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 in vivo effect of bradykinin on mucociliary (m.c.) activity in the rabbit maxillary sinus was investigated by administering the substance (0.01-10.0 micrograms/kg) via arteria maxillaris and recording the responses with a non-invasive photoelectric technique. Bradykinin accelerated the m.c. activity in a dose-dependent manner in the dose range 0.05-10.0 micrograms/kg. While the action of bradykinin was resistant to pretreatment with indomethacin 10.0 mg/kg, it was considerably weakened by the substance P antagonist [D-Pro2, D-Trp7,9]SP 1 mg/kg. The initial effect of bradykinin was also suppressed by atropine, suggesting that bradykinin accelerates m.c. activity by a dual mechanism comprising both SP and acetylcholine. Bradykinin probably stimulates a reflex arc in the airways involving afferent SP neurons and efferent post-ganglionic parasympathetic neurons.
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PMID:Bradykinin accelerates mucociliary activity in rabbit maxillary sinus. 242 26

The ionic basis for the rapid reduction in potential difference (dip) produced on luminal addition of substance P and related peptides was analysed by altering the electromotive force and chemical gradients across the isolated, canine tracheal epithelium. The dip could be exaggerated, minimised or reversed by increasing, decreasing or reversing the basal potential difference, and the intercept of the line relating the two was close to zero when the Cl- compositions of the two bathing solutions were identical. Luminal Cl- replacement by a non-permeant anion (isethionate) attenuated the dip which was, however, exaggerated by a permeant anion (nitrate). Replacement of serosal Na+ or luminal HCO3- had no significant effect on the magnitude of the dip. The tachykinins exhibited cross-tachyphylaxis with each other, indicating a common receptor. Bradykinin, a structurally unrelated peptide, also produced dips upon luminal addition, but showed no cross-tachyphylaxis with the tachykinins. Again, a linear relation between basal potential difference and the dip elicited by bradykinin was observed. Based on current awareness of the bioelectric properties of the canine tracheal epithelium, we suggest that these peptides modulate paracellular anion permeabilities.
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PMID:Peptides increase anion conductance of canine trachea: an effect on tight junctions. 243 14

Sympathetic reflexes elicited by stimulation of visceral receptors have been well investigated, but the central neurotransmitters mediating these reflexes are largely unknown. Therefore, experiments were done to evaluate the role of substance P in the central transmission of a sympathoexcitatory reflex elicited by stimulation of intestinal receptors. Activity of mesenteric and renal nerves was recorded electrophysiologically in chloralose/urethane-anesthetized rats. Stimulation of intestinal receptors by serosal application of 0.5-1.0 microgram bradykinin increased mesenteric nerve activity by 100 +/- 21%, renal nerve discharge by 33 +/- 9%, and systemic arterial pressure by 10 mm Hg. Chronic capsaicin treatment (cumulative dose 950 mg/kg) caused a 52% depletion of substance P-like immunoreactivity from dorsal root ganglia and a significant attenuation of these reflexes. Mesenteric nerve activity increased by 48 +/- 6% in the capsaicin-treated rats. Bradykinin did not cause significant changes in renal nerve activity or systemic arterial pressure in these rats. The excitation of mesenteric nerve activity was significantly greater than the increase in renal nerve activity int he untreated and capsaicin-treated rats; capsaicin treatment affected responses of both nerves similarly. Capsaicin treatment did not have generalized effects on sympathetic reflexes, as mesenteric and renal nerve activities were decreased by baroreceptor activation similarly in the untreated and capsaicin-treated rats. These results suggest that the central transmission of the reflex response to intestinal receptor stimulation is mediated in part by substance P or other capsaicin-sensitive peptides.
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PMID:Capsaicin treatment attenuates the reflex excitation of sympathetic activity caused by chemical stimulation of intestinal afferent nerves. 243 87

We investigated the properties of the novel dorsal root ganglion (DRG) hybrid cell line F-11 to see how closely these cells resembled normal DRG cells. Under normal growth conditions, F-11 cells appeared to contain several short neurite-like processes. However, these cells could also be grown under conditions in which they showed a much more extensive neuronal morphology, exhibiting many long neurites. Several differentiated features of DRG cells were present on F-11 cells. These included the presence of delta-opioid receptors, receptors for prostaglandins and bradykinin, and dihydropyridine-sensitive calcium channels. F-11 cells also synthesized and released a substance P-like compound, as determined by immunoreactivity. Both the number of bradykinin receptors and the voltage-sensitive calcium influx increased on cell differentiation. Opioid agonists (delta-specificity) were found to decrease cyclic AMP levels in F-11 cells in a naloxone- and pertussis toxin-reversible fashion. Bradykinin stimulated the synthesis of inositol-1,4-bisphosphate and inositol-1,4,5-trisphosphate. Ca2+ channel agonists stimulated voltage-sensitive Ca2+ influx in a dose-dependent, stereospecific manner, whereas Ca2+ channel antagonists inhibited Ca2+ influx. F-11 cells should, therefore, prove useful as models for authentic DRG neurons.
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PMID:Neurochemical characteristics of a novel dorsal root ganglion X neuroblastoma hybrid cell line, F-11. 243 52

