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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1993-7-15
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pubmed:abstractText |
To examine the interaction of protein kinase C (PKC) with agonist-induced calcium fluxes in hypertension, cytosolic free calcium ([Ca2+]i) was measured in vascular smooth muscle cells (vSMC) of normotensive and spontaneously hypertensive rats (SHR) after incubation with phorbol,-12 myristate,-13 acetate (PMA) and application of angiotensin II (AII). To distinguish between calcium influx through voltage-dependent calcium channels and calcium mobilization from intracellular stores, the calcium agonist BayK 8644 was used. Resting [Ca2+]i was 108.0 +/- 10.6 nM (mean +/- SEM, n = 25) in normotensive and 102.0 +/- 11.4 nM (n = 21) in hypertensive cells. After pretreatment with PMA 10(-7) M for 60 min, resting [Ca2+]i of normotensive vSMC increased to 145.0 +/- 13.8 nM (n = 17) while the resting level of the hypertensive cells decreased to 68.0 +/- 2.4 nM (n = 14, p < 0.05 as compared with normotensive cells) in hypertensive vSMC. Maximum increase in [Ca2+]i induced with 10 M AII for normotensive and hypertensive vSMC was similar: 230.5 +/- 34.4 nM (n = 14) and 212.5 +/- 26.7 nM (n = 17). After pretreatment with PMA 10(-7) M, the maximum increase in [Ca2+]i induced by AII in hypertensive cells was limited to 108.0 +/- 6.2 nM (p < 0.05 as compared with normotensive cells), whereas the increase in [Ca2+]i in normotensive vSMC remained the same as before: 211.5 +/- 23.4 nM. After administration of 10(-5) M BayK 8644, [Ca2+]i increased by 54.3 +/- 12.2 nM (n = 4) and 43.4 +/- 17.4 nM (n = 5) in normotensive and hypertensive vSMC, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3-Pyridinecarboxylic acid...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0160-2446
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
749-53
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7685444-3-Pyridinecarboxylic acid...,
pubmed-meshheading:7685444-Angiotensin II,
pubmed-meshheading:7685444-Animals,
pubmed-meshheading:7685444-Cells, Cultured,
pubmed-meshheading:7685444-Cytosol,
pubmed-meshheading:7685444-Enzyme Activation,
pubmed-meshheading:7685444-Fura-2,
pubmed-meshheading:7685444-Male,
pubmed-meshheading:7685444-Muscle, Smooth, Vascular,
pubmed-meshheading:7685444-Protein Kinase C,
pubmed-meshheading:7685444-Rats,
pubmed-meshheading:7685444-Rats, Inbred SHR,
pubmed-meshheading:7685444-Rats, Inbred WKY,
pubmed-meshheading:7685444-Tetradecanoylphorbol Acetate
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pubmed:year |
1993
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pubmed:articleTitle |
Angiotensin II responses after protein kinase C activation in vascular smooth muscle cells of spontaneously hypertensive rats.
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pubmed:affiliation |
Medinische Universitäts Poliklinik, University of Münster, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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