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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00696
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http://purl.obolibrary.org/obo/BFO_0000066
http://purl.obolibrary.org/obo/UBERON_0004237
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http://purl.obolibrary.org/obo/BFO_0000066
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http://resource.belframework.org/belframework/20131211/namespace/selventa-legacy-chemicals/cyclic%20AMP
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a(SCHEM:"cyclic AMP") -| p(RGD:Myl9,pmod(P,T,18))
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Cardiovascular Physiology Concepts
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Cardiovascular Physiology Concepts
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Other
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The Gs-protein coupled pathway stimulates adenylyl cyclase (AC) that catalyzes the formation of cAMP. In VSM, unlike the heart, an increase in cAMP stimulated by a b2-adrenoceptor agonist such as epinephrine or isoproterenol causes relaxation. The mechanism for this is cAMP inhibition of MLCK. Therefore, increased cAMP decreases MLC phosphorylation, which decreases the interactions between actin and myosin. Therefore, drugs which increase cAMP (e.g., b2-adrenoceptor agonists, phosphodiesterase inhibitors) cause vasodilation.
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Selventa
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2014-07-03T14:31:29.026+02:00
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