Linked Life Data

10545774

Source:http://linkedlifedata.com/resource/pubmed/id/10545774

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pubmed-article:10545774pubmed:dateCreated1999-12-16lld:pubmed
pubmed-article:10545774pubmed:abstractText(+)-MK801, a noncompetitive NMDA receptor antagonist, was reported to exhibit anticonvulsive and neuroprotective activities during the postischemic period. Intravenous administration of (+)-MK801 produced tachycardia in rats, but bradycardia in pigs. We examined the mechanical and electrophysiological effects of (+)-MK801 on rat cardiac tissues. (+)-MK801 dose-dependently increased (3-100 microM) twitch tension in rat atria and ventricular strips. The spontaneous beating rate in rat right atria, however, was dose-dependently decreased by (+)-MK801. The inotropic effect of (+)-MK801 was affected neither by alpha(1)-antagonist (1 microM prazosin) nor by beta(1)-adrenoceptor antagonist (3 microM atenolol), but significantly by a transient outward K(+) channel blocker (3 mM 4-aminopyridine). (+)-MK801 did not cause any significant change of intracellular cAMP content. Electrophysiological study in rat ventricular cells revealed that (+)-MK801 concentration-dependently prolonged the action potential duration with a concomitant decrease in the maximum rate of the action potential upstroke (V(max)) and an increase in the recovery time constant of V(max). Voltage clamp study showed that (+)-MK801 (3 microM) reduced inward Na(+) current (I(Na)), along with a slowing of its recovery from inactivation and a slight negative shift of its voltage-dependent steady-state inactivation curves. At a much higher concentration (30 microM), (+)-MK801 slightly reduced the amplitude of L-type calcium inward current (I(Ca)), although the voltage dependence of its steady-state inactivation was unaffected. For the potassium currents in rat ventricular cells, 3 microM of (+)-MK801 reduced the peak transient outward current (I(to)), steady-state outward current (I(ss)) and inward current through K(1) channels. The inhibition of I(to) was associated with a prominent negative shift in the voltage dependence of its steady-state inactivation curve. The outward current through K(1) channels was unaffected. These results indicate that (+)-MK801 may be a strong I(Na) and I(to) blocker with some I(Ca) blocking activity. The inhibition of I(to) and other K(+) efflux would prolong action potential duration, produce positive inotropic action and contribute to the negative chronotropic effect of (+)-MK801.lld:pubmed
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pubmed-article:10545774pubmed:authorpubmed-author:SuM JMJlld:pubmed
pubmed-article:10545774pubmed:authorpubmed-author:HuangC FCFlld:pubmed
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pubmed-article:10545774pubmed:pagination387-98lld:pubmed
pubmed-article:10545774pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:10545774pubmed:articleTitlePositive inotropic action of NMDA receptor antagonist (+)-MK801 in rat heart.lld:pubmed
pubmed-article:10545774pubmed:affiliationDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.lld:pubmed
pubmed-article:10545774pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10545774pubmed:publicationTypeIn Vitrolld:pubmed
pubmed-article:10545774pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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