Abstract
Potassium ions in dentifrices for treating 'hypersensitive' dentin are believed to act directly on intradental nerves by raising extracellular potassium ion concentration ([K+]o) sufficiently to prevent action potential generation by axonal accommodation. However, the [K+]o necessary to block nerve conduction is not precisely known, nor is it certain that K+ can diffuse from a dentifrice in sufficient amounts to inactivate intradental nerves. To establish more accurately the [K+]o required to block nerve conduction under controlled conditions, we studied the effects of increased [K+]o on the sizes of compound action potentials (CAP) recorded from rat spinal nerves in vitro. [K+]o was increased by the addition of either KCl or KNO3 to Krebs' solutions applied to the central portion of the nerves. CAP attenuation increased in a dose-dependent manner as [K+]o was raised in the 8 to 64 mmol/L range, and complete block was generally produced with solutions containing at least 32 mmol/L K+. CAP attenuation was reversible, and recovery times increased with increasing [K+]o. The effects of KCl and KNO3 solutions were the same for all [K+]o tested. Half-maximal (50%) reduction in the Aβ-fiber component of the CAP occurred with 17.4 mmol/L K+, and with 17.8 mmol/L and 19.3 mmol/L K+, respectively, for the AS- and C-fiber components. Control experiments with glucose and choline chloride confirmed that the conduction block observed with increased [K+]o was not due to increased solution osmolarity or ionic strength. Assuming that intradental axons are as sensitive to altered [K+]o as spinal nerve axons, we suggest that for K+ in dentifrices to block intradental nerve conduction: (1) [K+]o in excess of 8 mmol/L would have to be achieved around nerve axons in the inner dentin or peripheral pulp, and (2) increases in [K+]o of these magnitudes would have to be maintained in order for intradental nerve inactivation to be sustained.
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