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)

Substance P stimulation of salivation in rats has been studied as has its in vitro enhancement of amylase release by isolated parotid cells. The extent of the stimulation on amylase release by isolated parotid cells was dependent upon the concentration of substance P, with the minimum effective concentration being 1 nM. The substance P effect was detectable within 1 min after incubation and lasted for at least 50 min. Substance P stimulation was demonstrable at 25--37 degrees C but not at 0 degrees C. Adrenocorticotropic hormone (ACTH), thyrotropin-releasing hormone (TRH), vasopressin and neurotensin had no effect on amylase release. These results suggest that substance P may act directly on the parotid cells. Examination of the salivary-stimulating activity of fragments of substance P showed that the C-terminal octapeptide and (pyroglutamyl)hexapeptide were active, although less potent than substance P, whereas its free acid, C-terminal tetra- and tri-peptides were inactive. Vasopressin, angiotensin II and neurotensin could inhibit substance P induced salivation, whereas TRH, ACTH and somatostatin had no effect. Amylase activity per unit volume of saliva was not changed by the injection of vasopressin, angiotensin II or neurotensin. These vasoactive peptides did not affect substance P stimulation of amylase release by isolated parotid cells. The results indicate that vasopressin, angiotensin II and neurotensin inhibit the action of substance P on salivation at sites other than the parotid cells.
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PMID:Substance P stimulation of amylase release by isolated parotid cells and inhibition of substance P induction of salivation by vasoactive peptides. 22 41

Changes in the intracellular free calcium ([Ca2+]i) of cultured normal human epidermal keratinocytes (NHEK) were investigated in order to determine whether the adenylate cyclase cAMP (AC) system and phospholipase C activating system are involved in increasing [Ca2+]i. NHEK were obtained from neonatal foreskin and grown in serum-free medium (K-GM) supplemented with 2% bovine pituitary extract. [Ca2+]i was measured by fluorescence ratio imaging microscopy using Fura-2 as the indicator. In the case of the AC system, transient increases in [Ca2+]i were observed in response to stimulation with epinephrine, norepinephrine, isoproterenol and salbutamol. Methoxamine, clonidine and dobutamine did not induce any [Ca2+]i increase. The [Ca2+]i increase evoked by epinephrine was inhibited by pretreatment with propranolol, but not by prazosin or yohimbine, indicating that epinephrine-induced [Ca2+]i elevation via beta 2-adrenergic stimulation. Similar changes were observed when NHEK were stimulated with histamine, adenosine, GTP gamma S, forskolin and dibutyryl cAMP respectively. The absence of extracellular Ca2+ had no effect on the epinephrine-induced [Ca2+]i increase. It appears that activated protein kinase A, based on cAMP accumulation via stimulatory GTP binding protein, elicited the release of Ca2+ from intracellular stores. On the other hand, when drugs known to activate phospholipase C in a wide variety of cell types were tested, a transient increase in [Ca2+]i was demonstrated in response to the addition of thrombin, bradykinin and substance P. This reaction was not affected by the presence of EGTA, suggesting that these drugs raise [Ca2+]i via phosphatidylinositol breakdown. Vasopressin, angiotensin II, serotonin and acetylcholine did not induce any increase in [Ca2+]i. On the basis of these studies, it was concluded that NHEK possess the mechanism which increase [Ca2+]i via AC system and phospholipase C activating system. It seems probable that this rise in [Ca2+]i initiates a calcium-dependent cellular response, such as activation of calcium/calmodulin dependent kinase, and subsequently regulates the proliferation and differentiation of human epidermal keratinocytes.
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PMID:[Changes in the intracellular free calcium of cultured human epidermal keratinocytes]. 171 97

Somatostatin and substance P (10(-6)-3 X 10(-5) M) inhibited dose-dependently the specific binding of [3H] [D-Ala2, Met5]enkephalinamide [( 3H]-DALAMID) to rat brain membranes, by decreasing the number of binding sites. [Lys]-Vasopressin also inhibited the binding, by affecting both the number of binding sites and the affinity of receptors to [3H]DALAMID. The results indicate that somatostatin and substance P may interfere with the endorphin system by an apparently competitive manner.
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PMID:Somatostatin, substance P and [Lys]-vasopressin interfere with the binding of [3H][D-Ala2, Met5]enkephalinamide to rat brain membranes. 241 36

