Abstract
Other papers in this volume and elsewhere (Brown et al., 1979; Brown and DiFrancesco, 1980; DiFrancesco and Ojeda, 1980; Yanagihara and Irisawa, 1980) have already described the properties of an inward current, if (or ih), that is slowly activated during hyper polarization beyond about -50 mV in the SA node. In its time course, its voltage range for activation/deactivation and in its response to adrenaline, this current bears many resemblances to the s-mechanism described by Noble and Tsien (1968) as controlling an outward K+ current, iK2, in Purkinje fibres (DiFrancesco and Ojeda, 1980). As this resemblance became clear, so also did an obvious puzzle; the s-mechanism is described as activating on depolarization and controls an outward current. This produces the same overall current change as an inward current activated by hyper polarization; but had nature really developed two systems for producing this current change in the heart by such different means? It seemed rather unlikely.
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References
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DiFrancesco, D., Noble, D. (1982). Implications of the Re-Interpretation of iK2 for the Modelling of the Electrical Activity of Pacemaker Tissues in the Heart. In: Bouman, L.N., Jongsma, H.J. (eds) Cardiac Rate and Rhythm. Developments in Cardiovascular Medicine, vol 17. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-7535-4_7
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DOI: https://doi.org/10.1007/978-94-009-7535-4_7
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