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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. This study investigated tachykinin-evoked vasodilatation in the microvasculature of the hamster cheek pouch in vivo. Arterioles and venules were observed by intravital microscopy with video recording, and vasodilatation and constriction, defined as changes in blood vessel diameter, measured by image analysis. All agents were applied topically by superfusion. None of the agents tested had a significant effect on venule diameter. 2. When arterioles were preconstricted (by ca. 50%) with endothelin-1 present in the superfusing medium, substance P (0.3-30 nM) was a potent vasodilator, being 10 fold more active than both neurokinin A and the NK1 receptor-selective agonist, substance P methyl ester. The NK2 receptor-selective agonist, [beta-Ala8]-NKA(4-10)(0.1-10 microM) was active only at high concentrations, and the NK3 receptor-selective agonist senktide (0.1-10 microM) was virtually inactive (n = 8 hamsters). Dilatation evoked by tachykinins and analogues was rapid in onset (< 0.5 min) and readily reversible. 3. At low concentrations (1-10 nM), the non-peptide tachykinin NK1 receptor antagonist SR140333 ((S)1-(2-[3(3,4-dichlorophenyl)-1-(3-iso-propoxyphenylacetyl)pi peridin-3- yl]ethyl)-4-phenyl-1-azoniabicyclo[2.2.2]octone, chloride) had no effect on the diameter of preconstricted arterioles per se, but potently inhibited dilator responses to substance P methyl ester (apparent pKB 9.9 +/- 0.2; n = 5 hamsters, n = 10 estimates). SR140333 (10 nM) did not inhibit submaximal dilator responses evoked by human alpha calcitonin gene-related peptide (alpha CGRPh; 1.0 nM; P > 0.05; n = 5). 4 The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 microM) caused a51.3 +/- 5.4% arteriolar constriction. In the presence of L-NAME, submaximal vasodilator responses to substance P (10-I00 nM) and carbachol (0.1-1.0 microM) were significantly attenuated (n = 5 hamsters;P<0.05) as compared to responses obtained in preparations that were preconstricted to a similar extent by endothelin-l (48.0 +/- 5.6%). L-NAME (10 M) was without effect on submaximal vasodilator responses to alpha CGRPh (0.1 nM) or sodium nitroprusside (1O nM) (n = 5 hamsters; P> 0.05).5 We conclude that tachykinin-evoked arteriolar vasodilatation in the hamster cheek pouch is mediated via NK, receptor activation and depends, at least in part, on the release of nitric oxide. The NKI receptors mediating vasodilatation can be blocked by topical application of SR140333; which may therefore be useful in the investigation of the role of NK1 receptors in neurogenic inflammation in the microvasculature.
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PMID:Inhibition by SR 140333 of NK1 tachykinin receptor-evoked, nitric oxide-dependent vasodilatation in the hamster cheek pouch microvasculature in vivo. 753 May 73

1. In the present work, we have studied the microvascular reactivity of the arterial and venous mesenteric beds of the guinea-pig to bradykinin, neurokinins and other agents. 2. The vasoactive properties of three selective agonists for neurokinin receptors, namely [Sar9, Met (O2)11]SP (NK1), [beta-Ala8]NKA(4-10) (NK2) and [MePhe7]NKB (NK3), were evaluated on precontracted arterial and venous mesenteric vasculatures of the guinea-pig. The NK1-selective agonist, [Sar9,Met(O2)11]SP (1 to 1000 pmol), induced an endothelium-dependent and N omega-nitro-L-arginine methyl ester (L-NAME)-sensitive relaxation of the arterial vasculature precontracted with methoxamine, whereas the NK2 and NK3-selective agonists were virtually inactive at high doses (1000 pmol). 3. The three selective neurokinin receptor agonists were inactive in the non-precontracted arterial and venous mesenteric vasculatures as well as in the precontracted venous mesenteric vasculature. 4. Bradykinin (0.1 to 100 pmol) induced a marked dose- and endothelium-dependent vasodilatation of the precontracted arterial and venous vasculatures. ED50 values were 5.5 pmol on the arterial side and 1.9 pmol on the venous side. In contrast, desArg9-bradykinin was inactive at doses up to 1000 pmol. Furthermore, on the arterial and venous sides, a higher dose of bradykinin (1000 pmol), induced a biphasic effect, a transient constriction followed by a marked and sustained vasodilatation. The vasodilator effects of bradykinin were abolished by Hoe 140 (0.1 microM) and CHAPS, markedly reduced by L-NAME and were unaffected by [Leu8]desArg9-bradykinin (0.1 microM) on both sides of the mesenteric vasculature. Hoe 140 also abolished the arterial vasoconstrictions induced by high doses of bradykinin. 5. Noradrenaline, angiotensin II and endothelin-1 produced contractions on both sides of the mesenteric circulation, while acetylcholine (arterial side) and sodium nitroprusside (arterial and venous sides) caused vasodilatation.6. Our study supports the view that NK1 receptors responsible for vasodilatation are present solely in the endothelium of the arterial mesenteric vasculature of the guinea-pig. On the other hand, bradykinin(0.1 to 100 pmol) exerts predominantly vasodilator effects on both sides of the mesenteric vasculature via selective activation of B2 receptors located on the endothelium. The same receptor type located on the smooth muscle appears to be responsible for the arterial and venous constriction with high doses of bradykinin.
