Abstract：
:Indirect and direct experimental evidence demonstrates that both the entry of extracellular calcium and the liberation of calcium from intracellular stores can contribute to an increase in free cytoplasmic calcium concentration in endothelial cells, which seems to be an essential step in the synthesis and/or release of endothelium-derived relaxing factors(s). A variety of Ca2+ transport mechanisms may be involved in the regulation of cytoplasmic calcium in endothelial cells. Ca2+ entry may occur via voltage-operated Ca2+ channels. If they do exist, these channels may have characteristics different from those in underlying vascular smooth muscle cells. Sustained activation of the release of EDRF by various receptor agonists (e.g., acetylcholine, adenine nucleotides, and bradykinin) is also dependent on Ca2+ entry, but it is insensitive to organic Ca2+ channel antagonists. These findings indicate that, when used clinically in various cardiovascular diseases, organic calcium channel antagonists are not expected to interfere with endothelium-dependent relaxation evoked by endogenous vasoactive substances (e.g., ADP, serotonin). Since amiloride and its analogues blocked endothelium-dependent relaxations in different arterial preparations, Na+ transport and Na+/Ca2+ exchange were suggested to play a role in calcium-dependent release of EDRF. The exact nature of Ca2+ transport mechanisms and also the calcium-sensitive cellular processes that lead to the synthesis/release of endothelium derived relaxing factor(s) remain to be determined. However, the available data suggest that calcium handling by the vascular smooth muscle and endothelial cells may be different, allowing potentially selective modulation of Ca2+ activation in these two cell types.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Rubanyi GM,Vanhoutte PMdoi
10.1111/j.1749-6632.1988.tb33360.xsubject
Has Abstractpub_date
1988-01-01 00:00:00pages
226-33eissn
0077-8923issn
1749-6632journal_volume
522pub_type
杂志文章,评审abstract：:Although tissue injury can evoke significant hyperalgesia in infants from the first days of life, little is known about how injury affects emergent central pain networks at the synaptic level. Recent studies have investigated whether tissue damage at different ages has distinct consequences for synaptic function in th...
journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
pub_type： 杂志文章
doi：10.1111/j.1749-6632.1988.tb32984.x
更新日期：1988-01-01 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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更新日期：1993-05-28 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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更新日期：1998-10-23 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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更新日期：2006-08-01 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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更新日期：1996-10-31 00:00:00
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journal_title：Annals of the New York Academy of Sciences
pub_type： 杂志文章
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更新日期：1986-01-01 00:00:00
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journal_title：Annals of the New York Academy of Sciences
pub_type： 杂志文章
doi：10.1111/j.1749-6632.1988.tb33428.x
更新日期：1988-01-01 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
pub_type： 杂志文章,评审
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更新日期：2010-08-01 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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journal_title：Annals of the New York Academy of Sciences
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更新日期：1992-04-15 00:00:00
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journal_title：Annals of the New York Academy of Sciences
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