Abstract
1 The hypothesis that magnesium deficiency, linked to the magnesium content of drinking water, induces major tone increases in coronary arteries and enhances their responses to vasoactive agents to an extent sufficient to explain sudden death associated with ischaemic heart disease was examined in an in vitro preparation. 2 The spontaneous tone of cattle coronary arteries was not increased during a 30 min exposure to Mg2+-deficient Krebs until the mineral was omitted entirely from the bathing medium, and even then the observed increase was small. Only in strips maintained under extremely deficient conditions for a prolonged period, namely Mg2+ concentration of 0.2 mM and 0.0 mM for 3 h, was tone substantially greater than in controls in standard (1.2 mM) Mg2+-Krebs. 3 Responses to acetylcholine and to noradrenaline were not increased in Mg2+-free Krebs but those to potassium and to 5-hydroxytryptamine were enlarged over the lower parts of their concentration-response curves. Responses to potassium and to 5-hydroxytryptamine were also examined in Krebs containing very low concentration of Mg2+ (0.4 and 0.2 mM) and only modest increases in contraction size were detected. Increases in the Mg2+ concentration of the Krebs (to 4.8 mM) depressed responses to potassium and 5-hydroxytryptamine. 4 It is concluded that Mg2+ deficiency must be nearly complete (0.4-0.0 mM) to induce even moderate tone increases in coronary vessels, or to sensitize them to agonist responses, and that there is no reason to link marginally subnormal Mg2+ levels, occasionally reported in humans with heart disease, to marked changes in coronary dynamics.