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PMID:Characterization of receptors for kinins and neurokinins in the arterial and venous mesenteric vasculatures of the guinea-pig. 758 63

To examine the effect of tachykinins on Cl secretion across tracheal mucosa and the possible contribution of nitric oxide (NO) formation to their actions in vivo, we measured Cl diffusion potential difference (Cl-PD) with a high-impedance voltmeter in the presence of amiloride. Superfusion of each neurokinin A (NKA) and substance P (SP) increased Cl-PD in a concentration-dependent fashion, whereas neurokinin B (NKB) had no effect, with the rank order of potency being NKA > SP >> NKB. The tachykinin-induced increase in Cl-PD was inhibited by the NO synthase inhibitor NG-nitro-L-arginine methylester (L-NAME), an effect that was reversed by L-arginine but not by D-arginine. These results suggest that tachykinins increase Cl secretion across rabbit trachea from the submucosa toward the lumen via stimulation of NK2 receptors and that NO formation may be involved in at least part of this process.
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PMID:[Role of nitric oxide in tachykinin-induced increase in Cl diffusion potential difference of rabbit tracheal mucosa]. 759 41

This study compared the antinociceptive properties of systemic administration of selective, non-peptidergic antagonists at neurokinin (NK1 and NK2) receptors to those of other classes of antinociceptive agent. (All doses are in mg/kg.) In mice, the NK1 antagonist, CP 99,994, preferentially (inhibitory dose50 (ID50) = 4.4) inhibited the late phase (LP) as compared to the early phase (EP) (16.1) of formalin-induced licking (FIL). A high dose (17.6) elicited ataxia in the rotarod test. Acetic acid-induced writhing was reduced at intermediate doses (10.0) whereas the tail-flick (TF) response to thermal and mechanical stimuli was inhibited only at high doses (22.7 and 17.7, respectively). Modulation of stimulus intensity did not modify the influence of CP 99,994 upon the response to heat. A similar pattern of data was acquired with RP 67,580, although this NK1 antagonist more potently inhibited writhing (2.8). In contrast, RP 68,651, the inactive isomer of RP 67,580, neither reduced the LP of FIL nor modified writhing indicating that these actions of RP 67,580 were stereospecific. Three further NK1 antagonists, SR 140,333, WIN 51,708 and WIN 62,577, likewise inhibited the LP of FIL and failed to modify the TF response at non-ataxic doses. Further, SR 140,333 (0.5) and WIN 51,708 (1.4) were potent ligands in the writhing procedure. The NK2 antagonist, SR 48,966, mimicked NK1 antagonists in preferentially inhibiting the LP (7.7) as compared to the EP (26.9) of FIL. Further, only at doses higher than those evoking ataxia (20.9) did SR 48,968 modify the TF response (36.5 and 32.0 for heat and pressure, respectively). However, it differed to NK1 antagonists in being inactive in the writhing test (> 40.0). In comparison to these NK1 and NK2 antagonists, the mu-opioid agonists (morphine and fentanyl) and kappa-opioid agonists (enadoline and U 69,593) equipotently inhibited all nociceptive responses at doses not provoking ataxia. While the glycine B receptor partial agonist, (+)-HA 966, selectively blocked the LP of FIL and did not evoke