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)

The effects of pharmacological and nervous stimuli on the flow of secretion from the dog lateral nasal gland following catheterization are described. Drugs were injected close-arterially into the arterial supply to the nose, or intravenously. Cholinergic agonists (pilocarpine, methacholine), given intravenously (I.V.) or intra-arterially (I.A.), and stimulation of the vidian nerve produced a copious flow of secretion which was blocked by atropine. The adrenoceptor agonists phenylephrine (alpha) and salbutamol (beta 2), given I.V. or I.A., and stimulation of the vagosympathetic nerve produced a small but consistent flow of secretion. Histamine (50 micrograms), substance P (0.1 micrograms) and prostaglandin E1 (1-5 micrograms), injected I.A., produced small flows of secretion. Bradykinin (25 ng-50 micrograms), 5-hydroxytryptamine (100 ng-50 micrograms) and vasoactive intestinal peptide (VIP) (10 ng-50 micrograms) did not cause secretion. The total protein content, the composition of secretions as revealed by sodium dodecyl sulphate-polyacrylamide agarose gel electrophoresis, and changes in [Na] and [K] in relation to flow of secretion are described. Differences in ion and protein concentrations, and in protein composition, are described for vidian nerve-induced and vagosympathetically induced secretions. Electron microscopy revealed that the gland contains serous cells in the secretory region, and ducts morphologically similar to the intercalated, striated and excretory ducts of salivary glands.
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PMID:Lateral nasal gland secretion in the anaesthetized dog. 374 94

We have measured changes in tracheal mucosal thickness and tracheal vascular resistance in the dog. A probe was used to detect changes in height with time of the tracheal epithelium relative to an underlying cartilage. Tracheal vascular resistance was determined by perfusing a cranial tracheal artery at constant flow and measuring inflow pressure. Various drugs injected close-arterially were tested in 20 greyhounds anesthetized with pentobarbital sodium. Bradykinin, histamine, and methacholine significantly (P less than 0.01) decreased vascular resistance (-39.3 +/- 3.7, -47.3 +/- 4.2, and -22.5 +/- 5.2%, respectively) and increased the thickness of the mucosa (119.0 +/- 25.0, 61.9 +/- 25.0, and 46.3 +/- 6.4 micron). Substance P, vasoactive intestinal peptide, prostaglandin F2 alpha, and prostaglandin E, had large vasodilator actions (-31.4 +/- 5.0, -34.3 +/- 2.2, -21.9 +/- 2.8, and -31.5 +/- 2.4%) but only small effects on mucosal thickness (12.3 +/- 3.9, 13.0 +/- 3.4, 16.7 +/- 6.5, and 8.7 +/- 2.9 micron, respectively). Phenylephrine hydrochloride increased vascular resistance (19.8 +/- 1.7%) and decreased mucosal thickness (-23.9 +/- 3.1 micron). Thus airway vascular resistance and mucosal thickness always change in opposite directions, but drugs have different relative actions on the two variables. Even with large vasodilatations, the absolute changes in mucosal thickness were small and were unlikely to have an appreciable effect on tracheal airway resistance.
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PMID:Relationship between tracheal mucosal thickness and vascular resistance in dogs. 380 25

1 Increased vascular permeability following electric antidromic stimulation of the rat saphenous nerve was observed in the skin area supplied by the nerve, confirming previous results by other authors.2 The phenomenon was not affected by pretreatment of the rats with diphenhydramine, burimamide or their combination; atropine, methysergide, methysergide plus diphenhydramine, carboxypeptidase B, acetylsalicylic acid, indomethacin or methiazinic acid. It was partially reduced by previous injection of cellulose-sulphate, a kininogen-depleting agent.3 Perfusates from the subcutaneous tissue of the paw area supplied by the saphenous nerve contained permeability increasing activity as shown by intradermal tests in other rats. This activity was present in perfusates collected during nerve stimulation but not in those collected before stimulation. It was not destroyed by heating to 100 degrees C, or by alpha-chymotrypsin or trypsin.4 Bradykinin-like activity may appear later in the perfusates, depending on the intensity of the stimuli.5 It is concluded that following electrical antidromic stimulation of the saphenous nerve a permeability increasing factor is released, possibly from nerves. It is dialysable and can be distinguished from acetylcholine, histamine, 5-hydroxytryptamine, plasma kinins, substance P, prostaglandins and high molecular weight proteins. The increased vascular permeability induced by this factor leads to plasma exudation and activation of the kinin system.
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PMID:Formation of a factor increasing vascular permeability during electrical stimulation of the saphenous nerve in rats. 414 38

