Interaction between extracellular magnesium and the passage of calcium through the sarcolemma during depolarization of isolated feline coronary and femoral arteries.

The mode of action of Mg2+ on vascular smooth muscle has been examined in isolated feline coronary and femoral arterial segments using a sensitive in vitro method. Potassium (124 mM) was added to feline coronary and femoral arteries incubated in a calcium-free buffer solution containing 10 microM EGTA, and magnesium in various concentrations (1.2, 4.4 or 13.2 mM). Potassium induced during these conditions a small contraction whose magnitude was attenuated by raised concentrations of Mg2+ (4.4 and 13.2 mM). Subsequent cumulative addition of calcium (10(-6)-3 x 10(-3) M) resulted in concentration-dependent contractions. The magnitude of these contractions was magnesium-dependent; the contraction elicited was depressed and a dextral shift of the extracellular calcium concentration-response relation was noted in the presence of increased concentrations of Mg2+ (4.4 and 13.2 mM). In separate experiments performed on potassium-depolarized (124 mM) feline coronary arteries it was noted that magnesium-induced relaxation was not changed by the presence of propranolol (10(-6) M), cimetidine (10(-6) M) or atropine (10(-5) M). In addition, the mechanical removal of the endothelium did not affect the dilator effect of Mg2+, as examined in potassium-depolarized (124 mM) feline femoral arteries. Hence, it may be concluded that Mg2+ may interfere with the passage of extracellular calcium through the sarcolemma, and that the dilator effect of magnesium is not the result of a direct action on beta-adrenoceptors, histamine H2 or cholinergic receptors, or requires the presence of an intact endothelium.