Luminal addition of tachykinins to the open-circuited canine tracheal epithelium produces a biphasic response in the transmucosal potential difference (PD). A rapid, transient decrease is followed by a subsequent rise, both phases being associated with changes in conductance. Concentration-response curves demonstrated the following orders of potency: substance P greater than physalaemin greater than eledoisin = kassinin for the tachykinins, and substance P greater than substance P-(4-11) greater than substance P-(6-11) using the C-terminal fragments. Both sequences are similar to those reported for the dog carotid artery. These observations were confirmed by cross-tachyphylaxis experiments. SP-O-methyl ester, a selective agonist for the SP-P (or NK-1) receptor, elicited identical responses, and exhibited cross-tachyphylaxis to substance P. Bradykinin produced similar luminal responses, though different receptors are involved, since no cross-tachyphylaxis was observed between bradykinin and the tachykinins.
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PMID:Luminal tachykinin receptors on canine tracheal epithelium: functional subtyping. 244 1

The effect of vasoactive peptides on vascular smooth muscle in the cerebral microcirculation was examined using an isolated intracerebral arteriole preparation. Extraluminally applied vasoactive intestinal peptide (VIP) dilated the spontaneous tone of intracerebral arterioles to 118.9 +/- 3.1% of control diameter at pH 7.30, with an EC50 of 7.27 X 10(-8) M. Similar degrees of dilation to VIP were seen in vessels preconstricted by changing bath solution to pH 7.60. Substance P had no effect on vessel diameter at pH 7.30. However, in vessels precontracted by pH 7.60, significant dose-dependent dilation was observed with an EC50 of 2.55 x 10(-10) M. Neuropeptide Y constricted intracerebral arterioles to 81.22 +/- 2.7% of control diameter, with an EC50 of 6.23 x 10(-10) M. Bradykinin dilated intracerebral arterioles at pH 7.30 and pH 7.60 to 130 +/- 3.0% of control diameter. VIP and bradykinin are potent vasodilators of intracerebral arterioles. Neuropeptide Y is a vasoconstrictor. The effect of substance P appeared to be either pH-dependent or dependent on some degree of precontraction by another agonist, but no effect on vessel diameter was seen at pH 7.30.
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PMID:Vasomotor responses of rat intracerebral arterioles to vasoactive intestinal peptide, substance P, neuropeptide Y, and bradykinin. 244 45

The mechanism of the diuretic effect of atrial natriuretic factor is unclear. In this study, we compared the renal vasodilating and diuretic effects of renal arterial infusions of rat atriopeptin II in anesthetized dogs to see if natriuresis and increases in total renal blood flow were associated. The vasodilators substance P and bradykinin also were tested. Volume (V), Na+ and K+ concentration and Na+ and K+ content (UNaV; UkV) of urine from the infused and contralateral kidneys (IK; CK) were measured as well as mean total renal blood flow (RBF) of the IK. Atriopeptin II (30-1000 ng/kg/min) slightly promoted RBF by up to 20%, but raised V, UNaV and UkV by a maximum of 79, 190 and 100%, respectively. Substance P (0.01-30 ng/kg/min) raised RBF of IK by a maximum of 59%, reduced mean blood pressure by 26% and had a biphasic effect on IK excretion: V, UNaV and UkV were increased maximally by 105, 154 and 42% at 1.0 ng/kg/min, whereas progressively less diuresis, natriuresis and kaliuresis occurred at higher (hypotensive) doses. CK excretion was unchanged. Bradykinin (1-100 ng/kg/min) raised RBF, V, UNaV, and UkV of IKs by a mean maximum of 97, 70, 201 and 47%, respectively, with no changes in mean blood pressure or CK excretion. The natriuretic and hyperemic effects of nonhypotensive doses of each peptide were significantly correlated. However, atriopeptin II uniquely promoted Na+ excretion, but not RBF at the lowest dose tested, and, after 10 min washout of the 1000-ng/kg/min dose, and did not appreciably promote RBF after 10 min of infusion. It also caused CK diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natriuretic and vasodilating activities of intrarenally administered atriopeptin II, substance P and bradykinin in the dog. 245 90

