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 the neonatal administration of capsaicin on substance P (SP) immunoreactivity of the vagal sensory ganglion (nodose ganglion) and the CNS site of termination of vagal afferents (nucleus of the solitary tract-NTS) were evaluated with immunocytochemistry and radioimmunoassay. The SP content of the nodose ganglion was reduced by 58%, and a loss of immunoreactive cell bodies was found in capsaicin treated rats. Regional differences were found in the effects of capsaicin treatment on the SP immunoreactivity in the NTS. Whereas the SP in the medial portions of the nucleus was not altered, a reduction of SP immunoreactivity in the lateral portions of the nucleus was shown with immunocytochemistry and with radioimmunoassay. The data confirm that at least a portion of the vagal afferent cell bodies of the nodose ganglion and their projections to the brainstem are capsaicin sensitive. The finding that the SP in the lateral NTS is depleted by capsaicin administration may be of importance in the use of capsaicin in functional studies, particularly of the role of SP containing vagal afferents in respiration.
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PMID:Capsaicin reduces substance P immunoreactivity in the lateral nucleus of the solitary tract and nodose ganglion. 241 26

The effects of acetylcholine, substance P and vasoactive intestinal polypeptide (VIP) on the endogenous noradrenaline (NA) overflow were compared to those of two other vasodilators, nitroglycerin and felodipine, neither of which are thought to influence NA neurotransmission in blood perfused skeletal muscle. The lack of prejunctional effects of nitroglycerin was verified in vitro. The sympathetic nerve stimulation (SNS) evoked NA overflow was reduced by 37 +/- 9% by a dose of acetylcholine which reduced the perfusion pressure at rest by 44 +/- 6%. Conversely, atropine tended to enhance SNS evoked NA overflow. Acetylcholine reduced the vasoconstrictor responses to SNS when compared to the responses observed with an equipotent vasodilatory dose of, e.g. nitroglycerin. The SNS evoked NA overflow was not influenced by a moderate mechanical blood flow reduction or by pronounced reductions of vascular resistance induced by either substance P, VIP, nitroglycerin or felodipine, supporting the idea that the transport of NA from nerve terminal to blood is not importantly influenced by moderate decreases in blood flow or vascular tone. Prejunctional muscarinic inhibition of NA release in skeletal muscle was verified under in vivo conditions, but the other substances tested did not influence sympathetic neurotransmission. Endogenous NA overflow appears to mirror NA release in vivo also when diffusion is influenced by changes in blood flow or vascular tone in this experimental model.
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PMID:Influence of acetylcholine, peptides, and other vasodilators on endogenous noradrenaline overflow and vasoconstriction in canine blood perfused gracilis muscle. 241 14

Ring preparations from the carotid, coronary, renal, mesenteric and femoral arteries of the dog were precontracted with the thromboxane mimetic U46619, after ensuring that the resting conditions were comparable from the Laplace relationship. In the presence of prazosin (1 microM) and propranolol (3 microM), noradrenaline (NA) relaxed the arteries in the order coronary greater than carotid greater than femoral greater than renal = mesenteric. When maximum relaxation to nitroglycerin (10 microM) was taken to be 100% the maximum relaxation to noradrenaline in each artery was: coronary 70%; carotid 34%; femoral 19%; renal 7% and mesenteric 2%. In endothelium-intact arteries UK14304 mimicked the relaxation responses to NA and idazoxan shifted the curves to both agonists to the right, consistent with an alpha 2-adrenoceptor classification. Substance P relaxed the arteries in the same order as for NA but showed higher efficacy i.e.: coronary 100%; carotid 80%; femoral 71% renal 49%; and mesenteric 41%. Removal of the endothelium abolished the relaxation to NA. We conclude that endothelium-dependent relaxation to NA and substance P varies greatly across 5 large arteries of the dog. This may indicate that endothelium-derived relaxing factor (EDRF) release is site-dependent or that the efficacy of EDRF on smooth muscle varies; being greatest in the coronary and weakest in the renal and mesenteric arteries.
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PMID:Alpha 2-adrenoceptors and endothelium-dependent relaxation in canine large arteries. 242 47

