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)

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88

Receptor autoradiography was used to examine the distribution of muscarinic cholinoceptors ([3H]QNB), alpha 2-adrenoceptors ([3H]rauwolscine), beta-adrenoceptors ([125I]CYP) and substance P receptors ([125I]BHSP) in rabbit aorta, pulmonary artery, rat aorta, dog aorta, splenic, renal and coronary arteries, bovine aorta and coronary arteries. Muscarinic cholinoceptors and alpha 2-adrenoceptors were not associated with endothelium in any of the blood vessels examined. Substance P receptors were found on endothelium in dog renal but not bovine coronary arteries, and beta-adrenoceptors were found on endothelium in dog coronary arteries but not bovine aorta. The results suggest that endothelium-dependent relaxation can result either from activation of receptors located directly on the endothelial cells or, as is the case for ACh, by an indirect mechanism via activation of receptors located on the vascular smooth muscle.
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PMID:Autoradiographic analysis of receptors on vascular endothelium. 303 Jul 80

Motilin has a stimulating effect on gastrointestinal motility. The mechanism of its action is not known. Direct and neuronal effects have been postulated. To determine if receptors are present on smooth muscle cells we investigated the effect of synthetic porcine motilin and its interaction with acetylcholine on isolated guinea pig gastric smooth muscle cells. Motilin elicited a dose-dependent contraction of gastric smooth muscle cells. Minimal (8.3 +/- 1.3%) and maximal (33.9 +/- 2.4%) responses were observed at 10(-12) and 10(-6) M, respectively. The ED50 of motilin was 10(-9) M. Acetylcholine also elicited a dose-response muscle contraction with a maximal response observed at 10(-7) M. Atropine (10(-7) M) completely inhibited the maximal response to acetylcholine but did not have any effect on the contractile response to motilin. In addition, dibutyryl guanosine 3',5'-cyclic monophosphate (10(-3) M) and substance P antagonist, spantide (10(-4) M), also did not inhibit the action of motilin. Acetylcholine (10(-11) M) shifted the dose-response curve of motilin to the left by 1.5 log units. The maximal response to the combination of motilin (10(-6) M) and acetylcholine (10(-11) M) was 32 +/- 3.2%, which was similar to the maximal response to motilin alone. It is concluded that distinct motilin and muscarinic receptors are present on guinea pig gastric smooth muscle cells. The interaction between motilin and acetylcholine is additive and not potentiative.
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PMID:Motilin receptors on isolated gastric smooth muscle cells. 334 75

The reactivity of porcine intramyocardial resistance arteries (223 +/- 7 micron i.d., n = 30) was investigated with a pressurized in vitro preparation. Diameter changes in response to acetylcholine and to adrenergic drugs and dynamic changes in transmural pressure changes were investigated. Acetylcholine produced concentration-dependent constrictions, causing maximal reductions of 71 +/- 3% in lumen diameter, with EC50 values averaging 1.9 X 10(-7) M (n = 7). These responses were inhibited by atropine (10(-7) M) and therefore were mediated by muscarinic receptors. In addition, acetylcholine did not elicit relaxation in nine out of 10 vessels precontracted with U46619 (10(-7) M). Norepinephrine and epinephrine never produced constrictions (n = 6) even in the presence of propranolol (10(-6) M). Both norepinephrine and isoproterenol caused dose-dependent relaxations in acetylcholine-precontracted vessels, with IC50 values of 8.2 X 10(-7) M (n = 5) and 6.6 X 10(-8) M (n = 6), respectively. These relaxations were suppressed by propranolol. Between transmural pressures of 10 and 90 mm Hg, there was no intrinsic myogenic tone (n = 7). In addition, the vessels responded only passively to sudden pressure changes of 40 mm Hg. In all vessels, the functional integrity of the endothelium was verified by relaxations to substance P (10(-8) M) and/or bradykinin (10(-8) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reactivity of isolated porcine coronary resistance arteries to cholinergic and adrenergic drugs and transmural pressure changes. 334 75

The actions of substance P (SP), neurokinin A (NKA), neurokinin B (NKB), physalaemin (PHY), kassinin (KAS) and eledoisin (ELE) were investigated on transversally cut strips of pig coronary artery. All tachykinins produced vasodilatation of coronary arteries precontracted with ACh; 10(-5) M. The order of potency was: SP = PHY ELE greater than KAS greater than NKA greater than NKB, with the ED50 values being 0.38, 0.38, 1.2, 2.6, 8.3 and 34.0 nM, respectively. Continued superfusion of SP (7.4 X 10(-9) M) desensitized the coronary arteries which were refractory to the vasodilator action of NKA, NKB, PHY and KAS. The arteries nevertheless dilated upon the addition of noradrenaline (NA) and bradykinin (BK). Endothelium-removed preparations did not respond to any of the tachykinins. However, tissues devoid of endothelium relaxed in response to both NA and vasoactive intestinal polypeptide (VIP). Three octapeptide antagonists, [D-Pro4,Ala6,D-Trp7,9,Nle11]SP-(4-11) (compound I), [D-Pro4,Ser6,D-Trp7,9,Nle11]SP-(4-11) (compound II) and [D-Pro4,D-Trp7,9,10,Phe11]SP-(4-11) (compound III) were examined as potential antagonists of tachykinin-induced vasodilatation. Compounds I and II blocked the actions of SP and NKA but not that of PHY. Compound III effectively blocked the actions of SP and PHY. We conclude that the pig coronary artery possesses a 'NK-P/SP-P' type receptor, and that this receptor is probably localized on the endothelium.
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PMID:Effects of neurokinins on the isolated pig coronary artery. 360 37

