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. In healthy volunteers plasma concentrations of immunoreactive substance P were measured in response to changes in posture and dietary salt intake. 2. In 14 subjects plasma immunoreactive substance P was 168 +/- 31 pmol/l when subjects were supine and 401 +/- 51 pmol/l (P less than 0.001) when they were ambulant. 3. Measurement of supine plasma immunoreactive substance P at 6 h intervals gave a mean value of 240 +/- 39 pmol/l at 14.00 hours and a lowest value of 76 +/- 9 pmol/l at 02.00 hours. 4. In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 +/0 41 pmol/l, on a sodium intake ad lib., to 244 +/- 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 +/- 20 pmol/l (P less than 0.001) by day 4 of high sodium intake (350 mmol/day). 5. Although exogenous substance P was shown to be natriuretic in dog and rat, the present results do not favour a role of endogenous substance P as a circulating natriuretic factor in man.
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PMID:Immunoreactive substance P in human plasma: response to changes in posture and sodium balance. 616

The neuropeptide substance P forms polymeric fibrils similar to those previously reported for the hormone, insulin. Structural and chemical aspects of these two fibrillary forms have been compared and their possible existence in vivo considered. Numerous substance P fibrils are readily formed in vitro in mM solutions under conditions which are physiological with respect to salt concentration, pH and temperature, whereas more severe conditions (heat and acid) are apparently required for the rapid formation of numerous insulin fibrils. Morphologically, both fibrils appear to be relatively long and unbranched and the neuropeptide fibrils are similar in size to such naturally occurring structures as neurofilaments. Disaggregation of the neuropeptide fibril follows dilution (1000-fold) whilst more stringent (alkaline) treatment is apparently necessary for insulin fibril dissociation. These observations are discussed in relation to the role of an insulin-like peptide in the formation of certain types of amyloid and the possibility that fibrillary of similar polymeric forms of substance P may exist in normal tissue.
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PMID:Properties and possible significance of substance P and insulin fibrils. 617 29

Some factors influencing the oxidative activity of upper horizons of spruce forest soils (a mixture of fermentative and humus layers) toward intermediates of the oxidative part of the sulphur cycle were investigated. Preincubation of the soil with added cysteine, sulphide, elemental sulphur or thiosulphate was found to stimulate enzyme systems oxidating any of these compounds. Sulphite and sulphate were ineffective in this respect. The oxidation of elemental sulphur was stimulated by CaCO3, technical urea and high doses of superphosphate and potassium sulphate. It was inhibited by KH2PO4, pure urea, 40 % potassium salt, ammonium nitrate with calcium carbonate and the fertilizer NPK I. It proceeded at the highest rate at approximately 60 % capillary capacity (61 % of mass water content). Oxidation of thiosulphate was stimulated by KH2PO4, pure urea, superphosphate, potassium sulphate and only slightly by the fertilizer NPK I. It was inhibited by CaCO3, 40 % potassium salt and only slightly by ammonium nitrate with calcium carbonate. Potassium chloride, glucose and technical urea were without effect. The oxidation proceeded at the highest rate at 35 % maximal capillary capacity (48 % mass water content).
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PMID:Some factors influencing production of sulphate by oxidation of elemental sulphur and thiosulphate in upper horizons of spruce forest soils. 626 35

Rats were fed, from weaning through 11 weeks of age, dried leaf tissue of corn plants grown on soil amended with regular NPK fertilizer (150-22-62), with 33.6 ad 67.2 metric ton/ha of sewage sludge or with salts of cadmium (10kg/ha), lead (25kg/ha), and/or zinc (50kg/ha). A very high proportion of the cadmium (cd) consumed was eliminated in feces. Only in rats fed diets containing leaf tissue from plants grown on soil to which CdCl2 salt or the high level of sludge had been added did the metal accumulate in significantly greater quantity than in rats fed a standard diet without leaf tissue. Most of the carcass accumulation of Cd could be accounted for by that in the liver and kidneys. The proportion of dietary zinc (Zn) that was excreted in feces was less than that for Cd, indicating that more Zn was absorbed into the body. There was no correlation between intake and accumulation of Zn in the tissues, however, so that much of the absorbed Zn must have been eliminated in some way. Fecal elimination did not serve as a way to rid the body of excessive intake of lead (Pb). However, with intakes ranging from 2 to 11 mg total in this study, the carcass load did not exceed 1.1 mg of Pb. Thus absorbed Pb, like Zn, must also be eliminated efficiently. No gross signs of toxicity or of physiological impairment were observed in rats fed any of the plant tissue samples.
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PMID:Cadmium, lead and zinc in growing rats fed corn leaf tissue grown on soil amended with sewage sludge or heavy metal salts. 733 54

