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)

A method for demineralization of bone, preserving the antigenicity of neuroactive peptides, was developed. In all parts of rat long bones, nerves immunoreactive to substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY) and tyrosine hydroxylase (TH) were detected after immunohistochemical staining. The majority of nerves were vascular, although several non-vascular endings were observed at the growth plate and amidst marrow cells. An abundance of nerves were demonstrated near the epiphyseal plate and in the periosteum, regions of high osteogenic activity. The occurrence of different nerve types was analyzed at different stages of heterotopic osteogenesis, induced by allogeneic bone matrix. Nerve fibres immunoreactive to SP, CGRP, NPY and TH occurred amidst differentiating chondroblastic cells in the second week. They gradually increased in number during the ensuing eight weeks. In an in vitro study of osteoblastic cells (UMR 106-01, ROS 17/2.8, Saos-2, MC3T3-E1) receptors to CGRP, VIP, noradrenaline (NA) and NPY were demonstrated as assessed by analysis of cyclic AMP formation. In UMR cells, NPY inhibited the effects of NA and parathyroid hormone (PTH), which is the first demonstration of a receptor interaction between a local neuropeptide and a systemic calcium regulating hormone. The combined findings indicate a neuroendocrine influence on bone physiology.
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PMID:Neuroendocrine peptides in bone. 172 76

In atrial preparations obtained from reserpine-pre-treated guinea-pigs, incubated in the presence of 1 microM atropine plus 1 microM CGP 20712A (a beta 1 blocking drug), a positive inotropic effect due to CGRP release from capsaicin-sensitive sensory neurons was induced by electrical field stimulation (EFS). This response was concentration-dependently reduced by noradrenaline (0.01-3 microM), neuropeptide Y (NPY, 3-300 nM) and adenosine triphosphate (ATP, 1-30 microM). On the other hand, the overflow of [3H]-noradrenaline from sympathetic nerve terminals induced by EFS in isolated atria obtained from normal untreated animals was not modified in 10 nM calcitonin gene-related peptide (CGRP). Substance P (SP) and neurokinin A (NKA), at concentrations ranging from 0.01 to 1 microM did not affect the cardiac response to field stimulation of adrenergic terminals of atrial tissue. These findings demonstrate that all the co-transmitters stored in adrenergic nerve terminals have a modulatory role on the efferent function of cardiac capsaicin-sensitive sensory neurons, while cardiac adrenergic neurotransmission is not influenced by the peptidergic transmitters released from sensory neurons.
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PMID:Modulation by adrenergic transmitters of the efferent function of capsaicin-sensitive nerves in cardiac tissue. 172 21

The effect of acrylamide intoxication on the innervation and local control of the rabbit central ear artery was investigated. There was no difference in the noradrenaline, neuropeptide Y and calcitonin gene-related peptide tissue content between control and experimental animals. There was, however, a slight reduction in catecholamine histofluorescence. Although the contractile efficiency of the rabbit central ear artery as measured by responses to potassium chloride was unchanged, nerve-mediated contractile responses were significantly attenuated in acrylamide-treated animals. Contractile responses induced by exogenous alpha,beta-methylene ATP were markedly increased after acrylamide treatment, in contrast to contractions induced by exogenous noradrenaline which were attenuated at maximal concentrations. Modulatory effects of nerve-mediated contractile responses by neuropeptide Y were unaffected by acrylamide intoxication. It therefore appears that acrylamide intoxication damages sympathetic cotransmission, perhaps with preferential action on the purinergic component. Endothelium-dependent relaxant responses to acetylcholine and substance P were attenuated in acrylamide-treated animals, whereas relaxant responses mediated by calcitonin gene-related peptide (endothelium independent) were unaffected. The question of whether the damage to the endothelial cell action is a primary effect, or a secondary consequence of sympathetic nerve damage, is discussed.
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PMID:Changes in sympathetic and endothelium-mediated responses in the rabbit central ear artery after acrylamide treatment. 175 64

