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)

We have investigated with light and electron microscope immunocytochemistry the aminergic and peptidergic innervation of Onuf's nucleus in adult baboons. This nucleus, located in the ventrolateral part of the sacral spinal cord (S2 and S3), is considered to control urethral and anal sphincters and penile muscles. By comparison of intact and transected spinal cords, we have found that serotoninergic innervation has two origins: first, supraspinal, innervating the whole nucleus, with a possible predominance in the dorsal half; and second, intraspinal, corresponding to the ventral half of the nucleus. Thyrotropin-releasing hormone innervation appears largely coincident with serotonin, both in intact and transected spinal cords. Noradrenaline is exclusively of supraspinal origin, as attested by its disappearance below the level of the section. Substance P, calcitonin gene-related peptide, and Leu- and Met-enkephalin, which profusely innervate Onuf's nucleus, are on the contrary not affected by the transection. They most likely originate from the cord itself or the dorsal root ganglia. Thus, Onuf's nucleus innervation in the baboon arises both from supraspinal and intraspinal sources. The present study provides an anatomical basis for both voluntary and reflex controls of excretory and sexual functions in a primate. The same neurotransmitter (serotonin) according to its cell origin and discrete topography could exert different influences upon the same effector system.
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PMID:Serotoninergic, noradrenergic, and peptidergic innervation of Onuf's nucleus of normal and transected spinal cords of baboons (Papio papio). 137 63

Using isolated perfused porcine ileum we studied the release of substance P (SP) and neurokinin A (NKA) in response to electrical stimulation of the mixed periarterial nerves and to infusion of different neuroactive agents. Nerve stimulation (8 Hz) had no significant effect on the release of SP and NKA. Nerve stimulation also had no effect on the release of SP and NKA during infusion of atropine (10(-6) M) or phentolamine (10(-5) M), whereas a significant increase (from 8.2 +/- 1.9 to 20.1 +/- 4.6 pmol/l for SP and from 12.3 +/- 2.7 to 34.2 +/- 7.7 pmol/l for NKA, n = 7) was observed during nerve stimulation after pretreatment with both atropine and phentolamine. This increase was abolished by hexamethonium (3 x 10(-5) M). Also acetylcholine infusion causes a significant release of SP and NKA after infusion of both atropine and phentolamine (to 172 +/- 56% and 232 +/- 69% of basal release, n = 7), an effect that was abolished by hexamethonium infusion. Infusion of atropine alone increased the release of SP and NKA significantly (to 337 +/- 92% and 386 +/- 124% of basal output, n = 5). Norepinephrine (10(-6) M) inhibited the release of SP and NKA (to 69 +/- 6% and 80 +/- 6% of basal release, n = 7). Our results suggest that the SP- and NKA-producing neurons receive intrinsic tonic muscarinic inhibitory impulses, extrinsic nicotinic excitatory impulses, and extrinsic adrenergic inhibitory impulses.
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PMID:Nervous control of the release of substance P and neurokinin A from the isolated perfused porcine ileum. 137 30

The vascular smooth muscle contractile response to neuropeptide Y (NPY), potassium, noradrenaline, histamine and serotonin was studied in circular segments of isolated vessels in vitro from rabbits with alloxan-induced diabetes mellitus. The injection of alloxan resulted in a marked and maintained increase in serum glucose as early as 1 week after treatment. Four vessel types were examined: abdominal aorta, and renal, left anterior descending coronary and middle cerebral arteries. There was no difference in the contractile response to histamine or serotonin between control and diabetic vessels. However, in the cerebral artery the contractile response to noradrenaline was reduced in the diabetic group, while in the aorta and the renal artery no significant differences were seen. Noradrenaline failed to evoke any contractile response in the coronary arteries in either group. NPY induced strong, concentration-dependent contractions of coronary and cerebral arteries, but did not have any contractile effect per se in aorta or renal arteries, either in control or in alloxan-treated rabbits. The maximal contractile effect and the sensitivity to NPY was significantly less in diabetic coronary and cerebral vessels as compared to control. There was no difference in dilator effect of acetylcholine and substance P between the diabetic animals and the control group in any of the vessel types, indicating that the changed vascular responses to NPY and noradrenaline were not endothelium-dependent. In conclusion, the present study has shown that the postjunctional effects of NPY and noradrenaline in the peripheral sympathetic nervous system are selectively attenuated in this model of chronic diabetes.
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PMID:Diminished contractile responses to neuropeptide Y of arteries from diabetic rabbits. 158 98