The neurotransmitter substance P acts also as a potent vasodilator. Its participation in the pathogenesis of deoxycorticosterone acetate (DOCA)-salt hypertension was evaluated by an acute infusion of a newly synthesized, potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt rats but only small, transient, and nonsignificant rises in blood pressure of sham-treated control rats. The rise in blood pressure was not accompanied by changes in heart rate. Maximal blood pressure increase in DOCA-salt rats was 31.7 +/- 14.8 mm Hg. In a second series of experiments, the hemodynamic effects of this antagonist were evaluated under anesthesia in both DOCA-salt and sham-treated control rats by the thermodilution method. During CP 96,345 infusion, sustained increases in cardiac index and stroke volume and decreases in total peripheral resistance were observed in both DOCA-salt and control rats. In DOCA-salt rats, cardiac index rose by 79.4%, while total peripheral resistance fell by 27.9% of the baseline values. In control rats, the changes were smaller (+27.2% and -22.5%, respectively). Stroke volume changed in parallel to cardiac output in both groups. The data suggest that acute blockade of NK-1 receptors increases blood pressure in DOCA-salt rats mainly by an increase in cardiac output. We conclude that endogenous substance P tends to counteract the DOCA-salt-induced elevation of blood pressure by modulating both cardiac output and peripheral resistance.
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PMID:Cardiovascular effects of a specific nonpeptide antagonist of substance P (NK-1) receptor in DOCA-salt hypertension. 749 93

[3H]Senktide, a highly selective tachykinin NK3 receptor agonist, was used to study tachykinin NK3 receptors of rat and guinea pig brain. Guinea pig brain membranes had a Kd of 3.9 +/- 0.5 nM and a Bmax of 42 fmol/mg. Dose-displacement experiments with neurokinins and selective tachykinin receptor agonists revealed the following order of potency: [MePhe7]neurokinin B > neurokinin B > substance P > neurokinin A. This order is typical for a tachykinin NK3 receptor. To further characterize the specificity of this receptor, the effects of unrelated compounds such as: bradykinin, angiotensin II, bombesin and their structural analogs were also evaluated on the binding of [3H]senktide. Unexpectedly, the angiotensin AT1 receptor antagonists, DuP 753 (2-n-butyl-4-chloro-5-hydroxymethyl-1-[2'-(1H-tetrazol-5-yl)bip hen yl-4-yl)methyl]imidazole potassium salt), L-158,809 (5,7-dimethyl-2-ethyl-3-[(2'-(1H-tetrazol-5-yl) [1,1'-biphenyl]-4-yl) methyl]-3H-imidazo[4,5-beta]pyridine H2O) and EXP 3174 (2-n-butyl-4-chloro-1-[2'-(1H-tetrazol-5-yl)biphenyl-4-yl)methyl]i midazole- 5-carboxylic acid), inhibited the binding of [3H]senktide to its receptor in the guinea pig brain membranes with IC50 values of 18 microM, 25 microM and 50 microM, respectively. Similar effects were also observed with rat brain membranes. Angiotensin II, saralasin ([Sar1,Val5,Ala8]angiotensin II, a peptide angiotensin AT1 receptor antagonist) and PD 123,319 (1-[4-(dimethylamino)3-methylphenyl]methyl-5-(diphenylacetyl)-4,5, 6,7- tetrahydro-1H-imidazo[4,5-c]pyridine-6-carboxylic acid, a known non-peptide angiotensin AT2 receptor antagonist) did not inhibit the binding of [3H]senktide to either type of membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-peptide angiotensin receptor antagonists bind to tachykinin NK3 receptors of rat and guinea pig brain. 751 91

Many neurons within the ventrolateral hypothalamus in guinea pigs contain estrogen-induced progestin receptors as well as substance P. Retrograde tracing combined with immunocytochemistry was used to determine the specific projections of this subset of steroid-sensitive cells. Unilateral Fluoro-Gold injections into the dorsal midbrain, including the central gray, labeled a large proportion of the ventrolateral hypothalamic neurons immunoreactive for both progestin receptors and substance P (approximately 30%); substantially fewer of these neurons were labeled by unilateral Fluoro-Gold injections into the preoptic area (approximately 6%), medial amygdala (approximately 10%), or the bed nucleus of the stria terminalis (approximately 11%). The projections of progestin receptor-immunoreactive neurons in the ventrolateral hypothalamus were similar to those of progestin receptor/substance P double-labeled neurons, while a slightly lower percentage of the ventrolateral hypothalamic, substance P-immunoreactive neurons tended to project to each of these areas. These pathways may prove to be components of the neural circuitry underlying a variety of functions influenced by gonadal steroid hormones and substance P, such as female sexual behavior, salt intake, nociception and aggression.
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PMID:Projections from ventrolateral hypothalamic neurons containing progestin receptor- and substance P-immunoreactivity to specific forebrain and midbrain areas in female guinea pigs. 751 13