The strength of action of the parasympathetic innervation of the heart was tested, in anaesthetized dogs, by regular delivery of bursts of supramaximal electrical pulses at low frequency to the cut, cardiac end of the vagus nerve. Periods of 'conditioning' stimulation of the same nerve at relatively high frequencies (15-30 Hz, for 15-300 s) were found to cause a slowly developing potentiation (up to 280% increase in the vagally induced prolongation of pulse interval) of the cardiac action of the low-frequency stimulation. This potentiation lasted for periods of up to 30 min after the conditioning period. Similar potentiation could be elicited for the action of one vagus nerve by conditioning the vagus on the other side. Potentiation of vagal action was not associated with an enhancement of the response of the heart to injected methacholine. Several neuropeptides, reported to be present in cardiac autonomic nerves, were tested for ability to mimic this effect when administered by intravenous injection. Vasoactive intestinal polypeptide, neurotensin, somatostatin and substance P all failed to do so at the doses tested. Vasopressin did induce an enhancement of cardiac vagal efficacy, but effective pharmacological blockade of its action did not block the potentiation caused by conditioning stimulation. In the absence of any evidence of neuromodulation of vagal action by these neuropeptides, it was presumed that the effect could be attributed to a classical homosynaptic post-tetanic potentiation mechanism involving intracellular accumulation of calcium ions in prejunctional nerve terminals.
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PMID:Effects of periods of conditioning stimulation and of neuropeptides on vagal action at the heart. 243 Oct 28

Vasopressin and related peptides cause behavioral excitation after intracerebroventricular injection in mice. This behavioral excitation is characterized by excessive scratching and grooming behavior in the unrestrained animal and enhanced escape-directed activity in stressful situations. These effects of vasopressin were found to be blocked by the administration of analogs which act as competitive antagonists of the pressor-activity of vasopressin. The potencies of these analogs in suppressing the behavioral effect paralleled the pressor antagonist potencies. The antagonists did not cause the characteristic behavioral alterations by themselves, nor did they block grooming and/or scratching behavior induced by the structurally-unrelated substances, mescaline, bombesin and substance P. It is suggested that these antagonists provide useful tools for studying the role of endogenous vasopressin in behavior.
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PMID:Specific antagonists of the acute behavioral response to centrally-administered vasopressin in mice. 243 82

We compared responses to calcium ionophore A23187, vasopressin, and substance P in helical strips of dog middle cerebral, basilar, and posterior communicating arteries to obtain a better understanding of humoral control of cerebrovascular tone in different brain regions and its potential impact on mechanisms of cerebral vasospasm. A23187 relaxed these different arterial strips partially precontracted with prostaglandin F2 alpha to a similar extent. Vasopressin produced concentration-dependent relaxation in basilar and posterior communicating arterial strips, whereas middle cerebral arterial strips either contracted or relaxed slightly. Relaxations induced by A23187 and vasopressin were either abolished or converted to contractions by removal of the endothelium. In contrast, the relaxation of cerebral arterial strips to substance P was markedly attenuated but not abolished by endothelium denudation; the remaining relaxation was suppressed by indomethacin. In some cerebral arterial strips with intact endothelium, substance P caused a transient contraction that was reversed to a relaxation by indomethacin or ONO-3708, a prostaglandin antagonist. In arterial strips denuded of endothelium from the same dogs, substance P always produced relaxations. Relaxations of cerebral arterial strips to A23187 and vasopressin appear to be mediated by endothelium-derived relaxing factor. The function of vasopressin receptors in endothelial cells differs markedly in basilar and posterior communicating arteries versus middle cerebral arteries. Substance P-induced relaxations appear to be primarily associated with endothelium-derived relaxing factor and with prostaglandin I2, whereas contractions appear to be mediated by endothelium-derived prostaglandins.
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PMID:Endothelium-dependent and -independent responses to vasodilators of isolated dog cerebral arteries. 246 Sep 77