ataxia, the NMDA receptor channel blocker, (+)-MK 801, elicited antinociception only at doses close to those provoking ataxia. Finally, the NSAIDs, indomethacin and ibuprofen, the BK2 antagonist, Hoe 140 and the nitric oxide synthase (NOS) inhibitors, L-NAME and 7 nitroindazole, inhibited the LP (but not the EP) of FIL and (except for L-NAME) also reduced writhing: in contrast, they did not evoke ataxia and were inactive in the TF procedures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antinociceptive profiles of non-peptidergic neurokinin1 and neurokinin2 receptor antagonists: a comparison to other classes of antinociceptive agent. 765 44

1. Neuromuscular transmission in the circular muscle of the canine proximal colon was examined, in the presence and absence of nitric oxide synthase inhibitors, by use of mechanical and intracellular microelectrode recording techniques. 2. Electrical field stimulation (EFS; 0.1-20 HZ) produced frequency-dependent contractions of circular muscle strips which reached a maximum at 15 Hz. These responses were enhanced by NG-monomethyl-L-arginine (L-NMMA; 300 microM) and reduced by atropine (1 microM). The effects of L-NMMA were reversed by L-arginine (3 mM). All responses to EFS were abolished by tetrodotoxin (1 microM). 3. In the presence of atropine, phentolamine and propranolol (all at 1 microM; 'non-adrenergic, non-cholingergic (NANC) conditions'), EFS evoked frequency-dependent inhibition of phasic contractions which reached a maximum at 5 Hz. At higher frequencies of EFS, inhibition diminished, and these responses were followed by post-stimulus excitation. 4. Under NANC conditions and in the presence of L-NG-nitroarginine methyl ester (L-NAME; 200 microM), EFS evoked contractions at frequencies of 5 Hz or greater. These contractions were reduced by co-incubation with L-arginine (2 mM) and abolished by tetrodotoxin (1 microM). 5. In the presence of atropine (1 microM), EFS (5-20 Hz) caused frequency-dependent inhibition of electrical slow waves. In the presence of L-NAME (100 microM) and atropine, the inhibitory response to EFS was abolished and an increase in slow wave duration was seen at stimulation frequencies greater than 5 Hz. The effects of EFS on slow wave duration were abolished by tetrodotoxin (1 microM). 6. Atropine-resistant contractions to EFS were enhanced by indomethacin (10 microM) and reduced or abolished by the non-selective NK1/NK2 tachykinin receptor antagonist D-Pro2, D-Trp7,9 SP, and by the selective NK2 receptor antagonist MEN 10,376 (10 microM).7. Exogenous tachykinins mimicked non-cholinergic excitatory electrical and mechanical responses. The rank order of potency for contraction was neurokinin A>neurokinin B>substance P, suggesting a predominance of the NK2 sub-type of tachykinin receptors on colonic smooth muscle cells. Low concentrations of neurokinin A also increased the amplitude and duration of electrical slow waves.8. These results suggest that: (i) in previous studies, non-cholinergic excitatory responses were masked by the simultaneous release of NO; (ii) non-cholinergic excitatory responses occur throughout the period of stimulation and are not manifest only as 'rebound' excitation; (iii) one or more tachykinins, possibly,acting via NK2 receptors, may mediate non-cholinergic excitatory responses.