Chemical removal of the endothelium by saponin in the isolated dog femoral artery was investigated by comparing the relaxant responses to endothelium-dependent and -independent vasodilators of saponin-treated rings with the responses of non-treated rings. Saponin treatment was done by incubating rings with Krebs-Henseleit solution containing 0.1, 0.3 or 1 mg/ml of saponin for 45 min at 37 degrees C. In non-treated rings, acetylcholine (10(-8)-3 X 10(-6) M) caused a concentration-dependent relaxation of rings precontracted with prostaglandin F2 alpha (3 X 10(-6) M). The acetylcholine-induced relaxation was reduced in rings pretreated with 0.1 mg/ml of saponin and almost abolished with 0.3 or 1 mg/ml. Prostaglandin F2 alpha-induced contraction was suppressed weakly by treatment with 0.3 mg/ml and markedly with 1 mg/ml saponin. The treatment with 0.3 mg/ml saponin markedly reduced relaxations caused by substance P (10(-9)-3 X 10(-8) M) and by Ca2+-ionophore A23187 (10(-6) M). Relaxant responses of saponin-treated rings to nitroglycerin and to nitroprusside were almost identical with those of non-treated rings. These results showing selective suppression by saponin of the endothelium-dependent relaxation suggest that saponin removes the endothelial cells from the intimal surface of the artery, and this was confirmed by electron microscopy. The endothelium removing method with saponin seems to be useful as a pharmacological tool for vascular investigations.
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PMID:Chemical removal of the endothelium by saponin in the isolated dog femoral artery. 242 45

We have sought to determine if changes in arterial and gastric pressure occurred with selective chemical stimulation of the dorsomedial NTS. Substance P (SP) and L-glutamate (L-glu), but not acetylcholine (ACh), elicited a dose-dependent decrease in tonic gastric pressure and inhibited gastric phasic activity. As previously reported, L-glu and ACh, but not SP elicited dose-dependent arterial hypotension. The data support a putative role for SP in visceral reflexes mediated by vagal nerves.
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PMID:Central modulation of gastric pressure by substance P: a comparison with glutamate and acetylcholine. 243 Jun 70

The dependence of vascular relaxation on an intact endothelium and the relationship between relaxation and cyclic GMP accumulation were determined in coronary arteries isolated from cardiac transplantation patients with or without coronary atherosclerosis. In nonatherosclerotic arteries, the endothelium-dependent agent acetylcholine produced concentration-related relaxations. In atherosclerotic arteries, endothelium-dependent relaxations were abolished with acetylcholine, partly suppressed with substance P and histamine, and completely preserved with the ionophore A23187. In these arteries, the endothelium-independent agent nitroglycerin remained fully active. Accumulation of cyclic GMP in atherosclerotic strips was suppressed with acetylcholine but unattenuated with A23187 and nitroglycerin. In aortas from rabbits with diet-induced atherosclerosis, there was likewise an impaired cholinergic relaxation and cyclic GMP accumulation in the presence of preserved responses to A23187 and nitroglycerin. The results demonstrate that impaired cholinergic responses in atherosclerotic arteries reflect a muscarinic defect and not an inability of endothelium to release endothelial factor or smooth muscle to respond to it.
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PMID:Impaired muscarinic endothelium-dependent relaxation and cyclic guanosine 5'-monophosphate formation in atherosclerotic human coronary artery and rabbit aorta. 243 88

Microdissected areas of the rabbit brainstem were isolated at prenatal day E28, postnatal days P3, 7, 14, 21, at 2 months and adults. Substance P immunoreactivity (SPI) was assayed by RIA and SPI was expressed relative to the protein content of the extracted brain tissues. The developmental characteristics of SPI within specific brainstem nuclei are reported. In general, SPI was highest in the NTS (nucleus tractus solitarii) at all ages. The pattern of distribution of SPI, however, was age-specific. The development of SPI within select nuclei demonstrated marked variability and showed both age- and nucleus-specificity.
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PMID:Developmental characteristics of substance P immunoreactivity within specific rabbit brainstem nuclei. 246 6

