| pubmed-article:1700112 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C0007450 | lld:lifeskim |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C0001629 | lld:lifeskim |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C0391850 | lld:lifeskim |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C1325901 | lld:lifeskim |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:1700112 | lifeskim:mentions | umls-concept:C1879313 | lld:lifeskim |
| pubmed-article:1700112 | pubmed:dateCreated | 1990-12-19 | lld:pubmed |
| pubmed-article:1700112 | pubmed:abstractText | 1. Inactivation by voltage changes of 45Ca2+ uptake into and catecholamine release from cat adrenal glands perfused at a high rate (4 ml/min) at 37 degrees C with oxygenated Krebs-Tris solution has been studied. Experimental conditions were selected so that adrenal medullary chromaffin cells were depolarized for different time periods and with various K+ concentrations in the absence of Ca2+, prior to the application of 0.5 mM-Ca2+ for 10 s in the presence of 118 mM-K+ to test the rate of secretion (the 'Ca2+ pulse'). 2. Application of the Ca2+ pulse after perfusion with 5.9 mM-K+ led to a 100-fold increase of the basal rate of secretion. However, if the Ca2+ pulse was preceded by a 10 min period of perfusion with 118 mM-K+, the secretory response was decreased by over 80%. 3. Inactivation of secretion starts 10-30 s after high-K+ perfusion and is completed 2-5 min thereafter. Inactivation is readily reversed by perfusing the glands with normal K(+)-containing solution; the recovery phenomenon is also gradual and time-dependent, starting 30 s after repolarization and ending 300 s thereafter. 4. The rate of inactivation is much slower at 35 than at 118 mM-K+, suggesting that the process is strongly dependent on voltage. 5. Like catecholamine release, Ca2+ uptake into adrenal medullary chromaffin cells is inactivated in a voltage-dependent manner. This, together with the fact that Cd2+ blocked secretion completely and inactivation was seen equally using Ca2+ or Ba2+ as secretagogues, suggests that inactivation of a certain class of voltage-dependent Ca2+ channels is responsible for the blockade of secretion. Such channels must be slowly inactivated by voltage and highly sensitive to dihydropyridines, since (+)PN200-110 (an L-type Ca2+ channel blocker) enhanced the rate of inactivation and (+/-)Bay K 8644 (an L-type Ca2+ channel activator) prevented it, indicating that they might belong to L-subtype Ca2+ channels. 6. The effects of (+/-)Bay K 8644 (100 nM) were seen on both the voltage and time dependence of inactivation. At a moderate depolarization (35 mM-K+), the drug prevented inactivation and caused potentiation of secretion which developed gradually; at strong depolarizations (118 mM-K+), Bay K 8644 prevented the time-dependent development of inactivation. (+)PN200-110 (30 nM) did not suddenly decrease catecholamine release at the earlier times of depolarization; what the drug did was to accelerate the normal rate of inactivation induced by depolarization.(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
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| pubmed-article:1700112 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1700112 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1700112 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1700112 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1700112 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1700112 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:1700112 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:1700112 | pubmed:author | pubmed-author:GarcíaA GAG | lld:pubmed |
| pubmed-article:1700112 | pubmed:author | pubmed-author:LópezM GMG | lld:pubmed |
| pubmed-article:1700112 | pubmed:author | pubmed-author:GarridoBB | lld:pubmed |
| pubmed-article:1700112 | pubmed:author | pubmed-author:MoroM AMA | lld:pubmed |
| pubmed-article:1700112 | pubmed:author | pubmed-author:de PascualRR | lld:pubmed |
| pubmed-article:1700112 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1700112 | pubmed:volume | 428 | lld:pubmed |
| pubmed-article:1700112 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1700112 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1700112 | pubmed:pagination | 615-37 | lld:pubmed |
| pubmed-article:1700112 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:1700112 | pubmed:meshHeading | pubmed-meshheading:1700112-... | lld:pubmed |
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| pubmed-article:1700112 | pubmed:meshHeading | pubmed-meshheading:1700112-... | lld:pubmed |
| pubmed-article:1700112 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:1700112 | pubmed:articleTitle | Voltage-dependent inactivation of catecholamine secretion evoked by brief calcium pulses in the cat adrenal medulla. | lld:pubmed |
| pubmed-article:1700112 | pubmed:affiliation | Departamento de Farmacología, Facultad de Medicina, Universidad Autónoma de Madrid, Spain. | lld:pubmed |
| pubmed-article:1700112 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1700112 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1700112 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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