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 effect of galanin on the [3H]ACh release from myenteric plexus-longitudinal muscle strips of the guinea pig small intestine was studied. While galanin did not alter the basal spontaneous efflux of ACh, it significantly depressed the ACh release evoked by electrical stimulation or caused by VIP and substance P. These results suggest an important neuromodulatory role for galanin in the enteric nervous system.
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PMID:Evidence for galanin as an inhibitory neuropeptide on myenteric cholinergic neurons in the guinea pig small intestine. 243 87

Acetylcholine, released from splanchnic nerve terminals innervating adrenal chromaffin cells, is known to increase synthesis of adrenal tyrosine hydroxylase, the rate-limiting enzyme in catecholamine synthesis. The neuropeptide substance P is also present in the splanchnic nerve innervating the adrenal medulla, and this study examined whether substance P has any long-term effects on tyrosine hydroxylase activity and catecholamine levels in cultures of adult bovine adrenal chromaffin cells. When cultures were incubated for 3 days with substance P and carbachol, a cholinergic agonist, substance P (10(-6) M, and greater) completely inhibited the increase in tyrosine hydroxylase activity normally induced by carbachol. Long-term stimulation with carbachol also depleted endogenous catecholamines from the cells and substance P prevented this carbachol-induced depletion of catecholamine content. Substance P by itself, in the absence of carbachol, had only a slight effect on tyrosine hydroxylase activity. 8-Bromoadenosine 3':5'-cyclic monophosphate, an analogue of adenosine 3':5'-cyclic monophosphate, also increases tyrosine hydroxylase activity in chromaffin cells; however, substance P had no effect on the increase in tyrosine hydroxylase activity induced by this analogue. These results indicate that substance P's effects are relatively specific for the carbachol-induced increased in tyrosine hydroxylase activity and that the primary site of action of substance P is not a site common to the mechanism of tyrosine hydroxylase induction by carbachol and 8-bromoadenosine 3':5'-cyclic monophosphate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of substance P on the long-term regulation of tyrosine hydroxylase activity and catecholamine levels in cultured adrenal chromaffin cells. 243 94

Experiments were performed on cats anesthetized with thiopental sodium and gallamine triethiodide and ventilated artificially. Gastric motility was recorded by a balloon method. Electrical stimulation of the vagal trunk in cats with chronic supranodose vagotomy for 11 to 32 days caused an excitatory response of the stomach. The pulse duration of electrical stimulation to obtain a maximal excitatory response of the stomach was 3 msec. Administration of hexamethonium (10 mg/kg i.v.) did not inhibit but enhanced the excitatory response of stomach. Atropine (3, 10 and 30 micrograms/kg i.v.), hemicholinium (10 mg/kg i.v.) and morphine (5 mg/kg i.v.) inhibited this hexamethonium-resistant excitatory response of the stomach, whereas treatment with physostigmine (300 mu/kg i.v.) augmented it. A substance P antagonist, (D-Pro2, D-Trp7.9)-substance P (250 and 500 micrograms/kg i.v.), did not affect the hexamethonium-resistant excitatory response. Acetylcholine content of the nodose ganglion 6 to 8 days after supranodose vagotomy was assayed using the radioenzymatic method, and the level was about 48% that of the intact ganglion. These results suggest that the gastric excitatory response to stimulation of the supranodose denervated vagal trunk is produced by activation of vagal afferent fibers probably originating from the nodose ganglion; the fibers involved are cholinergic.
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PMID:Gastric excitation by stimulation of the vagal trunk after chronic supranodose vagotomy in cats. 243 91

