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)

1. Dispersed rat parotid acinar cells were used to study the effects of secretagogues on 22Na uptake. 2. Carbachol stimulated 22Na uptake, and caused a net gain in total Na and a loss in total K. These effects were accentuated in the presence of 10(-3) M-ouabain. 3. Substance P, epinephrine and phenylephrine also stimulated 22Na uptake while isoproterenol and angiotensin II did not. 4. The 22Na uptake due to carbachol was inhibited by atropine, procaine or CoCl2; the response to Substance P was inhibited by CoCl2 only. 5. Extracellular Ca was required for stimulation of 22Na uptake by carbachol. Strontium but not Ba could substitute for Ca in supporting 22Na uptake. 6. Uptake of 22Na was stimulated by the divalent cationophore, A-23187, and Ca was required for this effect. 7. It is concluded that activation of Ca influx by muscarinic, alpha-adrenergic or peptide agonists triggers, among other effects, an increased membrane permeability to Na.
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PMID:Calcium and receptor regulation of radiosodium uptake by dispersed rat parotid acinar cells. 9 91

Carbachol and substance P stimulated 45Ca2+ flux changes, 86Rb+ efflux, and amylase secretion from acinar cells isolated from rat parotid. The local anesthetic tetracaine blocked all of these measured responses to carbachol, but none of the responses to substance P. Tetracaine must act at either the cholinergic receptor or at a subsequent transducing step in the cholinergic stimulus-response sequence. If tetracaine acts at one of the transducing steps between cholinergic receptor occupation and the physiological responses then the action of tetracaine must be at a locus in the cholinergic reaction scheme not shared by substance P, because tetracaine did not block any response of the parotid to substance P.
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PMID:Tetracaine blocks the responses of isolated acinar cells from rat parotid to carbachol but not to substance P. 9 97

1. Carbachol, phenylephrine and substance P were each capable of producing a transient release of K (86 Rb) from rat parotid slices in the absence of extracellular Ca. 2. Each of the agonists was also capable of producing "cross-receptor inactivation"; that is, if a transient response was elicited by any one of the agonists then no transient response could be obtained by either of the other two. 3. Removal of carbachol from muscarinic receptors with atropine did not reverse the cross-receptor inactivation of the substance P response unless Ca was added with substance P or unless Ca was present when atropine was added. 4. It is concluded that the K release response in the parotid gland is mediated by receptor-controlled Ca influx sites. These influx sites also bind Ca at a location inaccessible to EGTA and release the bound Ca upon receptor activation. 5. It is also conlcuded that all three receptors (muscarinic, alpha-adrenergic, and peptide) appear to regulate the same Ca influx sites.
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PMID:Muscarinic, alpha-adrenergic and peptide receptors regulate the same calcium influx sites in the parotid gland. 19 43

1. A study was made of the role of Ca release in mediating the sustained phase of K release (86 Rb release) in the rat parotid gland due to receptor activation. 2. Sr could substitute for Ca in supporting the sustained phase of the 86Rb release due to carbachol. Sr was less effective than Ca, while Ba was ineffective. 3. Sr could also restore responsiveness of the transient phase to agonists in media lacking Ca. Again, Sr was less effective than Ca, and Ba was without effect. 4. Carbachol stimulated release of 45Ca from parotid gland slices. The amount of Ca released (about 0.2 micromole/g) was much greater than the estimated Ca influx for the same period. 5. Release of 45Ca by carbachol prevented release due to a subsequent exposure to substance P. 6. Release of 45Ca due to substance P was significantly increased if muscarinic receptors were activated during tissue labelling. 7. These results support an earlier hypothesis whereby different agonists (such as carbachol and substance P) stimulate the release of Ca from a common pool and the release of this Ca mediates the transient phase of the K release response.
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PMID:Relationship between calcium release and potassium release in rat parotid gland. 48 Feb 37

1. The effect on water intake of intracranial injections of Substance P was studied in the rat. 2. Substance P strongly inhibited drinking elicited by Angiotensin II, Carbachol water deprivation or sodium chloride load, in that order. 3. The peptide was particularly effective when water intake was induced by injections of Angiotensin II into the preoptic area. In these experiments, drinking was inhibited by doses of Substance P as low as 1 ng. 4. The results suggest that in the rat Substance P may play a role in the brain in the regulation of water intake, acting as a thirst inhibitor.
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PMID:Antidipsogenic effect of intracranial injections of substance P in rats. 67 47

The effects of cholinergic stimulation on K efflux from rat sublingual gland slices was investigated. The sublingual gland slices appeared stable on incubation as indicated by electrolyte content and ultrastructural analysis. Carbachol induced a biphasic increase in release of 86Rb (an index of K efflux); a transient phase lasting 2--4 min was followed by a sustained (or slowly falling) phase. Both phases of the response were blocked by atropine, but only the sustained phase was blocked by omission of Ca or by the addition of LaCl3. The divalent cationophore A-23187 produced a Ca-dependent release of 86Rb. Substance P stimulated a biphasic release of 86Rb, similar to that obtained with carbachol, but epinephrine did not. The response to substance P demonstrated a Ca dependence similar to that of carbachol. When a transient response to carbachol was elicited, no transient response to carbachol was elicited, no transient response to substance P could be obtained. This suggests that the receptors for these agonists may reside in the same cells. Also, the magnitude of the responses suggests that most of the affected cells are probably the mucous elements of the sublingual gland.
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PMID:Calcium and the control of potassium efflux in the sublingual gland. 69 15