It has been demonstrated that nerve fibres storing immunoreactivity of vasoactive intestinal polypeptide, peptide histidine iso-leucine, neuropeptide Y, substance P, calcitonin gene-related peptide, galanin, and cholecystokinin exists in the thyroid, though the content of these neuropeptides is lower in the thyroid than in other organs, like in the gut. Furthermore, the parafollicular C-cells have been shown to harbour several different peptides: calcitonin, somatostatin, calcitonin gene-related peptide, gastrin-releasing peptide, katacalcin and helodermin. In addition, other regulatory peptides like atrial natriuretic hormone, growth factors, and cytokines are also produced in the thyroid. This review summarizes today's knowledge on the effects of these peptides on thyroid hormone secretion and their possible role in thyroid physiology. So far, functional studies have failed to establish any convincing effect of substance P, calcitonin gene-related peptide, galanin and cholecystokinin on basal or TSH-stimulated thyroid hormone secretion. In contrast, vasoactive intestinal peptide has convincingly been demonstrated to stimulate thyroid hormone secretion, and neuropeptide Y to potentiate the inhibitory action of noradrenaline on TSH-induced thyroid hormone secretion. This suggests that these two neuropeptides are involved in the intrathyroidal neural regulation of thyroid function. Moreover, the C-cell peptides somatostatin, calcitonin, calcitonin gene-related peptide, and katacalcin seem to be involved as inhibitors of thyroid hormone secretion, whereas both gastrin-releasing peptide and helodermin stimulate thyroid hormone secretion. Atrial natriuretic hormone and growth factors, and cytokines seem to inhibit thyroid hormone secretion. Hence, studies undertaken so far suggest a local intrathyroidal peptidergic regulatory concept, the exact role of which remains to be established.
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PMID:Regulatory peptides in the thyroid gland--a review on their localization and function. 182 1

1. The effect of capsaicin pre-treatment on adrenal catecholamine (CA) secretion in response to stress is controversial. In earlier experiments performed under pentobarbitone anaesthesia, the release of CA in response to stress was complicated by the effects of the barbiturate anaesthesia. 2. In the present study we have used conscious freely moving rats with indwelling cannulae to study the effect of neonatal capsaicin pre-treatment on the plasma CA response to different types of stressors (swimming stress, hypovolaemic stress, immobilization stress and cold stress). 3. After swimming for 20 min, plasma noradrenaline (NA) levels increased by 8-fold and adrenaline by 2-fold in control rats. The increase in plasma NA levels in the capsaicin group was attenuated at 10 min of swimming compared with the vehicle group (P < 0.05). 4. With hypovolaemic stress, there were no differences in plasma CA levels, blood pressure and heart rate between the capsaicin group and the vehicle group. There were also no differences in plasma CA levels after immobilization stress between the two groups. 5. With cold stress, plasma NA levels increased 5-fold and adrenaline levels by 3-fold over basal at 45 min in the vehicle pre-treated rats. This increase was not observed in the capsaicin group. 6. Immunoreactive substance P was depleted by only 68% in the splanchnic nerve following capsaicin pre-treatment. If the remaining 32% was biologically active substance P then it could account for the maintenance of the response to hypovolaemic and immobilization stress. However, it might be possible that the responses to hypovolaemic and immobilization stresses could be attenuated if a more complete depletion were achieved. 7. These results in conscious rats indicate that capsaicin-sensitive sensory neurons are required for plasma CA response to selective stressors. They are required for CA output in response to cold stress and to the early phase of swimming stress, but not to hypovolaemic stress and immobilization stress.
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PMID:Capsaicin-sensitive sensory neurons are involved in the plasma catecholamine response of rats to selective stressors. 184 48