The physiological and pharmacological properties of tachykinin receptors have been examined by intracellular recording from intact chick lumbar sympathetic ganglia in vitro. In these ganglia, both substance P and eledoisin are potent agonists, producing a slowly developing depolarization in ganglion neurons which is associated with an increase in input resistance and inhibition of the M-current. In contrast, physalaemin is a considerably less potent tachykinin in chick ganglia, and kassinin is without activity even at high doses. The rank order of potencies of tachykinin agonists is consistent from cell to cell, indicating that a single type of tachykinin receptor may be responsible for the observed responses. A putative tachykinin antagonist, (D-Arg1,D-Pro2,D-Trp7,9,Leu11)-substance P, exhibits no intrinsic activity in the ganglia but does block the responses to subsequently applied substance P and eledoisin. This tachykinin antagonist also inhibits a portion of the slow excitatory postsynaptic potential (EPSP) elicited in ganglion neurons by repetitive nerve stimulation. Since substance P has been identified within nerve fibers in the ganglia, it appears that this or another endogenous tachykinin mediates a portion of the slow EPSPs observed in the ganglia. Acetylcholine acting via muscarinic receptors is also capable of producing slow EPSPs in the ganglia, since perfusion with atropine can reduce the size of some slow EPSPs. It is concluded that chick sympathetic neurons contain both tachykinin and muscarinic receptors, and that these receptors are involved in slow synaptic responses in the ganglion neurons which increase the excitability of the cells.
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PMID:Properties of tachykinin receptors examined by intracellular recording from chick sympathetic ganglia. 244 2

1 Acetylcholine, substance P, prostaglandin E1 and the nitrovasodilator glyceryl trinitrate induced concentration-dependent relaxations of endothelium-intact strips of rabbit coeliac artery precontracted with noradrenaline. 2 Endothelium-denuded strip preparations contracted to acetylcholine and showed no response to substance P. The relaxant response to prostaglandin E1 was unimpaired after removal of endothelium, whereas the response to glyceryl trinitrate was increased. 3 A 20 min exposure of endothelium-intact strips to gossypol, an irreversible inhibitor of the production and/or release of endothelium-derived relaxing factor, abolished vasodilatation in response to the endothelium-dependent agents acetylcholine and substance P, did not change relaxations to prostaglandin E1, but significantly enhanced relaxations in response to glyceryl trinitrate. 4 In view of the assumed common mechanism of action of endothelium-derived relaxing factor and nitrovasodilators, these results suggest an interference of the two active principles at the level of the vascular smooth muscle cell.
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PMID:Selective inhibition by gossypol of endothelium-dependent relaxations augments relaxations to glyceryl trinitrate in rabbit coeliac artery. 244

This study was undertaken to determine whether atherosclerosis impairs relaxations mediated by endothelium-derived relaxing factor (EDRF) in human coronary arteries. Epicardial coronary arteries were obtained from the hearts of cardiac transplantation patients with or without histologically documented coronary atherosclerosis (atherosclerotic arteries were from patients aged 42-55 years, nonatherosclerotic arteries were from patients aged 14-24 years). Transverse strip preparations were mounted in organ baths for isometric tension recording. Tension was induced with prostaglandins F2 alpha. Indomethacin (10(-5) M) was present to prevent possible interference from endogenously formed prostaglandins. The EDRF-mediated relaxations in response to substance P (10(-10) to 10(-8) M), bradykinin (10(-9) to 10(-7) M), and Ca2+-ionophore A23187 (10(-9) to 10(-7) M) were significantly attenuated in atherosclerotic arteries. In deendothelialized tissues these compounds had no effect. In contrast, endothelium-independent relaxations induced by isoprenaline (10(-7) to 10(-5) M) were not affected by atherosclerosis. Atherosclerotic arteries showed also normal relaxations with high concentrations of glyceryl trinitrate (10(-8) to 10(-7) M), but reduced relaxations with a lower concentration of the compound (10(-9) M). Acetylcholine (10(-7) to 10(-6) M) only produced endothelium-dependent relaxations in 8 of 60 arterial preparations (with or without atherosclerosis). In most of the arteries, it was a direct vasoconstrictor (which may have masked EDRF release in many cases). Omission of indomethacin from the bath solution increased the incidence of moderate acetylcholine-induced relaxations (9 of 16 preparations). It is concluded that atherosclerosis attenuates EDRF-mediated vasospasm and myocardial ischemia.
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PMID:Selective attenuation of endothelium-mediated vasodilation in atherosclerotic human coronary arteries. 244 55

The role of endothelium on the responses of the perfused rabbit renal artery segments to vasoconstrictor and vasodilator agents was studied. The vasoconstrictor responses of rabbit renal arteries to phenylephrine were enhanced by endothelium destruction. Acetylcholine (ACh), calcium-ionophore (A23187) and substance P (SP), in the presence of indomethacin, induced endothelium-dependent vasodilation of the phenylephrine-constricted renal arteries. Nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase, significantly reduced the dilator responses to ACh, A23187 and SP, but did not reduce the responses to sodium nitrite. In conclusion, our results provide evidence for the involvement of lipoxygenase products in the endothelium-dependent vasodilation of rabbit renal arteries to ACh, A23184 and SP.
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PMID:Endothelium-dependent vasodilator actions of acetylcholine, calcium-ionophore (A23187) and substance P in perfused renal arteries from rabbits. 245 9

