Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.1 (chymotrypsin)
 10,938 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Venom from Gila monster (family Helodermatidae) contains a pancreatic secretagogue. In dispersed acini from guinea pig pancreas, the venom increased enzyme secretion to the same extent as did vasoactive intestinal peptide, secretin, or PHI. The abilities of vasoactive intestinal peptide and Gila monster venom to stimulate enzyme secretion were not altered by boiling but were abolished by incubation with trypsin or chymotrypsin. Like vasoactive intestinal peptide, secretin, and PHI, the venom caused a 50- to 60-fold increase in cellular cAMP and inhibited binding of 125I-vasoactive intestinal peptide to its membrane receptors on pancreatic acini. The action of venom on enzyme secretion was inhibited by [Gln9]secretin-(5-27), a vasoactive intestinal peptide receptor antagonist, but was not altered by atropine, a cholinergic receptor antagonist, or by dibutyryl cGMP, a cholecystokinin receptor antagonist. Gila monster venom contained no immunoreactive vasoactive intestinal peptide by radioimmunoassay. These results indicate that venom from Gila monster contains a peptide that can stimulate pancreatic enzyme secretion by interacting with vasoactive intestinal peptide receptors on pancreatic acinar cells and thereby activating adenylate cyclase and increasing cellular cAMP.
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PMID:Actions of Gila monster venom on dispersed acini from guinea pig pancreas. 617 52

A comparison was made between the effects of several neuropeptides and ATP as possible mediators of the non-adrenergic, non-cholinergic excitatory response in detrusor strips from the guinea-pig urinary bladder. Both substance P and vasoactive intestinal polypeptide produced contractions of the guinea-pig bladder, but the form of the atropine-resistant neurogenic excitation was mimicked more precisely by ATP. Neither methionine enkephalin nor leucine enkephalin had a prominent direct action on the smooth muscle (up to 100 microM) and did not significantly modify the cholinergic or non-cholinergic components of the response elicited by field stimulation. A proteolytic enzyme, chymotrypsin (10 U/ml), antagonised the excitatory effect of substance P, but not that of the non-adrenergic, non-cholinergic excitatory response or ATP. The slow excitation elicited by a high concentration of vasoactive intestinal polypeptide (10 microM), in contrast to responses elicited by ATP or field stimulation, was attenuated by preincubation with the structurally related polypeptide PHI, which was itself inactive (up to 10 microM). The present observations argue against a role for the peptides studied as neuromuscular transmitters in the detrusor but do not preclude such a role for ATP.
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PMID:Neuropeptide action on the guinea-pig bladder; a comparison with the effects of field stimulation and ATP. 620 46

Non-adrenergic, non-cholinergic (NANC) nerve stimulation results in excitation (e.j.p., rebound depolarization, contractions) or inhibition (i.j.p., afterhyperpolarization, relaxations) of the gut. NANC neuronal mechanisms participate in the maintenance of the basal tone and spontaneous activity of the gut. There are however species differences, i.e. both NANC excitation and inhibition are present in the guinea pig and only NANC inhibition in the rat intestine. Substance P-like neuropeptide/s are suggested to be mediators released from excitatory NANC and sensory nerves. The latter are activated by histamine and degenerated by capsaicin. There is evidence in favor of a nitric oxide-like substance rather than ATP, dopamine, GABA and neuropeptides (e.g. VIP, PHI/PHM) as the inhibitory NANC mediator in the gut. TTX, high Mg(2+)-low Ca2+ media, 3,4-diaminopyridine, dipyridamol and adenosine deaminase modulate NANC excitation and inhibition. The NANC excitation is more sensitive than the NANC inhibition to the action of catecholamines, reserpine, 6-hydroxydopamine, chymotrypsin, prednisolon, bacitracin, opioids, free oxygen species and low concentration of local anesthetics.
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PMID:NANC transmission in intestines and its pharmacological modulation. 839 Nov 98