Porcine or bovine endothelial cells cultured on microcarrier beads, packed into adapted chromatographic columns, perfused with Krebs' buffer and activated with appropriate stimuli (e.g. bradykinin, ADP or phospholipase C) release EDRF and prostacyclin into the perfusing fluid. In the effluent EDRF and prostacyclin might be bio-assayed using the Vane's superfusion cascade (rabbit aortic strips and bovine coronary artery strips, respectively) against nitroglycerine (GTN) and synthetic prostacyclin standards. Prostacyclin might be also quantified as 6-keto-PGF1 alpha by RIA. A spatial separation of the generator (endothelial cells) from the effector (vascular smooth muscle) has allowed to prove that EDRF is nitric oxide, that its activity is inhibited by superoxide anions and by chemicals which act via free radicals, finally, that the release of EDRF and prostacyclin is coupled by a receptor-mediated activation of phospholipase C. Although so successful, the above technique suffers from its essentials, i.e. from using cultured cells instead of fresh intact endothelial cells. Cultured endothelial cells are not responsive to many receptor agonists including acetylcholine, substance P and 5-hydroxytryptamine. Unlike fresh intact endothelial preparations the cultured cells which are perfused with Krebs' buffer generate superoxide anions at such concentrations that it might be obligatory infusing superoxide dismutase in order to detect EDRF. Nonetheless, a couple of data obtained with the cultured endothelial cells have been reproduced in the fresh cell preparations, e.g. release of EDRF by ADP and ATP, a coupled release of EDRF and prostacyclin by phospholipase C or a paradoxical augmentation of the sodium-nitroprusside-induced vasorelaxation by methylene blue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelium-derived relaxing factor (EDRF) from cultured and fresh endothelial cells. 247 Mar 61

Acetylcholine, substance P and nitroglycerin applied intra- and extraluminally to the perfused dog femoral artery segment with endothelium caused depressor responses. Endothelium denudation abolished the responses to acetylcholine and substance P. EC50 ratios of extra- versus intraluminal acetylcholine and substance P were 43 and 79, respectively, whereas those of nitroglycerin did not differ. Physostigmine potentiated the response to extraluminal acetylcholine. Acetylcholine seems to be degraded partly by cholinesterase in the arterial wall. Acetylcholine and substance P applied extraluminally are expected to reach the endothelium and release endothelium-derived relaxing factor.
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PMID:Extraluminally applied acetylcholine and substance P on the release of EDRF. 247 88

Acetylcholine and substance P applied to the donor tissue, dog femoral artery segments with endothelium, produced moderate relaxations of the assay tissue, endothelium-denuded dog coronary artery strips. The relaxation was attenuated markedly by treatment of the assay tissue with hydroquinone and abolished by oxyhemoglobin or methylene blue. In this bioassay system, the effect of AA861 and TMK777, new 5-lipoxygenase inhibitors, was evaluated. When the donor tissue was treated with AA861 or TMK777, the responses to acetylcholine and substance P were attenuated moderately, whereas the relaxation by nitroglycerin was not influenced by AA861. However, the inhibitors when infused just below the donor tissue did not attenuate relaxant responses to acetylcholine and substance P. Application of superoxide dismutase (SOD) to the donor tissue caused a relaxation of the assay tissue, and potentiated the relaxation by acetylcholine and substance P. AA861 and TMK777 suppressed the relaxant responses to acetylcholine and substance P, respectively, in the presence and absence of SOD to a similar extent and abolished the SOD-induced relaxation. Pyrogallol abolished the relaxation by acetylcholine, but did not inhibit the response when the donor tissue was pretreated with SOD. Therefore, it appears that AA861 and TMK777 do not degrade endothelium-derived relaxing factor (EDRF) in the perfusate via generation of superoxide anion or block the action of EDRF on vascular smooth muscle, but interfere with the synthesis and/or release of EDRF. The findings obtained so far support the idea that lipoxygenase products participate in the generation of EDRF.
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PMID:Possible involvement of 5-lipoxygenase products in the generation of endothelium-derived relaxing factor. 247 45


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