP is unlikely to be a major mediator of this atropine-resistant vasodilatation. Experiments with a potentiator of acetylcholine, eserine, and with a depleter, suggest that acetylcholine plays some role in this vasodilatation, but it too does not appear to be the major physiological mechanism. Substance P and ATP were neither potent nor consistent vasodilators and are unlikely mediators.
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PMID:A study of vasoactive intestinal peptide and acetylcholine as possible mediators of vasodilatation in the cat submandibular gland. 614 96

The influence of substance P (SP) and somatostatin (SS) on contractions induced by electrical field stimulation, ATP and carbachol were investigated in isolated rabbit urinary bladder. Some experiments were also carried out in rat and guinea-pig detrusor. When added cumulatively to rabbit and rat preparations, SP and SS caused a gradual increase in tone of the preparations. There were no effects on the electrically induced contractions. In rabbit and rat detrusor pretreated with guanethidine, atropine and indomethacin, the contractile response to nerve stimulation was markedly reduced. In this situation SP and SS caused 2-4 fold increase in the electrically induced contractions. Indomethacin abolished the tonic response to ATP in the rabbit detrusor, and reduced the initial phasic contraction by about 30%. Both SP and SS were able to restore the phasic contraction to the level obtained before indomethacin addition. The contractions induced by carbachol in rabbit and rat detrusor were not affected by SP and SS, not even in indomethacin pretreated preparations. The SP-antagonist (D-Pro2, D-Phe, D-Trp9)-SP was tested in isolated rabbit, rat, and guinea-pig detrusor. Concentrations of the antagonist which effectively inhibited contractions induced by a submaximum concentration of SP had no effect on the contractile response to electrical field stimulation in rabbit and guinea-pig preparations, and rather tended to increase the contractions in the rat detrusor. The results suggest that neither SS nor SP is the mediator of excitatory non-cholinergic, non-adrenergic activation of rabbit urinary bladder. A role as local modulators of neuromuscular transmission cannot be excluded.
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PMID:Substance P and somatostatin and excitatory neurotransmission in rabbit urinary bladder. 617 Dec 17

In the rabbit iris sphincter muscle, electrical transmural stimulation produced fast and slow components of contraction which were markedly attenuated by tetrodotoxin. The fast component was augmented by physostigmine and was abolished by atropine, while the slow component was little affected. Adrenergic and ganglionic blocking agents did not inhibit the slow component. Therefore, the fast component is probably cholinergic, while the slow one is noncholinergic, nonadrenergic in nature. Capsaicin did produce a considerable contractile response, but there was a gradual decline with repetitive application and a tachyphylaxis occurred. Under such conditions the slow but not the fast component was abolished. Substance P and acetylcholine produced the largest contraction, while ATP, histamine, serotonin and noradrenaline produced little or no response. In cold stored preparations, the responses to electrical transmural stimulation and capsaicin were either markedly attenuated or abolished, whereas substance P and acetylcholine produced considerable contractions. Baclofen and theophylline did not inhibit the slow response to electrical transmural stimulation or the response to substance P and capsaicin. Thus, electrical transmural stimulation produces cholinergic and noncholinergic, non-adrenergic contractions in the rabbit iris sphincter muscle and the latter response is considered to be mediated by substance P or a related peptide released from the neural component.
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PMID:Noncholinergic, nonadrenergic contraction and substance P in rabbit iris sphincter muscle. 617 63

Peptide and non-peptide agents were tested for their stimulatory or inhibitory effects on circular strips of guinea pig isolated tracheae. Substance P, eledoisin, physalaemin, neurotensin, angiotensin, histamine and carbachol were found to contract, while noradrenaline, dopamine, bradykinin, nucleotides (AMP, ADP, ATP) and prostaglandins (PGE1, PGE2, PGA2) induced concentration-dependent relaxations of tracheae contracted with substance P or carbachol. Indomethacin (2.8 X 10(-6) M) significantly potentiated the effect of substance P and blocked that of bradykinin. The contractions to substance P of tissues treated with indomethacin were not modified by atropine, methysergide, diphenhydramine, cimetidine, propranolol, phentolamine, [Leu8]-ATII, [Leu8]-des-Arg9-bradykinin, naloxone and baclofen. The order of potency of C-terminal fragments of substance P was: hexa(6-11) greater than hepta(5-11) greater than substance P greater than = octa(4-11). It is concluded that the guinea pig isolated trachea is a pharmacological preparation sensitive to numerous agents and useful for studying structure-activity relationship and the mechanism of cellular action of several peptides, particularly substance P.
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PMID:Pharmacological effects of peptides on tracheal smooth muscle. 618 32

1. The effects of some putative non-adrenergic, non-cholinergic transmitters have been studied on longitudinal and circular smooth muscle from the stomach of the rainbow trout, Salmo gairdneri. 2. ATP, adenosine and vasoactive intestinal polypeptide (VIP) on certain occasions inhibited the activity of the stomach smooth muscle; ATP and adenosine only circular muscle. VIP both longitudinal and circular muscle. 3. Neurotensin produced a contraction, which in strips from the cardiac stomach in most cases occurred after the exposure to the peptide; this might be a rebound contraction after an inhibition which could not be recorded with the experimental set-up. 4. Bombesin, 5-hydroxytryptamine and substance P produced dose-dependent contractions over a wide dose range. Somatostatin and enkephalin contracted the preparations only in the highest doses tested (10(-9) moles, 10(-8) moles). 5. Atropine did not reduce or abolish the response to any of the substances tested, indicating that their effects are not via cholinergic neurons, which innervate the smooth muscle. 6. Of the substances tested ATP, adenosine, VIP and neurotensin may be involved in the inhibitory vagal non-adrenergic, non-cholinergic innervation of the rainbow trout stomach.
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PMID:The effects of putative non-adrenergic, non-cholinergic autonomic transmitters on isolated strips from the stomach of the rainbow trout. Salmo gairdneri. 618 77


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