Linked Life Data

10517809

Source:http://linkedlifedata.com/resource/pubmed/id/10517809

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2000-1-4
pubmed:abstractText
1. Nitric oxide (NO) has been shown to modulate neuropeptide secretion from the posterior pituitary. Here we show that NO activates large-conductance Ca2+-activated K+ (BK) channels in posterior pituitary nerve terminals. 2. NO, generated either by the photolysis of caged-NO or with chemical donors, irreversibly enhanced the component of whole-terminal K+ current due to BK channels and increased the activity of BK channels in excised patches. NO also inhibited the transient A-current. The time courses of these effects on K+ current were very different; activation of BK channels developed slowly over several minutes whereas inhibition of A-current immediately followed NO uncaging. 3. Activation of BK channels by NO occurred in the presence of guanylyl cyclase inhibitors and after removal of ATP or GTP from the pipette solution, suggesting a cGMP-independent signalling pathway. 4. The sulfhydryl alkylating agent N-ethyl maleimide (NEM) increased BK channel activity. Pretreatment with NEM occluded NO activation. 5. NO activation of BK channels occurred independently of voltage and cytoplasmic Ca2+ concentration. In addition, NO removed the strict Ca2+ requirement for channel activation, rendering channels highly active even at nanomolar Ca2+ levels. 6. These results suggest that NO, or a reactive nitrogen byproduct, chemically modifies nerve terminal BK channels or a closely associated protein and thereby produces an increase in channel activity. Such activation is likely to inhibit impulse activity in posterior pituitary nerve terminals and this may explain the inhibitory action of NO on secretion.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-1284313, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-1302271, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-1700301, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-1852778, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-1988937, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-2497467, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-6818840, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7499306, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7509733, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7511350, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7512692, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7516125, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7517025, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7519783, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7523633, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7530064, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7539993, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7685865, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7733655, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7870291, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-7898755, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8021831, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8084473, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8095406, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8395581, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8413832, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8782570, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8782593, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8789952, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-8816713, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-9208862, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-9357987, http://linkedlifedata.com/resource/pubmed/commentcorrection/10517809-9422697
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
520 Pt 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
165-76
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:10517809-Animals, pubmed-meshheading:10517809-Cell-Free System, pubmed-meshheading:10517809-Cyclic GMP, pubmed-meshheading:10517809-Electrophysiology, pubmed-meshheading:10517809-Enzyme Inhibitors, pubmed-meshheading:10517809-Guanylate Cyclase, pubmed-meshheading:10517809-Ion Channel Gating, pubmed-meshheading:10517809-Kinetics, pubmed-meshheading:10517809-Large-Conductance Calcium-Activated Potassium Channels, pubmed-meshheading:10517809-Male, pubmed-meshheading:10517809-Nitric Oxide, pubmed-meshheading:10517809-Nitric Oxide Donors, pubmed-meshheading:10517809-Oxytocin, pubmed-meshheading:10517809-Patch-Clamp Techniques, pubmed-meshheading:10517809-Photolysis, pubmed-meshheading:10517809-Pituitary Gland, Posterior, pubmed-meshheading:10517809-Potassium Channels, pubmed-meshheading:10517809-Potassium Channels, Calcium-Activated, pubmed-meshheading:10517809-Rats, pubmed-meshheading:10517809-Ruthenium Compounds, pubmed-meshheading:10517809-Signal Transduction, pubmed-meshheading:10517809-Vasopressins
pubmed:year
1999
pubmed:articleTitle
Direct actions of nitric oxide on rat neurohypophysial K+ channels.
pubmed:affiliation
Department of Physiology, University of Wisconsin-Madison, Madison, WI 53706, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.