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PMID:Inhibition of nitric oxide synthesis reveals non-cholinergic excitatory neurotransmission in the canine proximal colon. 768 1

In the present study we characterized the receptor(s) that mediates non-adrenergic non-cholinergic (NANC) contractions of isolated guinea pig cervical trachea, using CP-99,994, a selective neurokinin (NK1) receptor antagonist, and SR-48,968, a selective neurokinin (NK2) receptor antagonist. The activity of these two antagonists was determined against contractions to the selective agonists ([beta Ala8]NKA(4-10) for NK2 and [Sar9,Met(O2)11]SP for NK1) and the nonselective (SP and NKA) NK receptor agonists. CP-99,994 was inactive versus NKA and [beta Ala8]NKA(4-10) but antagonized SP- and [Sar9,Met(O2)11]SP-induced contractions with -log KB values of 5.6 +/- 0.2 and 7.7 +/- 0.2, respectively. SR-48,968 was inactive versus SP and [Sar9,Met(O2)11]SP but was active versus NKA and [beta Ala8]NKA(4-10), yielding -log KB values of 8.4 +/- 0.2 and 9.1 +/- 0.2, respectively. In the presence of 1 microM atropine, 1.4 microM indomethacin, 0.2 microM timolol, and 4 microM thiorphan, electrical field stimulation (16 Hz, 2.0 ms, 50 V for 10 every 30 min) elicited a NANC contractile response which was not significantly altered by CP-99,994 (3 microM) or the nitric oxide synthase inhibitor L-NAME (10 microM) but was completely inhibited by tetrodotoxin (TTX) (1 microM) and was also reduced to 58 +/- 12, 31 +/- 16, 8 +/- 4, and 0% of control by 15, 50, 150, and 1500 nM SR-48,968, respectively. Resiniferatoxin (1 and 10 nM) produced a well-maintained concentration-dependent contraction, which was 57.8 +/- 4.8 and 61.6 +/- 3.8%, respectively, of the carbachol-induced maximum response. Contractions were not significantly modified by L-NAME and were not blocked by TTX (1 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurokinin (NK2) receptors mediate nonadrenergic noncholinergic contractile responses to electrical stimulation and resiniferatoxin in guinea pig trachea. 805 60

1. Measurement of plasma protein extravasation induced by the natural tachykinins following intradermal administration in rat skin indicated equipotency between substance P (SP), neurokinin A (NKA) and neurokinin B (NKB). The selective NK1 receptor agonist, [Sar9]SP sulphone was 10-100 times more potent than SP. The synthetic hexapeptide, septide, [pGlu6, Pro9]SP-(6-11), which has been proposed to act on a distinct NK1 receptor subtype/binding site was equipotent with [Sar9]SP sulphone. 2. The selective NK2 receptor agonist [beta Ala8]NKA(4-10) (0.1-1 nmol) and the selective NK3 receptor agonist, senktide (0.1-1 nmol) were both ineffective in producing oedema. The selective NK2 receptor antagonist, SR 48, 968 (0.3 mumol kg-1) had no significant inhibitory effects upon oedema induced by approximately equiactive doses of SP (0.2 nmol), septide (0.002 nmol), [Sar9]SP sulphone (0.002 nmol), or NKB (0.3 nmol). These results together suggest that neither NK2 nor NK3 receptors are involved in oedema formation in rat skin. 3. The non-peptide tachykinin NK1 receptor antagonist, RP 67,580 (1-3 mumol kg-1), inhibited plasma protein extravasation induced by septide (0.002 nmol) to a greater extent than that to SP (0.2 nmol). RP 67,580 (1 mumol kg-1) produced a significant inhibition of approximately 66% of the response to septide (0.002 nmol) only. Increasing the dose of RP 67,580 3 fold resulted in inhibition of the response to SP (0.2 nmol) and [Sar9]SP sulphone (0.002 nmol) by approximately 66% and 64% respectively with the response to septide being inhibited by approximately 70%. 4. Co-administration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME)(0.1 micromol) with the relevant tachykinin, resulted in a significant attenuation of the oedemaresponse to septide (0.1 nmol) producing only an approximate 56% inhibition of the response. The response to 0.2 nmol SP was unaffected whereas the response to a higher dose of 1 nmol was lowered byL-NAME but this did not reach significance.5. Degranulation of mast cells, achieved by pretreatment with compound 48/80 (5 mg kg-1) for 3 consecutive days, significantly inhibited the oedema responses to only high dose SP (1 nmol) and[Sar9SP sulphone (0.002 nmol). SP (0.2 nmol), septide (0.002 nmol), NKA (0.2 nmol) and NKB(0.3 nmol) were unaffected by this treatment.6. RP 67,580 (0.3-3 microM kg-1) inhibited oedema induced by both 0.002 nmol and 0.1 nmol of septide.When using equiactive doses of SP only the response to the lower dose of 0.2 nmol SP was significantly inhibited, while RP 67,580 (3 micromol kg1) did not affect the response to 1 nmol SP.7 These results suggest distinct mechanisms of action for SP and septide in producing plasma protein extravasation in rat skin. The response induced by septide is blocked by RP 67,580 and is both NO dependent and mast-cell independent. In contrast the response to SP is only partially blocked by RP67,580 and is NO-independent. These data support the existence of a distinct 'septide-sensitive' receptor/binding site and suggest that this site is involved in tachykinin-induced oedema formation in rat skin.