The effect of gold salt therapy on substance P immunoreactivity levels in plasma and synovial fluid was studied in 42 patients with rheumatoid arthritis. Decreased levels of synovial fluid substance P, although not statistically significant, were found in rheumatoid patients who were currently receiving gold therapy when compared to either those patients previously treated or to those who never received this therapy. In addition, we found that patients who received more than 1000 mg of gold salts had significantly lower levels of substance P in synovial fluid than those treated with lower doses. Our results, therefore, seem to support the hypothesis that gold salts appear to be slow-acting neurotoxic drugs that significantly decrease the intrasynovial concentrations of substance P, a well-known inflammatory neuropeptide, in arthritis patients.
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PMID:The effect of gold salts on substance P levels in rheumatoid arthritis. 752 89

The present study investigated the effect of 24-h continuous ICV infusion of four different tachykinins on the enhanced need-free sodium intake induced by previous repeated sodium depletions in female rats. Female rats were employed because, in response to sodium depletions, they develop a higher need-free sodium intake than male rats. The following tachykinins were used: eledoisin, substance P (SP), [Sar9,Met(O2)11]SP and [Asp5,6,MePhe8]SP(5-11), also referred to as NH2-senktide, all at the same doses of 300 or 600 ng/h x 24 h. Food pellets, water, and 3% NaCl sodium solution were freely available. Eledoisin and NH2-senktide were more potent than SP in reducing the need-free sodium intake. On the other hand, [Sar9,Met(O2)11]SP had no effect. None of the tachykinins employed completely blocked the intake. Water intake was reduced, but this reduction was apparently a consequence of reduced intake of hypertonic sodium chloride solution, because at the same doses TKs did not inhibit water intake in a single-bottle test. Food intake remained unchanged at either dose used. These findings confirm previous studies in which pulse injection of the same drugs potently inhibited sodium intake. They also demonstrate that tachykinins endowed with high affinity for the NK3 receptor are the most potent in inhibiting sodium intake. Furthermore, these findings indicate that the tachykinins reduce the need-free sodium intake only during the infusion period, indicating that in these conditions they do not evoke either aversion for salt, or toxic consequences in the follow-up period.
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PMID:Effect of tachykinins on the need-free sodium intake of female rats: a continuous intracerebroventricular infusion study. 752 26

Afferent renal nerves (ARN) have been implicated in the development of one-kidney renal wrap (1K-WRAP) hypertension. The role of renal nerves in desoxycorticosterone acetate-salt (DOCA) hypertension, a low-renin model of hypertension, is controversial. The present study was designed to determine if spinal substance P (SP) and/or calcitonin gene-related peptide (CGRP) in ARN affects the development of 1K-WRAP or DOCA hypertension in adult rats. Selective long-term partial depletion of spinal SP and CGRP within small primary afferent nerve fibers including unmyelinated ARN was achieved by intrathecal administration of capsaicin. After capsaicin treatment, 1K-WRAP hypertension was induced by removing the right kidney and wrapping the left kidney with a figure-8 ligature. In a second group of rats, DOCA hypertension was induced by subcutaneous application of desoxycorticosterone pellets after unilateral nephrectomy. Systolic arterial pressure was monitored for 8 weeks by tail cuff plethysmography after which direct blood pressure measurement was performed followed by immunohistochemistry. Intrathecal capsaicin administration had no significant effect on SP-ir and CGRP-ir of ARN soma located within thoracic dorsal root ganglia whereas immunoreactivity against these peptides was reduced by one third to one half in the dorsal horn, indicating effective long-term spinal depletion of these neuropeptides. Intrathecal capsaicin enhanced the development of 1K-WRAP hypertension, since arterial pressure was greater in the treated group. In contrast, DOCA hypertension was unaffected by capsaicin pretreatment. Considering the neurotoxic action of capsaicin for SP-ir and CGRP-ir unmyelinated primary afferent neurons, we hypothesize that spinal SP, CGRP and/or related peptides existing in ARN and other capsaicin-sensitive unmyelinated primary afferent neurons in the lower thoracic spinal cord may ameliorate 1K-WRAP hypertension, but not DOCA hypertension.
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PMID:Intrathecal capsaicin enhances one-kidney renal wrap hypertension in the rat. 753 2


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