Presynaptic and postsynaptic actions of cadmium in cardiac muscle.
A transmembrane flux of Ca2+ has been demonstrated in many nerve and muscle cells. In cardiac muscle, Ca2+ channels in the sarcolemma transfer sufficient Ca2+ to trigger and partially control tension development. This time- and voltage-dependent Ca2+ current is also important in the development of the pacemaker potential, or diastolic depolarization. In addition, transmitter release from autonomic nerve varicosities in the myocardium exhibits a strong dependence on external calcium concentration [( Ca2+]o). Agents that selectively alter either pre- or postsynaptic Ca2+ channels are therefore of considerable interest. Our results illustrate two distinct effects of Cd2+ in cardiac muscle. Data from conventional electrophysiological recordings from primary pacemaker cells within the rabbit sinoatrial node indicate that Cd2+ (10(-6)-10(-5) M) may selectively inhibit acetylcholine release. Voltage clamp measurements of transmembrane Ca2+ currents in single isolated bullfrog atrial cells show that Cd2+ (10(-4)-10(-3) M) is also a very potent inhibitor of postsynaptic Ca2+ channels; these effects of Cd2+ mimic those seen after [Ca2+]o removal.
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D019256:Cadmium Chloride; D002118:Calcium / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000187:drug effects*; D006325:Heart Atria / Q000187:drug effects; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D011817:Rabbits; D011892:Rana catesbeiana; D012849:Sinoatrial Node / Q000187:drug effects; D013569:Synapses / Q000187:drug effects*
D007473:Ion Channels; D002104:Cadmium; D019256:Cadmium Chloride; D002118:Calcium