Vasopressin is one of numerous neuropeptides contained in sympathetic ganglia, but whose function remains unresolved. In this report, we present electrophysiological evidence that arginine-vasopressin (AVP) is a neurotransmitter in guinea pig inferior mesenteric ganglion (IMG). AVP superfused over the IMG, in vitro, produced in a population of neurons a membrane depolarization accompanied by a resistance increase, both of which were blocked by a specific V1 receptor antagonist. Moreover, slow excitatory postsynaptic potentials (EPSPs) elicited by repetitive nerve stimulation were attenuated in 75% of cells tested in the presence of excess AVP, and occasionally in the presence of the antagonist. Thus, AVP joins substance P as a putative transmitter of slow potentials in the guinea pig IMG.
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PMID:Vasopressin-mediated slow EPSPs in a mammalian sympathetic ganglion. 299 91

Vasopressin, oxytocin, substance P and enkephalin fibers were demonstrated to terminate synaptically in the nucleus of the solitary tract. The detergent Triton X-100 proved to be indispensable for the demonstration of vasopressin and oxytocin while enkephalin and substance P could be visualized very well without it. The differences with respect to morphology between these 4 peptides disappeared when Triton X-100 was used in both groups.
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PMID:An immuno-electronmicroscopical study comparing vasopressin, oxytocin, substance P and enkephalin containing nerve terminals in the nucleus of the solitary tract of the rat. 619 39

The actions of various peptides were studied using isolated spinal cord preparation of newborn rat. Vasopressin, substance P, thyrotropin releasing hormone, bombesin, gastrin releasing peptide, oxytocin, neurotensin, cholecystokinin-octapeptide and angiotensin II produced marked depolarizing responses of motoneurons with threshold concentrations of 5 X 10(-10)--8 X 10(-9) M. After the elimination of transsynaptic action by tetrodotoxin, the actions of these peptides were depressed to various extents, the former 5 peptides producing relatively large responses. Somatostatin and enkephalin depressed the dorsal root potential and produced slight hyperpolarization of dorsal root fibers. It is suggested that many of these peptides play important roles in synaptic transmission in mammalian spinal cord.
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PMID:Actions of vasopressin, gastrin releasing peptide and other peptides on neurons on newborn rat spinal cord in vitro. 730 Dec 1

The present study was designed to investigate general morphology and the response of human deferential artery to constrictor and dilator substances with special emphasis on endothelium-dependent responses. Human deferential artery segments were obtained from patients undergoing radical cystectomy (n = 7), suprapubic prostatectomy (n = 6), or radical prostatectomy (n = 6). Light microscopy revealed that human deferential artery is of muscular type, and fluorescence microscopy showed a dense adrenergic innervation. Paired rings, one normal and the other de-endothelialized by gentle rubbing, were mounted for isometric recording of tension in organ baths. Vasopressin, endothelin, serotonin, and potassium chloride induced endothelium-independent contractions, whereas norepinephrine and electrical field stimulation caused frequency-dependent contractions that were of greater magnitude in arteries denuded of endothelium. In precontracted arterial rings, acetylcholine and substance P induced endothelium-dependent relaxations. In contrast, papaverine and sodium nitroprusside caused concentration-dependent relaxations that were similar in the presence and in the absence of endothelium. NG-nitro-L-arginine methyl ester (10(-4) M), an inhibitor of nitric oxide synthase, potentiated the responses to norepinephrine in artery rings with endothelium, nearly abolished the acetylcholine-induced relaxation, and attenuated the relaxation induced by substance P. incubation with methylene blue (10(-5) M), an inhibitor of guanylate cyclase, completely prevented the relaxation induced by acetylcholine in arteries with endothelium. The results of this study indicate that the human deferential artery has a dense adrenergic innervation and marked ability to contract or relax in response to different agonists. Some of these responses are in part endothelium dependent and mediated through release of nitric oxide. These morphological and pharmacological observations could play an important role in regulating flow or pressure of blood that arrives to the vas deferens.
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PMID:Reactivity of human deferential artery to constrictor and dilator substances. 901 5


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