Abstract
Noradrenaline (NA) regulates arterial smooth muscle tone and hence blood vessel diameter and blood flow1. NA apparently increases tone by causing a calcium influx through the cell membrane1–3. Two calcium influx pathways have been proposed: voltage-activated calcium channels and NA-activated calcium-permeable channels that are voltage-insensitive1. Although voltage-activated calcium channels have been identified in arterial smooth muscle4, 5, voltage-insensitive calcium channels activated by NA have not. We show here that NA contractions of rabbit mesenteric arteries increase with depolarization. The increase parallels the elevation of open-state probability (P ) of single, voltage-dependent calcium channels. The action of noradrenaline can be explained by NA-activating voltage-dependent calcium channels, rather than by opening a second type of channel. We show directly that N A increases the open-state probability of single calcium channels. Thus, in the presence of NA, calcium entry through voltage-dependent calcium channels can regulate smooth muscle tone at physiological membrane potentials. These results may have relevance to pathophysiological conditions such as hypertension.
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Nelson, M., Standen, N., Brayden, J. et al. Noradrenaline contracts arteries by activating voltage-dependent calcium channels. Nature 336, 382–385 (1988). https://doi.org/10.1038/336382a0
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DOI: https://doi.org/10.1038/336382a0
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