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Török TL, Tóth PT, Rácz D, et al. The role of internal calcium-stores in the termination of noradrenaline release during sodium-pump reactivation in peripheral nerves. Neurochem Int. 1987;10(2):205-11doi: 10.1016/0197-0186(87)90129-x.
Török, T. L., Tóth, P. T., Rácz, D., Nguyen, T. T., Medhin, D. G., Azzidani, A. M., Fekete, M. I., & Magyar, K. (1987). The role of internal calcium-stores in the termination of noradrenaline release during sodium-pump reactivation in peripheral nerves. Neurochemistry international, 10(2), 205-11. https://doi.org/10.1016/0197-0186(87)90129-x
Török, T L, et al. "The role of internal calcium-stores in the termination of noradrenaline release during sodium-pump reactivation in peripheral nerves." Neurochemistry international vol. 10,2 (1987): 205-11. doi: https://doi.org/10.1016/0197-0186(87)90129-x
Török TL, Tóth PT, Rácz D, Nguyen TT, Medhin DG, Azzidani AM, Fekete MI, Magyar K. The role of internal calcium-stores in the termination of noradrenaline release during sodium-pump reactivation in peripheral nerves. Neurochem Int. 1987;10(2):205-11. doi: 10.1016/0197-0186(87)90129-x. PMID: 20501072.
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Neurochem Int. 1987;10(2):205-11. doi: 10.1016/0197-0186(87)90129-x.

The role of internal calcium-stores in the termination of noradrenaline release during sodium-pump reactivation in peripheral nerves.

Neurochemistry international

T L Török, P T Tóth, D Rácz, T T Nguyen, D G Medhin, A M Azzidani, M I Fekete, K Magyar

Affiliations

  1. Department of Pharmacodynamics, Semmelweis University of Medicine, Budapest, Hungary.

PMID: 20501072 DOI: 10.1016/0197-0186(87)90129-x

Abstract

The release of [(3)H]noradrenaline has been measured from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3 x 10(?5) M; corticosterone, 5 x 10(?5) M). K(+)-removal from Krebs solution increased the release of [(3)H]NA even in the absence of external calcium. K(+)-readmission to the external medium terminated the transmitter release. The rate of recovery was much faster than the rate of rise of transmitter release both in the presence and absence of external Ca(2+). The main aim of the present study was to examine whether the reactivated Na(+)-pump per se or the Na(+)-gradient dependent Ca(2+)-extrusion and -uptake into the internal calcium-stores is responsible for the termination of transmitter release. In Ca(2+)-free, 1 mM EGTA containing solution the "K-free" stimulated [(3)H]NA release was further enhanced by calcium-store releasers (CCCP, 10(?5) M; A23187, 3 x 10(?6) M). External K(+)-readmission was effective in abolishing the transmitter release evoked by CCCP and A23187. However when veratrine (10(?4) g/ml) was also present the readmitted K(+) was ineffective in inhibiting the [(3)H]NA release although the Na(+)-pump was fully activated by the elevated level of Na(+) inside. The results suggest that the Na(+)-gradient dependent Ca(2+)-metabolism of the nerves is responsible for the abolition of transmitter release rather than the Na(+)-pump reactivation per se.

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