Calcium dependency of the post-stimulatory potentiation of the neurogenic response in small mesenteric arteries from the rat
- 1 November 1989
- journal article
- research article
- Published by Wiley in Acta Physiologica Scandinavica
- Vol. 137 (3) , 443-448
- https://doi.org/10.1111/j.1748-1716.1989.tb08775.x
Abstract
We have previously shown that the contraction of small mesenteric arteries in response to nerve stimulation is enhanced by preceding high-frequency stimulation. We have now investigated the calcium dependency of this post-stimulatory potentiation. Small arteries (inner diameter 150-250 .mu.) from normotensive rats were dissected free from surrounding tissue, and segments were mounted in a myograph where the wall tension was measured at well-defined circumferences. Nerve stimulation was performed by field stimulation. A single stimulation of the nerve caused a contraction of 2.6 .+-. 0.25% of maximal adrenergic response. After a high-frequency nerve stimulation with 16 Hz and 480 pulses the response to a single nerve stimulation was enhanced 6.6 .+-. 1.3 times. The potentiation decayed with a time constant of 93.7 .+-. 20.0 s. The amplitude of the post-stimulatory potentiation was dependent on the extracellular calcium concentration during the conditioning stimulation. In a solution containing 2.5 mM calcium the single twitch was enhanced 6.6 times while after exposure to reduced calcium (0.5 mM) it was only enhanced twice. The contraction caused by a short burst of high-frequency nerve stimulation (20 Hz and 10 pulses) was potentiated four times by a conditioning stimulation (16 Hz and 480 pulses), and this potentiation seemed to be independent of the extracellular calcium concentration during the conditioning stimulation. Thus the magnitude of the post-stimulatory potentiation of single nerve stimulations is linearly related to the extracellular calcium concentration during the conditioning nerve stimulation. For the potentiation of the response to burst stimulation no relation was found between the potentiation and extracellular calcium.Keywords
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