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The primary beta-adrenergic receptor comes in several forms, the most common of which are arg389 and gly389. [30] The reasons for these effects are not fully understood but are probably related to blockade of beta-adrenergic receptors located on fat cells, liver cells, and other tissues, thus causing disruption of catecholamine-mediated control of lipid and carbohydrate metabolism in these tissues. In prior presentations, Cytokinetics scientists presented results that demonstrate that cardiac myosin activators increase cardiac contractility without increasing intracellular calcium and without stimulating beta-adrenergic receptors or inhibiting phosphodiesterase activity, mechanisms that may be arrhythmogenic and associated with other adverse clinical effects. |
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