Abstract:
:Several mechanisms of action for Ca2+ antagonists are possible at the vascular muscle cell membrane and at subsequent steps. In rat caudal artery, nitrendipine hyperpolarizes the resting vascular muscle cell, an action different from that of verapamil. Hyperpolarization might be expected to explain the relaxant action of nitrendipine because hyperpolarization per se causes a decrease in Ca2+ influx. SHR vascular muscle cells show a greater dependence on extracellular K+ concentration for the action of nitrendipine than WKY, as indicated by both tension and membrane potential measurements, suggesting an action on an ion pump. It is possible to directly test the hypothesis that inhibition of Ca2+ influx can directly account for the entire effect of nitrendipine by determination of intracellular Ca2+ with the metallochromic absorbence dye, arsenazo III. Nitrendipine not only decreased the magnitude of the Ca2+ signal but also enhanced the return to resting, or below resting, intracellular Ca2+ levels. Experiments on isolated single cells from the azygous vein of neonatal rats showed evidence of both blockade of Ca2+ influx and enhancement of Ca2+ efflux. These measurements suggest that nitrendipine might cause relaxation by stimulating Ca2+ efflux as well as by decreasing passive Ca2+ influx. Therefore, the action of nitrendipine might be more complicated than simply blocking Ca2+ channels, possibly involving stimulation of active ion transport.
journal_name
J Cardiovasc Pharmacoljournal_title
Journal of cardiovascular pharmacologyauthors
Hermsmeyer K,Kuthe Csubject
Has Abstractpub_date
1984-01-01 00:00:00pages
S933-6eissn
0160-2446issn
1533-4023journal_volume
6 Suppl 7pub_type
杂志文章abstract::The therapeutic strategy of heart rate control for atrial fibrillation (AF) is undergoing a renaissance since several recent randomized trials demonstrated clear advantages over the rhythm control for many patients. Heart rate control for AF is hampered, however, by a dearth of information relating target heart rates ...
journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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abstract::The acute hemodynamic, hormonal, and pharmacokinetic responses to the oral angiotensin-converting enzyme (ACE) inhibitor spirapril were studied in 15 patients with moderate to severe congestive heart failure in a baseline controlled dose-ranging study. Doses of 0.3, 1.0, 1.5, 3.125, and 6.25 mg were investigated for 2...
journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
pub_type: 杂志文章
doi:
更新日期:1989-08-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
pub_type: 杂志文章,评审
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journal_title:Journal of cardiovascular pharmacology
pub_type: 杂志文章,评审
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journal_title:Journal of cardiovascular pharmacology
pub_type: 杂志文章,评审
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更新日期:1987-01-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
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doi:
更新日期:1986-09-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
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更新日期:1985-05-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
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journal_title:Journal of cardiovascular pharmacology
pub_type: 杂志文章,评审
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更新日期:1984-01-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
pub_type: 杂志文章
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journal_title:Journal of cardiovascular pharmacology
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更新日期:1991-01-01 00:00:00
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更新日期:1993-01-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
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更新日期:1992-07-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology
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abstract::The new vasodilator and inotropic drug enoximone was given to dialysis patients as a single intravenous dose of 1 mg/kg. Plasma concentrations were measured up to 240 min. The mother compound enoximone reached a high plasma concentration intravenously, followed by a quick decline of the plasma concentration curve (t1/...
journal_title:Journal of cardiovascular pharmacology
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