Spontaneous oscillations in intracellular Ca2+ concentration ([Ca2+]i) and membrane potential were used to monitor rhythmicity in freshly dispersed and cultured interstitial cells (IC) from the canine colon. The frequency of oscillations and responses to a number of channel blockers, agonists, ionic substitutions, and temperature were similar in freshly dispersed and cultured cells. An increase in the amplitude of Ca2+ oscillations after 3-6 days in culture and an increase in the rate of decline of [Ca2+]i in cultured IC were two differences noted between freshly dispersed and cultured cells. The frequency and amplitude of oscillations were a function of extracellular Ca2+ concentrations, and oscillations were abolished when the transmembrane flux of Ca2+ was reduced by nicardipine, La3+, or removal of Ca2+ from the extracellular medium. Oscillations persisted in the presence of ryanodine and ouabain. Lowered temperatures or a reduction in the concentration of Ca2+ in the medium reduced the frequency of spontaneous oscillations. Carbachol and substance P caused a transient increase in [Ca2+]i. Substance P then abolished spontaneous events. ATP and calcitonin gene-related peptide increased the frequency of spontaneous activity. Vasoactive intestinal peptide caused a temporary delay in spontaneous oscillations when added to the medium. Results indicate that freshly dispersed and cultured IC may be useful in studies of the mechanisms of rhythmicity in the gastrointestinal system.
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PMID:Calcium oscillations in freshly dispersed and cultured interstitial cells from canine colon. 155 Feb 5

First incubating guinea pig pancreatic acini with carbachol reduced the subsequent stimulation of amylase release caused by carbachol, cholecystokinin octapeptide (CCK-8), and bombesin but not that caused by vasoactive intestinal peptide, substance P, 8-bromoadenosine 3',5'-cyclic monophosphate, A23187, or 12-O-tetradecanoylphorbol-13-acetate. Carbachol also reduced the subsequent binding of N-[3H]methylscopolamine, 125I-CCK-8, and 125I-[Tyr4]bombesin. Pancreatic acini possess a high-affinity class of cholinergic receptors and a low-affinity cholinergic receptors appears to produce the reduction in carbachol-stimulated amylase release and binding of N-[3H]methylscopolamine. First incubating acini with carbachol caused a complete loss of high-affinity cholinergic receptors with no change in the number or affinity of low-affinity cholinergic receptors. Carbachol occupation of low-affinity cholinergic receptors appears to produce the reduction in CCK-8- and bombesin-stimulated amylase release and in binding of 125I-CCK-8 and 125I-[Tyr4]bombesin. Acini possess two classes of CCK receptors. One class has a high affinity for CCK-8; the other class has a low affinity for CCK-8. First incubating acini with carbachol caused a 60% decrease in the number of high-affinity CCK receptors with no change in the number of low-affinity receptors or the affinities of either class of receptors for CCK-8. Acini possess a single class of bombesin receptors, and first incubating acini with carbachol caused a 40% decrease in the number of bombesin receptors with no change in their affinity for bombesin. 12-O-tetradecanoyl phorbol-13-acetate reproduced the action of carbachol on binding of N-[3H]methylscopolamine and 125I-CCK-8 but not on binding of 125I-[Tyr4]bombesin, suggesting that carbachol activation of protein kinase C may in some way mediate the effect of carbachol on receptors for carbachol and those for CCK but not that on receptors for bombesin.
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PMID:Carbachol desensitizes pancreatic enzyme secretion by downregulation of receptors. 168 17

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

Carbachol (CCH), serotonin (5HT), divalent ionophore A23187, cAMP, and certain neuropeptides, i.e. substance P (SP), inhibit the initial rate of uptake (influx) of 22Na into isolated chicken villus enterocytes. All these agents also increase cytosolic Ca. However, the increases stimulated by CCH, 5HT, and cAMP are not blocked by chelation of extracellular Ca, whereas those of A23187 and SP are. Only CCH and 5HT stimulate hydrolysis of membrane phosphoinositides to form inositol phosphates. CCH and 5HT also stimulate incorporation of [32P]-PO4 into membrane polyphosphoinositides. These studies suggest that at least three mechanisms exist to increase cytosolic Ca in chicken enterocytes and thereby inhibit Na influx. Certain neurohumoral agents such as SP open a plasma membrane permeability for Ca, permitting extracellular Ca to enter the cell down its electrochemical gradient. These agents do not stimulate phosphatidylinositol breakdown. CCH and 5HT stimulate phosphatidylinositol breakdown and via the formation of inositol trisphosphate release Ca from intracellular stores. A third mechanism exists for cAMP which mobilizes Ca from intracellular stores, but does not involve the metabolism of membrane phosphatidylinositols.
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PMID:Calcium mediated neurohumoral inhibition of chicken enterocyte Na influx: role of phosphatidylinositol metabolites. 169 50


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