To investigate the functional relationship between the enteric nervous system and the intestinal neurotensin (N) cells, the release of neurotensin (NT) was measured upon vascular 8-min infusion periods of various neurotransmitters and neuropeptides in an isolated vascularly perfused rat jejunoileum. NT-like immunoreactivity (NT-LI) was measured with an antiserum that specifically recognizes intact NT. The cholinergic agonists methacholine and carbachol produced a strong release of NT-LI (250% and 700% of basal, respectively at 10(-5) M). The infusion of a lower dose (10(-7) M) was less effective in both cases. The nicotinic receptor agonist DMPP (10(-4) M) had no significant effect on NT-LI release. Norepinephrine (10(-6) M) produced a moderate and well-sustained secretion of NT (200% of basal). Infusion of higher doses of these neurotransmitters dramatically increased the arterial pressure. G-amino-n-butyric acid (GABA), histamine, serotonin and dopamine administered at final concentrations up to 10(-5) M had no effect on NT-LI release. In contrast, gastrin-releasing peptide and bombesin induced a dose-dependent transient increase of portal NT-LI (maximal value at 10(-7) M: 1000% of basal) followed by a rapid return to near basal values. Substance P (10(-7) M) evoked a prompt release of NT-LI with a peak at 600% of basal followed by a decline to 200% of basal at the end of the session. Leu-enkephalin and calcitonin-gene-related-peptide (CGRP, 10(-7) M) produced a small rise in portal NT-LI, while Met-enkephalin, dynorphin, vasoactive intestinal peptide (VIP), galanin, neuropeptide Y (NPY), peptide histidine isoleucine (PHI), neuromedin U and thyrotropin releasing hormone (TRH) had no stimulatory effect. Our results indicate that additionally to the secretion of NT induced by cholinergic agents and bombesin, substance P and to a lesser extent Leu-enkephalin are capable of stimulating NT release in the rat.
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PMID:Release of ileal neurotensin in the rat by neurotransmitters and neuropeptides. 167 14

The spiral modiolar artery is the terminal artery in the cochlea, and as such is expected to play a major role in the control of cochlear blood flow. In this study, we examined the distribution of adrenergic and peptidergic nerve fibres on the spiral modiolar artery of the guinea pig using histofluorescence and immunofluorescence techniques. The spiral modiolar artery was dissected from the modiolus so that the entire length of the vessel and its branches, could be observed. Noradrenaline was identified using the glyoxylic acid histofluorescence technique. The presence of the vasoactive peptides substance P, calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), was investigated using antibodies against these peptides. Each putative transmitter tested yielded labelled nerve fibres throughout the length of the spiral modiolar artery and its branches. Double-labelling experiments confirmed that CGRP and substance P are contained in the same fibres but that VIP and substance P appear to be contained in different populations of fibres. These results establish that nerve fibres containing vasoactive peptides and noradrenaline supply the spiral modiolar artery and suggest that they are involved in the regulation of cochlear blood flow.
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PMID:Neural basis for regulation of cochlear blood flow: peptidergic and adrenergic innervation of the spiral modiolar artery of the guinea pig. 169 Jan 96

The present study tested whether release of dopamine from isolated bovine adrenal medullary cells in culture could be stimulated or inhibited by secretagogues and modulators known to affect noradrenaline and adrenaline release from adrenal medullary chromaffin cells. K+ depolarization or activation of voltage-sensitive Na+ channels by veratridine both stimulated dopamine release. Ca2+-dependent dopamine release was also stimulated by the mixed nicotinic-muscarinic agonist, carbachol. Carbachol-induced dopamine release was inhibited by a nicotinic but not by a muscarinic antagonist and dopamine release was also stimulated by a selective nicotinic agonist, 1,1-dimethyl-4-phenyl-piperazinium. Carbachol-induced dopamine release was inhibited by substance P and by neuropeptide Y. Histamine also stimulated dopamine release, while angiotensin II and glutamate produced no significant stimulation of dopamine release. Noradrenaline and adrenaline were released in response to the above agents with a profile almost identical to that of dopamine. The results indicate that dopamine can be directly released from adrenal medullary cells in response to stimulation of those cells and suggest that the dopamine release originates from chromaffin cells similar or identical to those storing noradrenaline and adrenaline. A possible role for dopamine, released from adrenal chromaffin cells, in modulating catecholamine release from the chromaffin cells and/or contributing to circulating plasma dopamine is discussed.
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PMID:Dopamine release from bovine adrenal medullary cells in culture. 169 90