The application of bradykinin or capsaicin to the rabbit eye evoked strong miosis. The effect could be prevented by pretreatment of the eye with tetrodotoxin (TTX) or a substance P (SP) antagonist. However, the miotic response could be elicited despite TTX or the SP antagonist if the dose of capsaicin or bradykinin was increased. Bradykinin and capsaicin contracted the isolated rabbit sphincter pupillae muscle. The contraction produced by bradykinin and capsaicin was unaffected by TTX but reduced by specific SP antagonists. This indicates that bradykinin and capsaicin exert their effects on the isolated sphincter muscle through the release of SP but independent of neuronal conduction. In vivo, the situation seems to be different. The finding that TTX is capable of blocking the miotic response to moderate doses of bradykinin and capsaicin suggests that the effect on the eye under these circumstances is dependent upon a normal impulse traffic.
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PMID:Pupillary constriction by bradykinin and capsaicin: mode of action. 608 73

Two cell culture systems were used for studies of neural functions in vitro. A neuronal hybrid cell line (neuroblastoma x glioma hybrid cells) and primary glial-rich cultures of newborn murine brain. The level of cyclic AMP in both systems is regulated by two groups of hormones, those that stimulate and those that inhibit formation of cyclic AMP. Among the inhibitory hormones active on the hybrid cells are opioids. Therefore the cells are being used in the elucidation of action of opioids. The list of stimulating and inhibitory hormones regulating the primary glial-rich cultures includes several peptide hormones such as the gastrointestinal peptides secretin and vasoactive intestinal peptide, the calcaemic hormones parathyrin and calcitonin, adrenocorticotropin and melanotropins, and somatostatin. Noradrenaline (via alpha- and beta-adrenergic receptors) and adenosine (via A1 and A2 receptors) inhibit and stimulate cyclic AMP synthesis in the primary glial-rich cultures. Bradykinin slowly hyperpolarizes the hybrid cells and elicits formation of cyclic GMP. Both responses desensitize rapidly. Substance P increases the permeability of hybrid cells for Na+, as measured by using 14C-guanidinium as substitute for Na+. Hybrid cells actively accumulate taurine, an amino acid that appears to fulfill important functions in the nervous system. The transport of taurine across the plasma membrane is highly specific for and strictly dependent on Na+. The pumped station hypothesis of taurine action in the nervous system views taurine gradient plus taurine carrier as a transport system for the elimination of sodium from neurons during phases of high neuronal activity.
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PMID:Cell culture as models for studying neural functions. 608 74

Extracts prepared from the dried skins of approximately one hundred amphibian species from Australia and Papua New Guinea were subjected to biological screening in order to determine the nature and amounts of peptides active on smooth muscle preparations and systemic blood pressure present in these extracts. The most frequently and abundantly occurring peptides were those of the caerulein, bombesin and tachykinin peptide families represented, respectively, by caerulein; litorin, Glu(OMe)2-litorin and Glu(OEt)2-litorin; uperolein and Lys5-Thr6-physalaemin. Bradykinin-like peptides seem to have a rather diffuse distribution, in the species examined, but so far no peptide of this family has been isolated and sequenced. The only angiotensin-like peptide ever found in amphibian skin, crinia angiotensin II, has been isolated from skin extracts of a few species, belonging to the genera Crinia, Geocrinia, Ranidella and Litoria. The array of peptides occurring in amphibians from Australia and Papua New Guinea is destined to increase, because several apparently novel peptides have been identified in skin extracts by bioassay and radioimmunoassay.
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PMID:Active peptides in the skins of one hundred amphibian species from Australia and Papua New Guinea. 614 90

Neutral thiol-activated peptidases present in the pH 5-soluble fraction of rabbit brain (separated by step-elution chromatography on diethylaminoethyl cellulose) were screened for the hydrolysis of bradykinin. Lys-bradykinin, Met-Lys-bradykinin, angiotensin I, angiotensin II, substance P, luteinizing hormone-releasing hormone (LH-RH), and neurotensin by bioassay. The column effluent was monitored for bradykinin inactivation and arylamidase activity and combined in six pools on the basis of bradykinin inactivation. The pools were characterized by determining the peptide fragments and amino acids released from bradykinin with an amino acid analyzer. Pools 1 through 3 contained 80% of the kininase activity and essentially all of the endopeptidase A and B activity, whereas pools 4 through 6 accounted for 98% of the recovered arylamidase activity. Bradykinin, angiotensin I, angiotensin II, and substance P were inactivated by all the pools, whereas LH-RH and neurotensin were inactivated by pools 3 and 4, and pools 3, 4, and 5, respectively. These data show that rabbit brain contains peptidases having some selectivity for the inactivation of neuropeptides. Endopeptidase B purified from pool 3 is inhibited by bradykinin-potentiating peptide 9a (BPP9a, SQ 20881) (< Glu-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro), a competitive inhibitor of the hydrolysis of bradykinin (Km = 3.5 X 10(-5) M, Ki = 3 X 10(-6) M) which also completely inhibits the inactivation of LH-RH.
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PMID:Screening for rabbit brain neuropeptide-metabolizing peptidases. Inhibition of endopeptidase B by bradykinin potentiating peptide 9a (SQ 20881). 616 Dec 9

