Linked Life Data

8055548

Source:http://linkedlifedata.com/resource/pubmed/id/8055548

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-9-13
pubmed:abstractText
The influx of calcium in response to vasopressin receptor stimulation is an important component of excitation-contraction coupling. We have examined the routes by which Ca2+ and other divalent cations enter vascular smooth muscle cells using a cultured vascular smooth muscle cell line (A7r5). Confluent A7r5 cells were loaded with Fura-2 to permit measurement of intracellular divalent cation concentration (Ca2+, Ba2+, Mn2+). Combinations of excitation wavelengths (340/380, 340/356, 356/380 and 340/370) were used depending on the divalent cation being studied. Emission was measured at 510 nm for all studies. Ca2+, Ba2+ and Mn2+ permeated unstimulated A7r5 cells. Vasopressin increased intracellular Ca2+ in cells both in the presence and absence of extracellular Ca2+, although responses in the absence of extracellular Ca2+ were smaller and had no sustained component. Amlodipine, a voltage-dependent calcium channel blocker, had no effect on Ca2+ entry, but Ni2+ did block Ca2+ influx. Vasopressin-induced elevations of intracellular Ca2+ in Ca(2+)-free physiological saline were abolished by ionomycin and thapsigargin. In the presence of extracellular Ba2+ vasopressin increased intracellular Ca2+ transiently and caused a small sustained increase in intracellular Ba2+ concentration. Ionomycin and thapsigargin increased intracellular Ca2+ but had no effect on Ba2+ influx. In contrast vasopressin, ionomycin and thapsigargin had no effect on Mn2+ influx. Econazole and SKF 96365, imidazoles reported to be blockers of receptor-induced cation entry, increased intracellular Ca2+ by releasing intracellular Ca2+ from a different site to that mobilized by vasopressin or thapsigargin in A7r5 cells. Econazole and SKF 96365 partially inhibited passive influx of Ca2+ and Ba2+ but did not inhibit passive influx of Mn2+, or vasopressin-induced influx of Ba2+. U73122, a putative inhibitor of phospholipase C partially inhibited passive entry of Ca2+ but not passive entry of Mn2+ and Ba2+. U73122 also inhibited vasopressin-induced release of intracellular Ca2+ and agonist-induced Ca2+ influx but did not block vasopressin-induced Ba2+ influx. Divalent cations enter A7r5 cells by a number of routes - 'passive' pathway(s) that admit Ca2+, Ba2+ and Mn2+ and receptor-operated pathway(s) that are permeable to Ca2+, Ba2+ but not Mn2+. On the basis of ionic permeabilities and the effect of various blocking agents, there appear to be two distinct passive influx routes. One is permeable to Ca2+ and Ba2+ and is blocked by econazole or SKF 96365. The other is permeable to Mn2+ and is blocked by Ni2+. There also appear to be two different routes of divalent cation entry involved in responses to receptor activation.(ABSTRACT TRUNCATED AT 400 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/1-(2-(3-(4-methoxyphenyl)propoxy)-4-..., http://linkedlifedata.com/resource/pubmed/chemical/1-(6-((3-methoxyestra-1,3,5(10)-trie..., http://linkedlifedata.com/resource/pubmed/chemical/Barium, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Cations, Divalent, http://linkedlifedata.com/resource/pubmed/chemical/Econazole, http://linkedlifedata.com/resource/pubmed/chemical/Estrenes, http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles, http://linkedlifedata.com/resource/pubmed/chemical/Manganese, http://linkedlifedata.com/resource/pubmed/chemical/Nickel, http://linkedlifedata.com/resource/pubmed/chemical/Pyrrolidinones, http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases, http://linkedlifedata.com/resource/pubmed/chemical/Vasopressins
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0143-4160
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
317-30
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Multiple pathways for entry of calcium and other divalent cations in a vascular smooth muscle cell line (A7r5).
pubmed:affiliation
Department of Clinical Pharmacology, St Mary's Hospital Medical School, Imperial College of Science Technology and Medicine, London, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't