Systemic capsaicin pretreatment (total cumulative dose 50 mg/kg administered s.c. over 2h) was performed in pigs under pentobarbitone anaesthesia and the effects on sensory and sympatho-adrenal mechanisms were examined acutely and 2 days after treatment. During pretreatment with capsaicin, pronounced sensory and sympatho-adrenal activation were noticed. This resulted in a several-fold increase in the systemic arterial plasma levels of calcitonin gene-related peptide (CGRP), neurokinin A (NKA), noradrenaline (NA), adrenaline (Adr) and neuropeptide Y (NPY), and a slight increase (39%) in plasma cortisol. Simultaneously, there was marked tachycardia, an increase in blood pressure, total skin erythema and some bronchoconstriction, all lasting for about 30 min. Upon repeated injections tachyphylaxis was observed. 2 days after capsaicin pretreatment, basal plasma levels of the neuropeptides, catecholamines and cortisol as well as basal cardiovascular and pulmonary parameters were similar in control and capsaicin-treated pigs. The tissue content of CGRP and NKA was reduced by 50-65% in the airways and by 80-90% in the skin 2 days after capsaicin pretreatment. In contrast, the CGRP content was unchanged or increased (by 195%) in the nodose and spinal ganglia, respectively. The corresponding tissue levels of vasoactive intestinal polypeptide (VIP) and NPY were basically unchanged in capsaicin-treated pigs. A bolus injection of capsaicin (1 mg/kg i.v.) in control animals resulted in a marked increase in plasma catecholamines and NPY, concomitant with elevation in blood pressure and heart rate. These effects were preceded by an initial bradycardia and decrease in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Capsaicin-induced local effector responses, autonomic reflexes and sensory neuropeptide depletion in the pig. 185 42

The effects of intrathecal pretreatment with the neurotoxins capsaicin, 6-hydroxydopamine and 5,7-dihydroxytryptamine on spinal antinociception by adenosine analogs (NECA, 5'-N-ethylcarboxamido adenosine and CHA, N6-cyclohexyl adenosine) and morphine were examined using the rat tail flick and hot plate tests. Pretreatment with 50 micrograms capsaicin for 7 to 11 days (which reduced substance P immunoreactivity in the superficial layers of the dorsal spinal cord) produced a slight increase in the action of NECA and CHA, and reduced the action on morphine in the hot plate test but not in the tail flick test. Pretreatment with 50 to 100 micrograms 6-hydroxydopamine for 7 to 14 days (which reduced spinal cord noradrenaline levels by 54-65%) reduced spinal antinociception by NECA and CHA but not that by morphine. Pretreatment with 50 micrograms 5,7-dihydroxytryptamine (which reduced spinal cord serotonin levels by 74-89%) had no effect on any agent. Acute pretreatment with 7.5-30 micrograms phentolamine reduced the spinal antinociceptive action of noradrenaline, NECA and CHA, primarily in the hot plate test. Phentolamine (30 micrograms) also reduced the action of morphine (hot plate greater than tail flick), but did not affect the action of L-baclofen. These results suggest that spinal antinociception by adenosine analogs: 1) occurs primarily at a postsynaptic site of action (capsaicin results), and 2) is dependent on release of endogenous noradrenaline and activation of spinal adrenergic receptors (6-hydroxydopamine and phentolamine results). The reduction in the effect of morphine by capsaicin (removes a source of adenosine release) and phentolamine (antagonizes the action of endogenously released adenosine) can be explained in terms of the adenosine release hypothesis of morphine action within the spinal cord.
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PMID:Spinal antinociception by adenosine analogs and morphine after intrathecal administration of the neurotoxins capsaicin, 6-hydroxydopamine and 5,7-dihydroxytryptamine. 190 40