The effects of local intraarterial infusions of VIP, acetylcholine (ACh), substance P, isoprenaline and bradykinin on submandibular gland blood flow and salivary secretion were studied in cats. It was found that VIP (10(-14) to 10(-10) mol/min) caused an atropine resistant vasodilation but no salivary secretion. Several hundred fold higher doses of exogenous VIP had to be infused than the amounts of VIP seen in the venous outflow during maximal nerve stimulation at a similar vasodilatory response. ACh infusions (5 X 10(-12) to 5 X 10(-8) mol/min) caused both a muscarinic vasodilation and salivary secretion. ACh was about 100 times less potent than VIP as a vasodilating agent. Both ACh and VIP induced in high doses a vasodilatory response similar to that seen during parasympathetic nerve stimulation at 15 Hz. ACh by itself did in the present doses, however, only induce about 50-60% of the maximal secretory response. Combined infusions of ACh and VIP, had mostly an additive effect on vasodilation. The salivatory volume response to ACh was potentiated by VIP and to a smaller extent also by isoprenaline. This potentiating effect may be due to a direct effect on secretory elements as well as partly to the additional increase in blood flow. Bradykinin was about 1 000 times less potent than VIP as a vasodilating agent. Substance P (10(-9) mol/min) only caused a weak vasodilation. Since there is evidence that ACh and VIP coexist within the same neurons and are both released upon parasympathetic nervous activation, the present findings suggest that the secretory and vasodilatory responses may be caused by an interaction between these two agents.
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PMID:Complementary role of vasoactive intestinal polypeptide (VIP) and acetylcholine for cat submandibular gland blood flow and secretion. 618 51

Angiotensin-converting enzyme was solubilized with papain from a particulate fraction of rat brain and purified to apparent homogeneity by a procedure including DEAE-cellulose, hydroxylapatite, Sephadex G-200, Cys(Bzl)-Pro-Sepharose, and ricin-Sepharose chromatography. Bradykinin potentiators, SQ 14,225, and Arg-Pro-Pro strongly inhibited the activity of the purified enzyme, whereas Phe-Ala, phosphoramidon, and pentobarbital exerted little inhibitory effect on the activity. Among neuropeptides investigated, substance P, bradykinin, and Leu-enkephalin (Arg6) exerted strong inhibitory actions on the enzyme. Furthermore, the latter two peptides were shown to be good substrates for the enzyme. Thus, angiotensin-converting enzyme of rat brain is distinct from endogenous enkephalinase and may interact with various neuropeptides located in the brain.
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PMID:Purification and inhibition by neuropeptides of angiotensin-converting enzyme from rat brain. 619 11

Bradykinin contracts the isolated rabbit sphincter pupillae muscle. The contraction produced by 10(-8) M bradykinin was resistant to atropine but not to tetrodotoxin, suggesting a non-cholinergic nervous mechanism. The contraction was blocked by specific substance P (SP) antagonists, suggesting the involvement of SP. The SP antagonists tested were [D-Pro2,D-Trp7,9]SP-(1-11) and [Arg5,D-Trp7,9]SP-(5-11). The bradykinin-induced contraction exhibited marked tachyphylaxis in contrast to that induced by SP. It appears that the tachyphylaxis reflects the depletion of a bradykinin-sensitive neuronal pool of SP. Injection of bradykinin into the vitreous chamber of the rabbit eye caused miosis and disruption of the blood-aqueous barrier (manifested as aqueous flare). A second administration of bradykinin a few hours after the first injection evoked a reduced response; the response to SP upon repeated administration was unchanged. Atropine was without effect on the response to bradykinin whereas tetrodotoxin and the SP antagonists reduced the response. The results suggest that bradykinin causes miosis and aqueous flare at least partly through local release of neuronal SP.
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PMID:Bradykinin contracts the pupillary sphincter and evokes ocular inflammation through release of neuronal substance P. 619 73


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