Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitro effects of the Bordetella HLT on the isolated perfused lung and some other tissue preparations from guinea pigs were examined. When HLT (30 to 300 MNDs/ml) was administered, an increase of the perfusion pressure was induced in the perfused lungs, indicating vasoconstriction. When 100 or 300 MNDs/ml of HLT was given, the pressure increase appeared after a lag period of 3.5 to 4 min, reached a maximum within 8 to 13 min, and then slowly decreased by 60 to 80% 25 min after exposure. In calcium-free medium, the pressure increase due to HLT did not occur, but these HLT-treated lungs manifested an increase without any lag period immediately after the calcium-free medium was replaced by normal medium containing calcium. No difference in the response of the perfused lungs to histamine was observed before and after exposure to HLT. The arterial strip did not respond to HLT, but after predigestion with a collagenase and elastase solution the contractive response to 100 MNDs/ml of HLT appeared with a lag period of 1 min. HLT had no effect on the pharmacological responses of the isolated atria, deferent canal or intestinal preparations, or on the ciliary movement of cultured tracheal rings.
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PMID:Effect of Bordetella heat-labile toxin on perfused lung preparations of guinea pigs. 357 56

Free cells isolated from adult rat heart by the collagenase method were maintained in culture up to 21 h with or without an islet-activating protein (IAP) that had been purified from the culture medium of Bordetella pertussis. Short-term stimulation of beta-adrenergic or glucagon receptors in these cultured cells caused more accumulation of cAMP in cells precultured with IAP (IAP-treated) than in nontreated cells, although there was no significant difference in the baseline (non-stimulated) content of cAMP between these cells. Stimulation of muscarinic cholinergic or adenosine R-site receptors caused a marked inhibition of cAMP accumulation in nontreated cells in either the presence or absence of a beta-agonist (or glucagon); no such inhibition was essentially observed in IAP-treated cells. These actions of IAP developed gradually and were dose-dependent with the half-maximal concentration of approximately 80 ng/ml in culture. It is concluded that IAP may exert its unique influence on the heart cell membrane causing profound modification of the coupling mechanism involved in the receptor-mediated activation or inhibition of adenylate cyclase. This action of IAP differs clearly from that of cholera toxin which activates adenylate cyclase rather independently of the receptor functions in heart cells.
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PMID:Modification by islet-activating protein of receptor-mediated regulation of cyclic AMP accumulation in isolated rat heart cells. 616 42