Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pilocarpine contracts the sphincter pupillae muscle via an effect on muscarinic receptors and phenylephrine contracts the dilator pupillae muscle via an effect on alpha-adrenergic receptors. These effects are thought to mimic the action of the parasympathetic and sympathetic nervous systems, respectively. Intracellular injection of substance P (SP) produces an atropine-resistant constriction of the pupil. This response is thought to mimic the effect of local sensory reflexes on the sphincter pupillae muscle, involving SP-containing trigeminal nerve endings. Repeated intraocular injections of tetrodotoxin, a general blocker of nervous conduction, over a period of 3 weeks produced supersensitivity to pilocarpine, phenylephrine and SP in the rabbit iris. These findings support the view that, like acetylcholine and noradrenaline, SP or an SP-like compound acts as a neurotransmitter in the iris. Also, long-term topical application of an SP antagonist, (D-Pro2,D-Trp7,9)-SP or (Arg5,D-Trp7,9)-SP5-11, to the rabbit eye produced supersensitivity to SP but not to pilocarpine, thus supporting the view that the SP antagonists interact specifically with the SP receptors. The isolated rabbit iris sphincter muscle responds to electrical stimulation with a cholinergic twitch followed by a slow non-cholinergic contraction that can be blocked by antagonists to SP. Analysis of the motor activity of the iris sphincter muscle after long-term topical treatment of the eye with an SP antagonist followed by an interval of 2 days after termination of treatment revealed a greatly enhanced non-cholinergic contraction compared with the cholinergic twitch, a finding that seems to be consistent with the idea that supersensitivity to SP had developed.
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PMID:Pupillary supersensitivity to substance P following prolonged treatment with tetrodotoxin or substance P antagonists. 258 Jul 17

The effect of pilocarpine and substance P on the amplitudes of the postganglionic compound action potentials (unconditioned response, UR and post-train conditioned response, PTR) were studied in the isolated rabbit superior cervical ganglion (SCG). Pilocarpine (50 microM) and substance P (1 microM) produced an increase in the amplitudes of both UR & PTR responses in the rabbit SCG. Facilitation and subliminal fringe values decreased. It was concluded that both pilocarpine and substance P increase the amplitudes of the transmitted postganglionic compound action potentials and they may facilitate ganglionic transmission in the rabbit SCG.
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PMID:Effect of pilocarpine and substance P on ganglionic transmission. 619 38

Pilocarpine releases histamine from mast cells of cat submandibular gland and rat liver. In the salivary gland, histamine is released into the saliva and venous outflow. Atropine blocks the salivation, but not histamine release from the submandibular gland into the blood. Histamine release from the gland could be due to a direct action of pilocarpine on tissue mast cells or to an indirect action of mediators (acetylcholine and peptides). These hypotheses were further investigated in our present studies on rat peritoneal mast cells. Our results show: (1) histamine release from rat peritoneal mast cells induced by pilocarpine (ED50 = 1.7 x 10(-2) mol/l) occurs at 1000-fold higher concentrations than by substance P (ED50 = 1.7 x 10(-5) mol/l) and in 6.5-fold higher concentrations than by atropine (ED50 = 2.6 x 10(-3) mol/l), (2) pilocarpine injected directly into the rat peritoneal cavity causes histamine release from peritoneal mast cells in 1.8-fold higher concentrations than from isolated rat peritoneal mast cells. These results would support the hypothesis that histamine release from cat submandibular gland is caused by peptidergic co-transmission during the stimulation of the organ.
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PMID:The mechanism of histamine release induced by pilocarpine from different tissues: studies on rat peritoneal mast cells. 752 51

1. During heat exposure, rats secrete large amounts of saliva. Salivation started when body temperature exceeded 39 degrees C and was reduced by kininogen deficiency or by HOE 140, a bradykinin antagonist. This secretory response was associated with a partial depletion of glandular kallikrein from the submaxillary glands. The depletion was abolished by simultaneous treatment of the animals with an alpha- and a beta-adrenergic antagonist. During heat exposure, plasma levels of kininogens were reduced. 2. Pilocarpine and substance P induced a similar flow of saliva in normal and kininogen-deficient rats and released low amounts of kallikrein from salivary glands. Phenylephrine and isoproterenol induced a larger flow of saliva in normal rats than in kininogen-deficient rats. Both agents released large amounts of kallikrein in saliva but isoproterenol was only active at large doses. 3. During heat exposure, the blood content of submaxillary glands in normal as well as in kininogen-deficient rats increased as a function of the ambient temperature. This increase was suppressed by atropine and NG-nitro-L-arginine, a NO-synthase inhibitor, but was not modified by HOE 140. Simultaneously, a swelling of the glands and of the surrounding soft tissues occurred in normal but not in kininogen-deficient rats. Kallikrein was present in the edema fluid. 4. The kallikrein-kinin system would thus participate in heat-induced salivary secretion and kinins may be a factor responsible for electrolyte and water exchanges in the glands.
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PMID:Involvement of the kallikrein-kinin system in the salivary secretion elicited in rats by heat stress. 753 74

Evans blue accumulated in parotid glands of conscious rats in response to feeding (over 60 min), in the absence of atropine and adrenoceptor antagonists and in their presence, and after pretreatment with the sensory neurotoxin capsaicin. Stimulation of the auriculo-temporal nerve (40 Hz, 10 or 20 min), without and with the blockers, caused Evans blue to accumulate. A periglandular oedema also contained the dye. Administration (i.v.) of neurokinin A accumulated Evans blue, while substance P, vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating peptide (PACAP), calcitonin gene-related peptide (CGRP) and pilocarpine lacked effect. Pilocarpine enhanced the action of neurokinin A and, furthermore, substance P combined with either VIP, PACAP or CGRP resulted in accumulation of Evans blue. In the sublingual + submandibular glands, Evans blue increased in response to neurokinin A and pilocarpine; furthermore, substance P and VIP, and substance P and CGRP, interacted positively. Bradykinin lacked effect in the glands. Comparisons were made with the urinary bladder. Accumulation of Evans blue reflects plasma protein extravasation. In salivary glands, the phenomenon occurred during feeding and was independent on intact sensory innervation; instead, the parasympathetic innervation containing the neuropeptides was in focus. In the clinic, the present findings may have implications for the aetiology of gland swelling and pain.
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PMID:Vascular protein leakage in the rat parotid gland elicited by reflex stimulation, parasympathetic nerve stimulation and administration of neuropeptides. 980 4