1. Bradykinin and capsaicin were compared for their ability to elicit functional effects and to release sensory neuropeptides from guinea-pig isolated perfused hearts. 2. Both bradykinin (10 microM) and capsaicin (1 microM) produced a marked increase in coronary flow, a large positive chronotropic effect and a significant reduction in contractile strength. These actions were associated with a marked release of substance P-like immunoreactivity (SP-LI) and calcitonin gene-related-like immunoreactivity (CGRP-LI). The percentage of the tissue content of SP-LI and CGRP-LI released by each agent was similar, although bradykinin was less effective than capsaicin. The ratio of SP-LI/CGRP-LI released by both agents was similar to that present in cardiac tissue. 3. Neuropeptide release could be evoked only once with capsaicin but at least four times with bradykinin. Also, functional responses to capsaicin underwent desensitization. After either in vitro or systemic capsaicin pretreatment, the release of SP-LI and CGRP-LI by bradykinin was reduced and the positive chronotropic effect of bradykinin was significantly reduced, while the increase in coronary flow and negative inotropic responses remained unchanged. 4. Pretreatment with indomethacin (10 microM) strongly antagonized the release of SP-LI and CGRP-LI by bradykinin and reduced the increase in heart rate. 5. These findings suggest that activation by bradykinin (probably through indirect mechanisms) of capsaicin-sensitive sensory nerves in the heart, leads to a local release of sensory neuropeptides. These neuropeptides, in turn, could participate in determining the complex functional effects of this kinin on cardiac performance.
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PMID:A comparison of bradykinin- and capsaicin-induced myocardial and coronary effects in isolated perfused heart of guinea-pig: involvement of substance P and calcitonin gene-related peptide release. 247 43

Vascular leakage in the middle ear cavity was studied after i.v. administration of various substances in rats and determined by the Evans blue technique. Bradykinin, histamine, serotonin, acetylcholine, substance P (SP) and vasoactive intestinal polypeptide (VIP) resulted in extravasation of Evans blue. In the case of bradykinin and histamine, the leakage was dose dependent. Calcitonin gene-related peptide (CGRP) did not affect vessel permeability. In other experiments the effect of histamine antagonists was tested on production of middle ear effusion, caused by blowing air at 14 degrees C into the external auditory canal (EAC). The increase in vessel permeability in this otitis media model was inhibited by the H2-receptor antagonist cimetidine, at doses 0.1 and 1.0 mg/ml. Diphenhydramine, an H1-receptor antagonist, arrested only partly middle ear fluid accumulation. Our study demonstrated that various inflammatory mediators and neuropeptides are capable of inducing vascular leakage in the middle ear cavity. It was also concluded that H2-receptors are involved in the regulation of middle ear vascular permeability.
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PMID:Middle ear effusion induced by various inflammatory mediators and neuropeptides. An experimental study in the rat. 247 18

1. Bradykinin (1 nm-1 microM) produced a contraction of bladder strips excised from the dome of the guinea-pig urinary bladder, an effect which was greatly enhanced by removal of the mucosal layer or by thiorphan (10 microM). All subsequent experiments were performed in mucosa-free strips and in the presence of thiorphan. 2. In carbachol (5 microM)-contracted strips, bradykinin produced a concentration (1 nm-1 microM)-dependent transient relaxation. 3. Kallidin was slightly more potent than bradykinin in producing a contraction and a relaxation of the carbachol-induced tone. By contrast, [des-Arg9]-bradykinin, a selective B1 receptor agonist was barely effective up to 1 microM. 4. The contractile response to bradykinin was: (a) unaffected by either tetrodotoxin (1 microM), in vitro capsaicin desensitization (10 microM for 30 min) or apamin (0.1 microM); (b) antagonized by indomethacin (5 microM), the prostaglandin receptor antagonist SC-19220 (100 microM) or the B2 receptor antagonist [D-Arg0, Hyp3, Thi5,8, Phe7]-bradykinin (10 micron) and (c) almost abolished by nifedipine (1 microM). 5. The antagonism of the contractile response to bradykinin produced by indomethacin and SC-19220 was non-additive while that produced by indomethacin and the B2 receptor antagonist was additive. 6. The relaxant response to bradykinin was unaffected by tetrodotoxin, in vitro capsaicin desensitization or indomethacin but antagonized in a competitive manner by the B2 receptor antagonist. Further, this response was abolished by apamin (0.1 microM) but unaffected by glibenclamide (1 microM). 7. Bradykinin (10 microM) produced a consistent release of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) but not substance P-LI from the guinea-pig bladder muscle. CGRP-LI release by bradykinin was greatly reduced in bladders exposed to indomethacin. [des-Arg9]-bradykinin (10 microM) was ineffective. 8. We conclude that: (a) bradykinin-induced contraction involves activation of both B2 receptors and prostanoid synthesis, via distinct mechanisms which act by inducing calcium influx via nifedipine-sensitive channels; (b) bradykinin-induced relaxation involves activation of B2 receptors and opening of apamin-sensitive potassium channels; (c) bradykinin stimulates sensory nerves in this tissue largely via prostanoid production.
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PMID:Multiple mechanisms in the motor responses of the guinea-pig isolated urinary bladder to bradykinin. 247 41


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