The effects of chronic acrylamide treatment on the autonomic nervous system were investigated by histochemical and pharmacological studies. Histochemical studies showed that acrylamide caused different degrees of damage to different nerve fibre types: calcitonin gene-related peptide (CGRP)-immunoreactive (IR) nerves showed the greatest reduction in intensity and number; noradrenaline (NA)-containing nerves were somewhat less affected; substance P (SP)-IR nerves were reduced in number, but this was not significant. The profiles of SP- and particularly of CGRP-IR nerves from treated animals were noticeably different to those from the control group, being flattened and irregular. Periarterial nerve stimulation (4-32 Hz) of the isolated rat mesenteric arterial bed preparation at basal tone elicited frequency-dependent vasoconstrictor responses. The magnitude of these responses was significantly reduced at higher frequencies in acrylamide-treated animals. In preparations with tone raised by the addition of methoxamine (10(-5) M), and in the presence of guanethidine (5 x 10(-6) M), periarterial nerve stimulation elicited vasodilator responses. These responses, which result from stimulation of sensory nerves, were greatly reduced in acrylamide-treated animals. There was a tendency for mesenteric beds from acrylamide-treated animals to show increased vasoconstrictor responses to doses of exogenous NA, although this was not significant. Responses to exogenous adenosine 5'-triphosphate (a cotransmitter with NA from sympathetic nerves) were not affected. In the raised-tone preparation, vasodilator responses to exogenous CGRP (the principal vasodilator sensory transmitter of rat mesenteric arteries) were not affected by acrylamide treatment. Hence, it is unlikely that the reduced responses to nerve stimulation were due to defects in the postjunctional receptors for the principal transmitters of sympathetic and sensory-motor nerves. There was no difference in the ability of mesenteric beds from control and treated animals to vasodilate in response to acetylcholine or sodium nitroprusside, or to vasoconstrict in response to potassium chloride, indicating normal smooth muscle and endothelial responses. These results suggest that chronic acrylamide treatment produces peripheral autonomic neuropathy of rat mesenteric vessels, manifested as a dysfunction of sympathetic and sensory-motor nerves. Furthermore, the graded destruction of nerve types, such that damage occurred in the order: CGRP-IR greater than NA greater than SP-IR, indicated a differential sensitivity of different nerves to this toxin.
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PMID:Acrylamide-induced autonomic neuropathy of rat mesenteric vessels: histological and pharmacological studies. 194 19

The effects of various neuroactive substances on the intracellular free Ca2+ concentration ([Ca2+]i) in cultured type-2 astrocytes were examined by fura-2-based microfluorometry. Type-2 astrocytes showed [Ca2+]i elevation in response to all the substances examined, i.e. carbachol (10(-4) M), histamine (10(-4) M), noradrenaline (10(-4) M), serotonin (10(-4) M), substance P (10(-6) M), vasopressin (10(-6) M) and glutamate (10(-4) M). Not all type-2 astrocytes, however, responded to these substances at the concentrations tested, and the percentages of astrocytes showing a Ca2+ response differed depending on the substance. These results indicate that type-2 astrocytes are potential targets for widely diverse neuroactive substances and heterogeneous in response to them.
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PMID:Type-2 astrocytes show intracellular Ca2+ elevation in response to various neuroactive substances. 194 45

Non-cholinergic, non-adrenergic vasodilation has been studied by transmural field stimulation of the isolated rat hepatic artery and compared with responses in the splenic artery. In the hepatic artery with rubbed endothelium, transmural stimulation caused a contracture that was blocked by phentolamine and potentiated after capsaicin. After pretreatment with guanethidine in order to deplete the neuronal stores of noradrenaline, the methoxamine-contracted hepatic artery was significantly relaxed by transmural stimulation; more efficiently than the splenic artery. This relaxation of the hepatic artery was attenuated following a 30 min exposure to capsaicin and largely blocked by tetrodotoxin (TTX). The relaxation by exogenous CGRP was independent of a functional endothelium. In contrast, vasodilation by substance P (SP) and neurokinin A (NKA), was completely dependent on an intact endothelium. Exogenous CGRP caused a near-complete relaxation of the methoxamine-contracted hepatic artery both before and after capsaicin treatment. CGRP was a more efficient relaxant of the hepatic than the splenic artery. These findings show that responses to transmural stimulation of the hepatic artery are modulated after pretreatment with capsaicin, indicating release of relaxing substances such as CGRP, presumably from capsaicin-sensitive neuronal stores. In conclusion, CGRP is a likely mediator of neuronal vasodilation in the rat liver, independent of the state of the endothelium.
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PMID:Vasodilation by calcitonin gene-related peptide (CGRP) and by transmural stimulation of the methoxamine-contracted rat hepatic artery after pretreatment with guanethidine. 194 24


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