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Albert, A. P. 
ORCID: https://orcid.org/0000-0002-3596-9634 and Large, W. A.
(2002)
Activation of store-operated channels by noradrenaline via protein kinase C in rabbit portal vein myocytes.
Journal of Physiology, 544 (1).
pp. 113-125.
ISSN 0022-3751
Abstract
In the present study we have investigated the role of diacylglycerol (DAG) and protein kinase C (PK) in mediating activation of Ca2+-permeable store-operated channels (SOCs) by noradrenaline in rabbit portal vein smooth muscle cells. With cell-attached recording, bath application of noradrenaline, 1-oleoyl-acetyl-sn-glycerol (OAG) and phorbol 12,13-dibutyrate (PDBu) evoked single channel currents. The biophysical properties of these channel currents were similar to those of the channel currents activated by depletion of internal Ca2+ stores with cyclopiazonic acid (CPA). The activation of SOCs in cell-attached recording by noradrenaline, OAG, PDBu, CPA and the acetoxymethyl ester form of BAPTA (BAPTA-AM) was markedly inhibited by the PKC inhibitors chelerythrine and RÖ-31-8220. In isolated outside-out patches CPA did not evoke SOCs but noradrenaline stimulated SOC activity, which was reduced by about 90 % by PKC inhibitors. The addition of the serine/threonine phosphatase inhibitors calyculin A and microcystin also stimulated SOCs in isolated outside-out patches. It is concluded that in rabbit portal vein myocytes, noradrenaline activates SOCs via DAG and PKC, possibly by a store-independent mechanism. In addition in this cell type it appears that PKC and phosphorylation may play an important role in stimulating SOC activity in response to depletion of internal Ca2+ stores by CPA and BAPTA-AM.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | physiology ,/dk/atira/pure/subjectarea/asjc/1300/1314 |
| Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
| Related URLs: | |
| Depositing User: | LivePure Connector |
| Date Deposited: | 29 Oct 2024 09:30 |
| Last Modified: | 03 Nov 2024 07:31 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/97280 |
| DOI: | 10.1113/jphysiol.2002.022574 |
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