1. The mechanical and electrical properties of smooth muscle cells of the rabbit aorta were recorded simultaneously using respectively a force transducer and a 3 M-KCl-filled glass microelectrode. 2. Acetylcholine had two effects depending on concentration. At low concentration, it caused a persistent endothelium-dependent relaxation and hyperpolarization. At higher concentrations the acetylcholine endothelium-dependent relaxation summed with an endothelium-independent contraction. 3. Substance P caused a transient endothelium-dependent relaxation and hyperpolarization. 4. Acetylcholine and substance P depolarized and contracted de-endothelialized smooth muscle. When the de-endothelialized strip was pre-contracted by noradrenaline, acetylcholine depolarized the muscle but substance P did not. 5. In a 'cascade' experiment, the perfusate from an upstream intact aorta passed over a downstream de-endothelialized strip. Acetylcholine and substance P relaxed the downstream strip showing that they released an endothelial humoral factor which relaxes smooth muscle. 6. The results suggest a constant release of a factor from the endothelial cells which hyperpolarizes the smooth muscle cells in the media. Activation of acetylcholine and substance P receptors on the endothelium accelerates the release of this factor and causes vasodilatation.
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PMID:Electrophysiological and mechanical effects of substance P and acetylcholine on rabbit aorta. 245 99

Two structurally related tetrapeptides, the N-terminal tetrapeptide of substance P SP(1-4) and tuftsin, exerted some similarities in modifying immune reactions and normalizing stress-induced disorders in the catecholamine system of adrenals. This paper presents results about the effects of tuftsin and SP(1-4) on the cholinergic-adrenergic interaction in rat adrenal gland slices. Both, tuftsin and SP(1-4) inhibited the nicotine-evoked [3H]noradrenaline outflow (postsynaptic effect), but the effect of SP(1-4) was more pronounced. SP(1-4) also inhibited the electrically stimulated [3H]ACh outflow (presynaptic effect), whereas tuftsin did not affect the ACh outflow. It is suggested that the regulation of the cholinergic-adrenergic interaction in adrenals is mediated by specific receptors, which are different on the pre- and postsynaptic side.
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PMID:Effect of the N-terminal tetrapeptide of substance P SP (1-4) and tuftsin on the pre- and postsynaptic transmitter outflow in rat adrenal gland slices. 246 17

1. Removal of the endothelium (DE) enhanced the in vitro release of prostacyclin (PGI2) by rat aortae in response to adrenaline (Ad), noradrenaline (NA), thromboxane A2 analogue U46619, phorbol dibutyrate (PDBU) and sodium fluoride (NaF) when assessed at 3 h post DE. At 6 h post DE, there were no differences between the dose-response curves obtained from aortic rings with or without endothelium. 2. At 3 h post DE the antagonism of Ad- and NA-stimulated PGI2 synthesis by yohimbine and prazosin, and NA-stimulated PGI2 synthesis by nifedipine was markedly reduced in aortae without endothelium when compared with controls. These effects were reversed by protracted incubation of aortic tissue post DE (6 h and 9 h). 3. Acetylcholine, carbachol, substance P and nitroprusside were without effect on de novo or NA-stimulated PGI2 synthesis, whether or not the endothelium was present and irrespective of incubation time, post-DE. 4. These results indicate that: (a) PGI2 synthesis linked to excitatory receptors (alpha-adrenoceptors, thromboxane A2) and associated systems (G proteins, protein kinase C) in the smooth muscle component of the rat aorta is not influenced by endothelium-derived relaxing factor (EDRF); (b) the changes of response to stimulators and inhibitors of PGI2 synthesis may be due to an increased reactivity of the vessels caused by the trauma of DE; and (c) vasodilators (parasympathomimetics, substance P and nitroprusside) that do not act directly on excitatory receptors do not influence PGI2 synthesis.
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PMID:Effect of endothelium removal on stimulatory and inhibitory modulation of rat aortic prostacyclin synthesis. 246 14


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