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rdf:type |
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lifeskim:mentions |
umls-concept:C0001473,
umls-concept:C0003483,
umls-concept:C0017887,
umls-concept:C0027481,
umls-concept:C0031469,
umls-concept:C0034493,
umls-concept:C0035028,
umls-concept:C0036226,
umls-concept:C0182537,
umls-concept:C0243077,
umls-concept:C1140999
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pubmed:issue |
3
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pubmed:dateCreated |
1993-7-14
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pubmed:abstractText |
Using three putative, selective inhibitors of the Ca+(+)-pump ATPase of sarcoplasmic reticulum (SR), cyclopiazonic acid, thapsigargin and 2,5-di-(tert-butyl)-1,4-benzohydroquinone, the mechanisms of relaxation of the arterial smooth muscle by cyclic GMP-generating vasodilators were studied in the ring preparations of the rabbit aorta. Nitroglycerin (NTG) and atrial natriuretic factor (ANF) were used as representative cyclic GMP-generating vasodilators. When the above three inhibitors of SR Ca+(+)-pump ATPase were present during the period of reloading of intracellular store sites with Ca++, the phasic contractions induced by phenylephrine or caffeine in the succeeding period in Ca+(+)-free media containing 2 mM EGTA were inhibited in a concentration-dependent manner. With 3 x 10(-5) M of cyclopiazonic acid the inhibition was almost complete for both agonists. NTG and ANF relaxed the aorta contracted by phenylephrine (10(-6) M) and produced an increase in cyclic GMP content. All the three SR Ca+(+)-pump ATPase inhibitors produced a concentration-dependent inhibition of the relaxation by NTG and ANF without affecting the increment of cyclic GMP content. These results indicate that the proper functioning of SR Ca+(+)-pump ATPase is necessary for elicitation of relaxation by NTG and ANF. Enhanced sequestration of Ca++ by SR may be an important mechanism by which these compounds induce relaxation in this type of smooth muscle.
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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/2,5-di-tert-butylhydroquinone,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Transporting ATPases,
http://linkedlifedata.com/resource/pubmed/chemical/Diltiazem,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroquinones,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroglycerin,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Terpenes,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin,
http://linkedlifedata.com/resource/pubmed/chemical/cyclopiazonic acid
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-3565
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
265
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1187-92
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:8389854-Adenosine Triphosphatases,
pubmed-meshheading:8389854-Animals,
pubmed-meshheading:8389854-Aorta,
pubmed-meshheading:8389854-Atrial Natriuretic Factor,
pubmed-meshheading:8389854-Calcium,
pubmed-meshheading:8389854-Calcium-Transporting ATPases,
pubmed-meshheading:8389854-Diltiazem,
pubmed-meshheading:8389854-Drug Interactions,
pubmed-meshheading:8389854-Hydroquinones,
pubmed-meshheading:8389854-Indoles,
pubmed-meshheading:8389854-Male,
pubmed-meshheading:8389854-Muscle Contraction,
pubmed-meshheading:8389854-Muscle Relaxation,
pubmed-meshheading:8389854-Nitroglycerin,
pubmed-meshheading:8389854-Phenylephrine,
pubmed-meshheading:8389854-Rabbits,
pubmed-meshheading:8389854-Sarcoplasmic Reticulum,
pubmed-meshheading:8389854-Terpenes,
pubmed-meshheading:8389854-Thapsigargin
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pubmed:year |
1993
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pubmed:articleTitle |
Putative, selective inhibitors of sarcoplasmic reticulum Ca+(+)-pump ATPase inhibit relaxation by nitroglycerin and atrial natriuretic factor of the rabbit aorta contracted by phenylephrine.
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pubmed:affiliation |
Department of Pharmacology, Niigata University School of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro
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