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PMID:Demonstration of a 'septide-sensitive' inflammatory response in rat skin. 856 45

The effect of capsaicin-induced stimulation of afferent neurons on peristalsis and the possible neural mediators involved in this action were examined in the guinea-pig isolated ileum. The intraluminal pressure threshold for eliciting peristaltic waves was used to quantify facilitation (decrease in threshold) or inhibition (increase in threshold) of peristalsis. Capsaicin (0.1-1 microM) caused an initial short-lasting stimulation of peristalsis followed by a prolonged inhibition of peristaltic activity. Capsaicin (1 microM) was ineffective when the gut segments had been pretreated with 3.3 microM capsaicin, which is indicative of an afferent neuron-dependent action of the drug. In contrast, the abolition of peristalsis caused by a high concentration of capsaicin (33 microM) was fully reversible on removal and reproducible on readministration of capsaicin, a feature characteristic of a nonspecific depression of smooth muscle excitability. Baseline peristalsis and the excitatory/inhibitory effect of capsaicin (1 microM) on peristalsis remained unaltered by a combination of the tachykinin NK1 receptor antagonist (+)-(2S, 3S)-3-(2-methoxybenzylamino)-2-phenyl piperidine (CP-99,994; 0.3 microM) and the tachykinin NK2 receptor antagonist (L(-)-N-methyl-N[4-acetylamino-4-phenyl-piperidine-2-(3,4- -dichlorophenyl)butyl]-benzamide (SR-48,968; 0.1 microM). Further experiments, performed in the presence of a low concentration of atropine (10 nM) showed that the calcitonin gene-related peptide (CGRP) antagonist human alpha-calcitonin gene-related peptide (8-37) [hCGRP(8-37); 10 microM] attenuated the delayed inhibitory effect of capsaicin on peristalsis, but did not influence baseline peristaltic activity and the capsaicin-induced facilitation of peristalsis. Blockade of nitric oxide (NO) synthesis by NG-nitro-L-arginine methylester (L-NAME, 300 microM) facilitated baseline peristaltic activity and reduced the delayed inhibition of peristalsis caused by capsaicin (1 microM) without affecting the initial peristalsis-stimulating action of capsaicin. The effects of L-NAME were prevented by L-arginine (1 mM). The data of the current study indicate that capsaicin-sensitive afferent neurons do not participate in the neural pathways subserving peristalsis in the guinea-pig small intestine, but modulate peristaltic activity upon stimulation with capsaicin. The initial stimulant action of capsaicin on peristalsis is independent of tachykinins acting via NK1 or NK2 receptors, while the delayed capsaicin-induced depression of peristalsis involves CGRP and NO.
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PMID:The inhibitory modulation of guinea-pig intestinal peristalsis caused by capsaicin involves calcitonin gene-related peptide and nitric oxide. 875 Sep 23

Casomokinin L (Tyr-Pro-Phe-Pro-Pro-Leu), a derivative of beta-casomorphin and casoxin D, showed endothelium-dependent vasorelaxing activity on the canine mesenteric artery (EC50 = 7 x 10(-8) M). This relaxing activity was partly blocked by 10(-5) M NAME (nitric oxide synthase inhibitor), and the inhibition by NAME was restored by addition of 10(-4) M arginine, suggesting the involvement of nitric oxide as an endothelium-dependent relaxing factor. The relaxing activity was blocked by 10(-8) M CP-99994 and 10(-7) M FK888 (NK1 antagonists), but not by 10(-6) M SR-48968 (NK2 antagonist). Casomokinin L binds to neurokinin NK1 receptors (Ki = 5.8 x 10(-5) M), and lowered blood pressure in SHR (0.1 mg/kg, i.v. and 3 mg/kg, PO). Thus, despite its only three residues in common with substance P, casomokinin L binds to NK1 receptors, relaxes the artery, and exerts an antihypertensive effect.
