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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-6-17
pubmed:abstractText
Angiotensin II (AngII) is one of the most important vasoconstrictive hormones but is also known to act as a neuromodulator and a neurotransmitter in the central and peripheral nervous systems. In a previous study, we have shown that AngII, mediated by AT(1) receptors, inhibits voltage-dependent calcium channel (VDCC) currents (I(Ca)) via G-proteins in submandibular ganglion (SMG) neurons. In this study, we further characterized the signal transduction of AngII-induced inhibition of I(Ca). Application of 1 microM AngII inhibited I(Ca) by 32.1+/-2.7% (mean+/-S.E.M., n=9). Intracellular dialysis of anti-G(q/11) antibodies attenuated these inhibition (8.8+/-1.3%, n=6). In addition, treatment of protein kinase C (PKC) activator and inhibitor also attenuated these inhibition (8.0+/-0.9 and 9.8+/-0.9%, n=6 and 9, respectively). We therefore conclude that AngII inhibits VDCC via G(q/11)-proteins involving in SMG neurons. In addition, such PKC-dependent pathways mediated mainly L-type VDCC inhibition.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0168-0102
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
179-89
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Angiotensin II-induced inhibition of calcium currents via G(q/11)-protein involving protein kinase C in hamster submandibular ganglion neurons.
pubmed:affiliation
Department of Physiology, Tokyo Dental College, 1-2-2 Masago, Mihama-ku, Chiba 261-8502, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't