| Autor: |
Sonna LA; Division of Pulmonary and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA., Hirshman CA, Croxton TL |
| Jazyk: |
angličtina |
| Zdroj: |
The American journal of physiology [Am J Physiol] 1996 Aug; Vol. 271 (2 Pt 1), pp. L251-7. |
| DOI: |
10.1152/ajplung.1996.271.2.L251 |
| Abstrakt: |
Magnesium ion (Mg2+) is a bronchodilator, but little is known about its mechanism of action on airways. We hypothesized that Mg2+ inhibits voltage-dependent Ca2+ channels of airway smooth muscle. Smooth muscle cells were freshly dispersed from pig trachea with collagenase. Depolarization-induced inward Ca2+ currents, measured in whole cell patch-clamp experiments, were inhibited by nifedipine and stimulated by BAY K 8644. Increasing bath Mg2+ from 1 to 21 mM caused a reversible approximately 30% inhibition of current and a positive shift of the peak current-voltage relationship. Voltage-dependent steady-state inactivation had a half-maximal potential (Vh) of -12 mV and a Boltzmann slope factor (k) of 6.0 mV. High Mg2+ caused a positive shift in Vh without affecting k, whereas nifedipine caused a negative shift in Vh and increased k. The inhibition of voltage-dependent Ca2+ channel currents by Mg2+ was quantitatively similar to Mg(2+)-induced relaxation of KCl-contracted tracheal smooth muscle strips. We conclude that inhibition of Ca2+ influx through dihydropyridine-sensitive, voltage-dependent channels by Mg2+ accounts for much of its relaxant action on airway smooth muscle. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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