Isolated precontracted arteries of various vascular beds relax in response to acetylcholine only if the endothelium is present. One explanation for this is that this drug stimulates the endothelial cells to release a vasodilator substance that in turn relaxes the underlying smooth muscle. To determine whether this mechanism is concerned also in the acetylcholine contraction of isolated porcine coronary arteries transverse strips of the extramural part of the left circumflex artery were used for recording isometric tension in the muscle bath. Dose-response curves for acetylcholine showed no significant difference before and after removal of endothelium. As a functional check on the removal of endothelium, the responsiveness of each preparation to a known endothelium dependent dilator (substance P) was tested before and after removal. These findings suggest that endothelial cells are not concerned in the acetylcholine induced contraction of porcine coronary arteries. Acetylcholine appears to act directly on smooth muscle of the porcine artery.
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PMID:Absence of role of endothelium in the response of isolated porcine coronary arteries to acetylcholine. 371 11

Acetylcholine dropped onto the meatal surface of the tympanic membrane evoked vasodilatation and a vascular leakage to the middle ear cavity. The vasoreactions were atropine-resistant. Substance P and vasoactive intestinal polypeptide (VIP) injected intravenously caused a marked vascular leakage and VIP also vasodilatation. These blood vessel changes seem to be regulated by the parasympathetic nerves as they were inhibited by vagotomy. Constriction of the tympanic membrane vessels was mediated through alpha-receptors.
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PMID:Pharmacological characterization of receptors on blood vessels in the tympanic membrane involved in otitis media. 383 88

Simultaneous recordings of focal slow potentials (sVs) and chemosensory discharges were made from cat carotid body-nerve preparations in situ. Chemoreceptor stimulants (100% N2, asphyxia, NaCN, ACh and nicotine), and depressants (100% O2, spontaneous gasps and dopamine) changed receptor polarization. sVs evoked by stimulants had a negative polarity whereas depressants elicited positive deflections. There was a direct correlation between maximal frequency of chemosensory discharges and peak sV amplitude when NaCN injections or N2 inhalation were used. However, cholinergic agents, dopamine and substance P evoked sVs which lacked correlation in time-course, amplitude or polarity with changes in sensory frequency. After a 6-day carotid nerve crush, different stimuli still evoked sVs even in the absence of sensory discharges. Both sVs and chemosensory discharges were abolished after 1 h ischemia produced by ligature of carotid body blood vessels. Thus, sVs from carotid body chemoreceptors probably include a neuronal component (the generator potential) directly responsible for the origin of chemosensory discharges, and a non-neuronal component (receptor or secretory potentials) probably originating in glomus and/or sustentacular cells.
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PMID:Bioelectric potentials in the carotid body. 392 Nov 96

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

1. Cuneate cells in anaesthetized cats were strongly excited by L-glutamate, and somewhat less by D-glutamate; cells which receive afferents from hair receptors were particularly sensitive.2. Glutamate could be used to demonstrate post-synaptic inhibitory inputs from the dorsal column, the medial lemniscus and the frontal cortex.3. Many cuneate cells were also strongly excited by adenosinetriphosphate (ATP); this was probably due to the chelating action of ATP, as citric acid was also quite effective.4. gamma-Aminobutyric acid (GABA) readily blocked all forms of spontaneous and evoked activity, except antidromic invasion of cuneothalamic neurones; cells which receive proprioceptive afferents were particularly sensitive to GABA. Glycine had a comparable effect.5. Acetylcholine (ACh), catecholamines, histamine, 5-hydroxytryptamine (5-HT) and an extract containing substance P mostly had only weak depressant actions. Cholinergic and mono-aminergic mechanisms are probably not very significant in the cuneate.6. These results are consistent with the possibility that glutamate and GABA (or glycine), or some closely related compounds, are the main excitatory and inhibitory transmitters in the cuneate nucleus.7. If ATP is released from afferent nerve endings, it could also play a significant role in excitation.
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PMID:Micro-iontophoretic studies on neurones in the cuneate nucleus. 429 9


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