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)

Human cervical tissue specimens were excised after hysterectomy at various phases of the menstrual cycle (n = 12), and small intracervical arteries were dissected free by microtechnique. Ring preparations of the vessels were prepared and mounted in organ baths, and isometric circular tension was recorded. Norepinephrine, 3 X 10(-8) to 10(-5) mol/L, produced concentration-dependent contractions, whereas 3 X 10(-7) to 10(-6) mol/L prostaglandin F2 alpha inconsistently produced weak contractions and slightly increased tension induced by 10(-5) mol/L norepinephrine. Prostaglandin I2, 10(-9) to 10(-6) mol/L, prostaglandin E2, 3 X 10(-9) to 10(-6) mol/L, vasoactive intestinal polypeptide, 10(-9) to 10(-7) mol/L, and substance P, 10(-12) to 10(-9) mol/L, induced relaxation of vessels precontracted by 10(-5) mol/L norepinephrine. It is suggested that several mechanisms for the local release of vasoactive compounds may influence cervical blood flow. Thus, sympathetic control of cervical blood flow may be modulated by peptide neurotransmitters such as vasoactive intestinal polypeptide and substance P and by local synthesis of prostaglandins E2 and I2.
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PMID:Effects of some neurotransmitters and prostanoids on isolated human intracervical arteries. 245 Apr 61

The substances stimulating the release of immunoreactive corticotropin-releasing factor from cultured human placental cells were investigated. Monolayer primary cultures of trophoblast cells from pregnant women at term were used. The immunoreactive corticotropin-releasing factor released in the culture medium eluted from high-performance liquid chromatography with the same retention time as human corticotropin-releasing factor. Norepinephrine and acetylcholine increased immunoreactive corticotropin-releasing factor release into the culture medium in a dose-related manner. Epinephrine was partially active, whereas dopamine and serotonin did not induce significant changes of immunoreactive corticotropin-releasing factor release from placental cultures. Angiotensin II, interleukin-1, oxytocin, and arginine-vasopressin also increased placental immunoreactive corticotropin-releasing factor release in a dose-related manner, whereas other peptides (vasoactive intestinal peptide, substance P, somatostatin, atrial natriuretic factor, interleukin-2) were ineffective. These results showed that several neurotransmitters and peptides stimulate the release of immunoreactive corticotropin-releasing factor from placental cells, suggesting their possible involvement in the physiologic regulation of placental immunoreactive corticotropin-releasing factor release during pregnancy and parturition.
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PMID:Neurotransmitters and peptides modulate the release of immunoreactive corticotropin-releasing factor from cultured human placental cells. 256 97

Putative neurotransmitters of the lower urinary tract were investigated in apes, rabbits and cats using immunohistochemical techniques of PAP (Peroxidase antiperoxidase) staining and IGSS (Immunogold silver staining) methods for Neuron specific enolase (NSE), Acetylcholine (Ach), Noradrenaline (NA), Vasoactive intestinal polypeptide (VIP), Substance P (SP) and Calcitonin gene related peptide (CGRP). 1) The localization of pelvic ganglions exhibited more striking evidence of species difference. Huge pelvic ganglions were found particularly in the dorsolateral area of the prostate in apes. On the other hand, in cats and rabbits, many ganglion cells were found around the uretero-vesical junctions. 2) In the pelvic ganglions of the apes, Ach immunoreactives were detected in nearly 70 percent of the cell bodies. 10-15 percent were NA immunoreactive cells. In addition, 15-20 percent VIP and a smaller percentage of SP immunoreactive cells were detected in the same ganglions. Axons extending from the ganglion cells showed the intense neurotransmitters immunoreactivity. 3) In the apes, varicose fibers containing SP were widely distributed in the epithelium, submucosa, muscle layer, and around the vessels of the bladder. SP immunoreactive cell bodies were found in the dorsal root ganglion at levels of L7, S1 and at the same levels in the posterior horn. On the other hand, the bulbourethral gland and the seminal vesicle contained SP immunoreactive cell bodies. 4) CGRP containing fibers were distributed in similar locations as SP containing fibers in the bladder. 5) VIP immunoreactive fibers were also widely distributed, being most dense at the base of the bladder.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunohistochemical studies of putative neurotransmitters in the lower urinary tract]. 257 46

