Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1994-6-6
pubmed:abstractText
Because endothelin-1 (ET-1) may be a neuromodulator in sensory systems, we examined whether this peptide could alter release of substance P (SP) and calcitonin gene-related peptide (CGRP) from isolated sensory neurons. Although ET-1 had minimal actions on spontaneous neuropeptide release, pretreating cultures with 500 nM resulted in a 50% augmentation of SP and CGRP release evoked by 50 nM capsaicin. Moreover, 2000 nM ET-1 enhanced capsaicin-evoked release of CGRP two fold. In an analogous manner, ET-1 alone did not alter intracellular cGMP content, but enhanced the increase in cGMP caused by 50 nM capsaicin. Intracellular cAMP was not altered by capsaicin and/or ET-1. These data suggest that ET-1 may play a role in modulation of peptide release from primary afferent neurons.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
14
pubmed:volume
167
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
128-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Endothelin-1 enhances capsaicin-induced peptide release and cGMP accumulation in cultures of rat sensory neurons.
pubmed:affiliation
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis 46202-5120.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't