Abstract
In addition to the beta-1 adrenergic receptor that mediates an increase in cardiac rate and force of contraction, myocardial alpha-1 adrenergic receptors are known to mediate a positive inotropic response with little effect on cardiac rate (Wagner and Brodde, 1978; Shibata et al., 1980). The mechanism by which cardiac alpha-1 adrenergic receptors increase force of contraction has not been established, but it appears not to be associated with accumulation of cyclic AMP or stimulation of adenylate cyclase (Brodde et al., 1978). In this respect, the alpha-1 adrenergic receptors differ from myocardial beta-adrenergic receptors. Another difference between alpha-1 and beta-1 adrenergic receptors in cardiac tissue is the slower onset and washout for alpha-1-mediated responses (Schumann et al., 1975). Electrophysiologic differences resulting from alpha-1 and beta-1 receptor activation have also been observed (Govier et al., 1966; Govier, 1967). Although beta-1 adrrenergic receptor-mediated inotropic responses occur at all rates of contraction, the effect mediated by the myocardial alpha-1 adrenergic receptor is most prominent at low heart rates (Broadley, 1982).
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Hieble, J.P., Ruffolo, R.R. (1987). Therapeutic Applications of Agents Interacting with alpha-1 Adrenergic Receptors. In: Ruffolo, R.R. (eds) The alpha-1 Adrenergic Receptors. The Receptors. Humana Press. https://doi.org/10.1007/978-1-4612-4582-7_12
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