The roles of putative central neurotransmitters in the control of blood pressure have been reviewed with respect to the cardiovascular functions of individual nerve pathways in the medulla oblongata and spinal cord. Vasomotor activity of sympathetic preganglionic neurones originates from spinally-projecting neurones in the ventrolateral medulla which may include adrenaline neurones of the C1 group and serotonin neurones in the lateral B1 and B3 groups. Other bulbospinal monoamine nerves may modulate vasomotor activity at the spinal level, but the mechanism of this modulation is controversial. Evidence for two descending sympatho-inhibitory pathways has emerged: a noradrenergic projection from the A5 cell group and a serotonergic projection from the medullary raphe (medial B1 and B2 groups). The vasomotor influence of other bulbospinal pathways is unclear. Baroreflex control of blood pressure is mediated through the solitary tract nucleus (NTS). L-Glutamate and substance P are considered as candidates for transmitters in baroreceptor afferents to the NTS. Transmitters in efferent nerves relaying baroreflex activity from the NTS to cardiovagal motoneurones, medullary vasomotor neurones or sympathetic preganglionic neurones have not been identified but the monoamine transmitters present in the NTS appear to modulate baroreflexes. Noradrenaline and serotonin nerve endings may facilitate the vasodepressor component of the baroreflex while adrenaline nerves possibly inhibit the cardiovagal mechanism. Enkephalins and vasopressin act in the NTS to raise blood pressure and nerves containing these neuropeptides may constitute important links in reciprocal cardiovascular pathways between the lower brainstem and hypothalamus.
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PMID:Blood pressure control by neurotransmitters in the medulla oblongata and spinal cord. 286 Jan 49

The responses of the circular muscle of canine colon to stimulation of intrinsic nerves and to the probable mediators of these nerves were studied in vivo. In vivo studies were carried out using close intra-arterial injections and local field stimulation of proximal, mid-, and distal colon while recording circumferential contractions. Our results suggest that acetylcholine is the major excitatory mediator, but another excitatory mediator could be released by high frequency field stimulation after atropine. Norepinephrine had mixed inhibitory and excitatory effects, but no evidence was obtained that it was released by field stimulation. Substance P had mainly excitatory effects partly by a mechanism involving nerves and partly by a direct effect on muscle; it in addition to norepinephrine deserves further evaluation as the mediator of noncholinergic excitation to high frequency field stimulation. There is no explanation of the inhibition it produced after initial excitation during field stimulation. Vasoactive intestinal peptide had inhibitory effects but these were incomplete and inconsistent. This may be related to our inability to demonstrate relaxation or inhibition to field stimulation after atropine. Further evaluation of the possible role of vasoactive intestinal peptide and other agents as nonadrenergic, noncholinergic inhibitory mediators is required.
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PMID:Neural control of canine colon motor function: studies in vivo. 290

The responses of strips of the canine colon to stimulation of intrinsic nerves and to the probable mediators of these nerves were studied in vitro. Studies were carried out using longitudinal and circular muscle strips from proximal and distal colon with field stimulation and addition of agents to the bath. Overall, these and other studies in vivo suggested that acetylcholine was an ubiquitous mediator of neural excitation. Norepinephrine had mixed inhibitory and excitatory effects, the latter only in circular muscle. Inhibitory effects of norepinephrine seemed to be both pre- and post-synaptic but no evidence that it was released by field stimulation was obtained. Substance P had excitatory effects chiefly by release of acetylcholine. It, in addition to norepinephrine, at least in circular muscle, deserves evaluation as the mediator of noncholinergic excitation to high frequency field stimulation. Although vasoactive intestinal peptide sometimes had inhibitory effects, these were incomplete and inconsistent. However, further evaluation of its possible role as a nonadrenergic, noncholinergic inhibitory mediator is required to determine if it is involved as one component in the response. Few qualitative differences existed between responses of various regions of the colon to potential neuromediators, although there were some consistent differences between responses of longitudinal and circular muscle. Some differences existed in responses obtained earlier in vivo and in vitro. In particular, inhibitory effects following excitation by substance P on field stimulation were found only in vivo. Nonadrenergic, noncholinergic inhibitory responses to field stimulation were consistently present only in vitro. These differences have not been explained.
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PMID:Neural control of canine colon motor function: studies in vitro. 290 1