The possible influence of spinal receptors coupled to Gi/Go regulatory proteins on chronic pain adaptive processes of neural tissues was investigated in normal and arthritic rats. Pain-suffering animals showed an enhanced immunoreactivity to substance P (ir-SP) in the lumbar spinal cord, pons-medulla oblongata region and thalamus. Norepinephrine (NE) levels were increased in the spinal cord, while serotonin (5-HT) was elevated in both spinal cord and midbrain. The intrathecal injection of 1 micrograms pertussis toxin 6 days before sacrifice of rats produced in these arthritic animals a pronounced reduction of ir-SP in the pons-medulla, midbrain and thalamus, but not in the spinal cord. The level of 5-HT was diminished in dorsal spinal cord and midbrain, whereas NE appeared unchanged. In contrast, the toxin only reduced ir-SP of normal rats in the midbrain, without altering the levels of NE or 5-HT, in all the areas analysed. These results suggest the involvement of certain spinal receptors coupled to Gi/Go transducer proteins in processes leading to the elevation of ir-SP and 5-HT in various neural structures of arthritic rats.
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PMID:Effect of intrathecal injection of pertussis toxin on substance P, norepinephrine and serotonin contents in various neural structures of arthritic rats. 170 96

The site of action of cholinergic, adrenergic, peptidergic and opioid agents was studied in myenteric plexus-longitudinal muscle strips from the guinea pig ileum. A preparation in a special triple bath was drawn through two rubber membranes, dividing the strip into three segments. Neurogenic stimulation of the oral segment, set up nerve action potentials also in the neurones projecting axons up to the aboral segment. These axons, turning into varicose nerve terminals, conducted action potentials aborally across the middle segment, that was up to 10 mm wide. Finally, the nerve terminals, extending into the aboral segment, might be also invaded triggering twitches. Agents were added, either to the oral segment, to affect the genesis and spread of action potentials in the proximal parts of cholinergic neurones (cell bodies, axon hillocks, initial segments and axon preterminals) or they were added to the middle segment to affect propagation of action potentials in varicose nerve terminals. As a result, the amplitude of aboral twitches reflected their effects at each site, quantitatively. Noradrenaline and ethylketocyclazocine were more effective at the site of varicose nerve terminals, whereas substance P, acetylcholine and oxotremorine were more effective at the proximal parts; pilocarpine and nicotine were effective at both sites. Changes in membrane polarization might be the final common effect in the mechanism of action of all the stimulatory agents used.
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PMID:An attempt to localize the site of action of different agents within cholinergic motor neurones of the myenteric plexus-longitudinal muscle preparation of the guinea pig ileum by the triple bath method. 171 55

Blood flow in the tracheobronchial airways is regulated by three main nervous pathways: 1) sympathetic motor nerves (adrenergic and nonadrenergic); 2) parasympathetic motor nerves (cholinergic and noncholinergic); and 3) afferent or sensory nerves (peptidergic). Noradrenaline is the main adrenergic mediator which produces short-lasting constrictions in both tracheal and bronchial vascular beds and in both arteries and veins. These responses are mediated via alpha-adrenoceptors. The nonadrenergic mediator neuropeptide Y is a vasoconstrictor which produces long-lasting responses with larger doses. Acetylcholine is the principal mediator of the cholinergic nerves and causes short-lasting dilations at all levels of the tracheobronchial circulation (arteries, veins and bronchopulmonary anastomoses). These responses are mediated via muscarinic receptors. Vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (in man peptide histidine methionine) are the main mediators of the noncholinergic nerves. Both of them produce vasodilation in the tracheobronchial circulation; VIP can cause longer-lasting responses with larger doses. The afferent or sensory nerves contain tachykinins, i.e. substance P and neurokinins A and B, which are potent vasodilators in the tracheobronchial circulation and also potent inducers of postcapillary permeability. Calcitonin gene-related peptide is another sensory neuropeptide with ability to produce long-lasting vasodilations without affecting microvascular permeability.
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PMID:Effects of neurotransmitters on tracheobronchial blood flow. 198 76

The levels of noradrenaline, neuropeptide Y, 5-hydroxytryptamine, and substance P were measured and compared between the large arteries of the circle of Willis and the small cerebral vessels of the pia mater in the rat, rabbit, cat, and monkey. In all species, noradrenaline and neuropeptide Y concentrations were greater in the larger arteries than in small pial vessels. Noradrenaline concentrations were dramatically reduced following cervical sympathectomy, with the extent of diminution differing greatly in the various species; the effects of cervical ganglionectomy on neuropeptide Y concentrations were less pronounced. 5-Hydroxytryptamine concentrations in rats, cats, and rabbits were significantly greater in the small pial vessels, although measurable concentrations existed in the circle of Willis. In cats and monkeys, substance P was found in major arteries, but was not detectable at the level of the small pial vessels. The differences in the regional distribution of the various neurotransmitter candidates in the cerebrovascular bed may reflect their physiological significance.
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PMID:Concentrations of putative neurovascular transmitters in major cerebral arteries and small pial vessels of various species. 244 Sep 1


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