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  • Title: Barium-induced diastolic depolarization and controlling mechanisms in guinea pig ventricular muscle.
    Author: Shen JB, Vassalle M.
    Journal: J Cardiovasc Pharmacol; 1996 Sep; 28(3):385-96. PubMed ID: 8877585.
    Abstract:
    Barium-induced diastolic depolarization (Ba(2+)-DD) and its modulation were studied in guinea pig papillary muscle and single ventricular myocytes. In papillary muscles, Cs+ (4 mM) abolished the DD induced by Ba2+ (0.05-0.2 mM) by abolishing the undershoot at the end of the action potential (AP; consistent with a block of an outward current). Acetylcholine (ACh 1 microM) had little effect on Ba(2+)-DD, whereas norepinephrine (NE 1 microM) enhanced it by increasing the undershoot and by inducing an oscillatory potential. Low [Ca2+]o (0.54 mM) decreased the resting potential and increased Ba(2+)-DD amplitude. High [Ca2+]o (8.1 mM) had opposite effects. Cs+ also reduced Ba(2+)-DD in low [Ca2+]o. In isolated myocytes, Ba(2+)-DD and the pacemaker current induced by Ba2+ (Ba(2+)-IKdd) increased on depolarization and reversed on hyperpolarization. Although not significantly, high [Ca2+]o slightly decreased and low [Ca2+]o slightly increased Ba(2+)-IKdd. Cd2+ markedly reduced the slow inward current ICa and the AP duration (APD), but did not affect Ba(2+)-IKdd. We conclude that Ba(2+)-DD (a) is entirely due to a voltage- and time-dependent decrease in gK1, since it is abolished by Cs+ (no contribution of a nonblocked decaying IK) by eliminating the undershoot (no If), (b) is potentiated by NE through an increased undershoot and an oscillatory potential, (c) is modified by high and low [Ca2+]o mostly through changes in the resting potential, and (d) is not affected by the block of the slow channel by Cd2+.
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