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 Substance P infused intracerebrally via chronically implanted electrode-cannulae on self-stimulation induced from the same site was studied in rats. Substance P caused a significant depression of self-stimulation at 60 and 120 microgram/rat. Morphine infused into this site also caused significant depression of self-stimulation, but the doses were considerably lower than those of Substance P (5 and 10 microgram/rat). Pretreatment with naloxone, a narcotic antagonist, significantly antagonized the effects of Substance P on self-stimulation. It is proposed that Substance P modulates self-stimulation by the release of an endogenous morphine-like substance, but the possibility of a direct effect of Substance P was not ruled out.
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PMID:Effect of substance P on medial forebrain bundle self-stimulation in rats following intracerebral administration. 59 92

Using the method of Chang and Leeman for isolation the sialogogic undecapeptide from bovine hypothalamus partly purified Substance P was obtained. The final steps of purification were omitted to prevent losing of other peptides possessing biological activity of Substance P. The qualitative and quantitative content of amino acids in the hypothalamic extract was determined and fourteen amino acids were found. Four of them were not present in the sialogogic undecapeptide or neurotensin. It can be concluded that in the hypothalamic tissue apart from sialogogic undecapeptide and neurotensin, there are other peptides related to these two.
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PMID:Substance P isolated from bovine hypothalamus: amino acid composition. 59 88

1. Rat brain synaptosomes were incubated under different conditions to study the release of substance P (SP). 2. Potassium ions and electrical field stimulation induced a loss of SP from synaptosomes. The release of SP by potassium in high concentrations (23.8 mM) was shown to be calcium dependent. 3. Substance P was retained in synaptosomes during incubation in 0.32 M sucrose at +4 degrees C up to 120 min. During incubation at 30 degrees C the SP content fell initially (30 min) but was gradually restored (120 min). 4. If these pre-incubated synaptosomes were reincubated for 45 min at 30 degrees C in potassium free Krebs-Ringer-phosphate buffer a further rise in their SP content occurred which was taken as indication that SP is being synthesized in synaptosomes. 5. The newly synthesized SP is presumably stored by binding to phosphatidyl serine until a sudden release is initiated by depolarization.
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PMID:Substance P in rat brain synaptosomes. 60 Mar 16

It has been reported that Xenopsin, Neurotensin and Substance P change plasma glucagon and insulin levels when they are administered in vivo. In order to clarify whether these agents have a direct effect on glucagon and insulin secretion from the pancreas, the action of each substance was examined by using the rat pancreas perfusion technique. The results were as follows: The perfusion with 1 and 5 nmole/min of Xenopsin for ten minutes resulted in a significant but transient release within two minutes. Neurotensin did not show any stimulatory effect on glucagon release in the concentration of 1 or 5 nmole/min for ten minutes. However, Substance P lowered significantly the glucagon concentration in the perfusate in a similar concentration. None of these substances influenced significantly insulin release from the perfused pancreas. These findings suggest that the hyperglucagonemia caused by these three agents in vivo may not be attributed to the direct effect on the pancreatic A-cell.
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PMID:[Glucagon-releasing activity of xenopsin, neurotensin and substance P in the perfused rat pancreas (author's transl)]. 63 79

Nine anesthetized dogs were provided with acute common duct fistulas after exclusion of the gallbladder. Synthetic Substance P was administered as caval infusions in a dosage of 0.5-20 ng x kg-1 x min-1, duration 10 min. The output of hepatic bile, sodium and amylase decreased during infusion by 40-52 per cent at the highest doses. After termination of infusion all 3 parameters increased by 19-60 per cent above the basal level. The biliary concentration of sodium was constant, while that of amylase increased during infusion. The responses were dose-related. The anticholeresis induced by substance P might be due to inhibition of the canalicular bile fraction, which presumably is mediated by active sodium transport and independent of bile salt excretion.
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PMID:Anticholeretic effect of substance P in anesthetized dogs. 64 72

The activity and distribution of substance P-catabolizing enzyme(s) were studied in the rat kidney. Kidney homogenates inactive substance P 5-20 times as fast as do homogenates of intestine, liver, lung, heart or brain. The catabolizing activity was highest in the cortex and decreased progressively down the papilla. Cortex of rat kidney was homogenized and fractions enriched in microsomal membrane, final supernatant, plasma membrane, endoplasmic reticulum, brush border and intact glomeruli were prepared. The identity and homogeneity of the preparations were determined by assaying marker enzymes and by morphological examination. Substance P was catabolized most rapidly by the microsomal and plasma-membrane-enriched fractions, and least rapidly by endoplasmic reticulum or final supernatant fractions. Purified brush border of proximal tubules inactivated substance P more than 10 times as fast as isolated glomeruli. Our experiments show that substance P is catabolized at a rate that is similar to the rates of inactivation of bradykinin and angiotensin II. Further, the distribution of substance P-catabolizing activity in various kidney fractions is similar to the distribution of kininase and angiotensinase activities previously reported.
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PMID:Renal inactivation of substance P in the rat. 64 14

Substance P (a peptide of eleven amino acids) caused a Ca-dependent release of K+ from rat parotid slices. The response to substance P differed from the alpha-adrenergic and the cholinergic responses in that it was transient, of smaller extent, and was not inhibited by phentolamine and atropine. Substance P caused little, if any, amylase secretion. Successive additions of the peptide to the slice system maintained the effect of C+ release indicating that the transient response to a single addition of the peptide was due to inactivation of substance P and not due to a decline in the response of the tissue.
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PMID:A transient release of potassium mediated by the action of substance P on rat parotid slices. 67 31

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 effect of Substance P (SP) on the intestine in situ of the dog was investigated. Five female dogs were used. At the same time, mechanographic recordings, using balloon kymography, were taken, while the myoelectric activity was recorded by means of electrography. Differences in SP action on the mechanogram and electromyogram of the stomach and the small intestines were reflected in the following phenomena: (a) SP in the doses used was less active on the ileum than on the stomach; (b) SP increased basal tonus but inhibited peristaltic contraction; (c) SP acted predominantly on spike discharges in the electromyogram. These results are likely to support the assumption that SP acts as a physiological modulator of smooth muscle activity.
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PMID:Effect of substance P on mechanical and myoelectrical activities of stomach and small intestines in conscious dog. 68 15

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


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