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

Electrical transmural stimulation evoked a transient contraction in the isolated mesenteric artery of the dog. This contraction was abolished by guanethidine or tetrodotoxin and was partially inhibited by prazosin. Noradrenaline was competitively antagonized by prazosin. Similarly, in the reserpine-treated artery, electrical transmural stimulation produced a transient contraction which was abolished by guanethidine or tetrodotoxin. However, prazosin failed to inhibit this contraction. The contraction to noradrenaline was not significantly different from the response it produced in control vessels. Tyramine (10(-5) M), which acts on sympathetic nerves to release noradrenaline, evoked a tonic contraction in the untreated artery. This contraction was abolished or markedly attenuated by prazosin or guanethidine. The response was not observed in the reserpine-treated artery, indicating that reserpine had depleted the nerves of noradrenaline. In the control vessel alpha,beta-methylene-ATP produced a transient contraction which was followed by a complete relaxation to the basal level. This contractile response was not significantly different in the presence of guanethidine or prazosin or in the reserpine-treated artery. After desensitization of the vessel to alpha,beta-methylene ATP (5 X 10(-6) M) the prazosin-resistant contractions induced by electrical transmural stimulation were abolished both in reserpine-treated and untreated arteries. Also the contractile responses to ATP and alpha-beta-methylene-ATP were abolished but the responses to tyramine (control vessels), noradrenaline and KCl were not affected. 8-Phenyltheophylline (10(-5) M) showed no inhibitory effect on the contractile responses to electrical transmural stimulation, tyramine, ATP or alpha,beta-methylene-ATP. 7. Neuropeptide Y, peptide YY, vasoactive intestinal polypeptide, bombesin and substance P (10-7 and 10-6 M for each peptide) caused no contractile response in the dog mesenteric artery. 8. These experiments provide further evidence that the sympathetic contraction of the isolated mesenteric artery of the dog induced by electrical transmural stimulation consists ofan adrenergic and a purinergic component and that the latter component is mediated through postsynaptic P2- purinoceptors.
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PMID:The effect of reserpine on sympathetic, purinergic neurotransmission in the isolated mesenteric artery of the dog: a pharmacological study. 303 38

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

Experiments were conducted to study the regulation of the developmental pattern of aromatase in the forebrain of the perinatal rat. Two experimental designs were used: aromatase measured in primary cultures of fetal hypothalamic cells and in cell-free preparations of forebrain tissue excised at varying ages. In cultured cells, aromatase decreased logarithmically at a slow rate (t1/2 = 7.8 days). Norepinephrine caused a pronounced dose (4 x 10(-6) M) and time-dependent (2-6 days) drop in aromatase without affecting the levels of 5 alpha-reductase or substance P. In isolated tissue, aromatase activity was compared with the concentrations of norepinephrine and dopamine in the forebrain of males vs females at different perinatal ages and in discrete forebrain areas at postnatal day 4. In no case was a sex difference in catecholamines seen. An overall developmental decline in aromatase was associated with developmental increases in catecholamine levels. Acute treatment with the beta-agonist, isoproterenol, had no effect on brain aromatase activity.
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PMID:Studies on the role of catecholamines in the regulation of the developmental pattern of hypothalamic aromatase. 350 14


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