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rdf:type |
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lifeskim:mentions |
umls-concept:C0003018,
umls-concept:C0021469,
umls-concept:C0028351,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0042360,
umls-concept:C0086376,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1314939,
umls-concept:C1709059,
umls-concept:C1711351,
umls-concept:C1963578
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pubmed:issue |
7
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pubmed:dateCreated |
2006-10-23
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pubmed:abstractText |
The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Autoreceptors,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/G-protein Beta gamma,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein beta Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein gamma Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0197-0186
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
698-707
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:16962210-Adrenergic alpha-Antagonists,
pubmed-meshheading:16962210-Angiotensin II,
pubmed-meshheading:16962210-Animals,
pubmed-meshheading:16962210-Autoreceptors,
pubmed-meshheading:16962210-Electric Stimulation,
pubmed-meshheading:16962210-Enzyme Inhibitors,
pubmed-meshheading:16962210-GTP-Binding Protein beta Subunits,
pubmed-meshheading:16962210-GTP-Binding Protein gamma Subunits,
pubmed-meshheading:16962210-Male,
pubmed-meshheading:16962210-Neural Inhibition,
pubmed-meshheading:16962210-Norepinephrine,
pubmed-meshheading:16962210-Pertussis Toxin,
pubmed-meshheading:16962210-Presynaptic Terminals,
pubmed-meshheading:16962210-Protein Kinase C,
pubmed-meshheading:16962210-Rats,
pubmed-meshheading:16962210-Rats, Wistar,
pubmed-meshheading:16962210-Receptor, Angiotensin, Type 1,
pubmed-meshheading:16962210-Receptor Cross-Talk,
pubmed-meshheading:16962210-Receptors, Adrenergic, alpha-2,
pubmed-meshheading:16962210-Signal Transduction,
pubmed-meshheading:16962210-Sympathetic Fibers, Postganglionic,
pubmed-meshheading:16962210-Synaptic Transmission,
pubmed-meshheading:16962210-Tritium,
pubmed-meshheading:16962210-Type C Phospholipases,
pubmed-meshheading:16962210-Vas Deferens
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pubmed:year |
2006
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pubmed:articleTitle |
Involvement of G-protein betagamma subunits on the influence of inhibitory alpha2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens.
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pubmed:affiliation |
Laboratory of Pharmacology, CEQOFFUP, Faculty of Pharmacy, University of Porto, Rua Aníbal Cunha, 164, 4050-047 Porto, Portugal.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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