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PMID:Vasorelaxation by casomokinin L, a derivative of beta-casomorphin and casoxin D, is mediated by NK1 receptor. 880 74

1. This study tested the hypothesis that a nitric oxide synthase (NOS) was activated in guinea-pig ileum in vitro in response to substance P (SP), and attempted to characterize the tachykinin receptor involved in this activation by the use of selective receptor agonists and antagonists. 2. Strips of guinea-pig ileum (8 x 2 mm) were superfused (Krebs, 37 degrees C, 2 ml min-1) with: (i) tachykinin receptor agonists: SP, GR 73,632 (NK1), GR 64,349 (NK2), senktide (NK3), and neuropeptide (NP) gamma; (ii) tachykinin receptor antagonists: CP 99,994 (NK1), SR 48,968 (NK2), SR 142,801 (NK3); (iii) nerve-related agents: carbachol (CCh), atropine, tetrodotoxin (TTX), hexamethonium; (iv) NOS inhibitors: N omega-nitro-L-arginine-methyl-ester (L-NAME), N omega-monomethyl-L-arginine (L-NMMA) and aminoguanidine (AG); (v) NO-related agents, L-arginine (L-Arg), D-arginine (D-Arg), sodium nitroprusside (NaNP) and methaemoglobin. Muscle contractility was recorded isometrically and quantified as integrated area of activity. 3. SP, tachykinin receptor agonists and NP gamma (10 pM to 10 microM), produced concentration-dependent contractions of ileal strips, with EC50s in the nanomolar range, and maximal responses (Emax) attained at 0.1 microM for SP and 1 microM for the other agonists. The Emax response to SP equalled that to KCl (60 mM) taken as a 100% control (99.3% [93.0-105.7]; mean and 95% CI; n = 12); a comparable Emax contraction was obtained with the other tachykinin receptor agonists (1 microM) as well as with CCh (1 microM). 4. Under baseline conditions, L-NAME (1 microM), L-NMMA (1 microM) and AG (1 microM), failed to contract the muscle strip. In contrast, when superfused for 3 min, 10 min after SP (0.1 microM), they induced a transient contraction of the strip (e.g. for 1 microM L-NAME: 50 to 70 s duration; amplitude 73 +/- 12%, n = 24). 5. The NOS inhibitor-induced contractile response was not obtained after KCl (60 mM), GR 73,632, GR 64,349, senktide or CCh (all up to 1 microM). In contrast, this contractile response was obtained after NP gamma (1 microM). 6. Blockade of tachykinin NK1, NK2 and NK3 receptors by continuous superfusion of CP 99,994, SR 48,968 and SR 142,801 (1 microM) respectively, starting 5 min before SP, did not modify the response to L-NAME, superfused 10 min after SP (0.1 microM). The contractile response to L-NAME (1 microM) was blocked by atropine (1 microM), superfused either before or after SP. In contrast, it persisted after TTX or hexamethonium (1 microM) superfused in the same conditions. 7. The amplitude of NOS inhibitor-induced contraction (1 microM) was dependent on the concentration of priming SP (1 pM to 1 microM). In contrast, the contractile response to NOS inhibitors (1 nM to 10 microM) of the ileum strip primed with SP (0.1 microM) was not concentration-related. 8. L-NAME-induced contraction was prevented by continuous superfusion of L-Arg (1 microM), but not D-Arg (1 microM). In addition, the NO donor, sodium nitroprusside (1 microM) and the NO scavenger, methaemoglobin (10 micrograms ml-1), both prevented the contractile response to L-NAME. 9. In summary, SP and to a lesser extent NP gamma, exert a permissive action allowing contractile stimulating effects of L-NAME, L-NMMA and AG, in guinea-pig ileum in vitro, by a mechanism which apparently does not involve tachykinin NK1, NK2 and NK3 receptors. This action is likely to result from the activation of a NO-synthase by SP in the vicinity of intestinal myocytes. Thus, L-NAME, L-NMMA or AG, by blocking this SP-induced NO production, unveiled a smooth muscle contraction which involves a cholinoceptor (atropine-sensitive) mechanism.
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PMID:Functional evidence for NO-synthase activation by substance P through a mechanism not involving classical tachykinin receptors in guinea-pig ileum in vitro. 881 51


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