Noradrenaline modulation of calcium channels in single smooth muscle cells from rabbit ear artery
1. Whole-cell recordings of voltage-gated Ca2+ current in single smooth muscle cells from rabbit ear artery were obtained with 110 mM-Ba2+ as charge carrier. 2. Noradrenaline (NA, 1-20 microM) produced a sustained increase in the dihydropyridine-sensitive L-type Ca2+ current, ranging up to 3-fold in...
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Published in | The Journal of physiology Vol. 404; no. 1; pp. 767 - 784 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford
The Physiological Society
01.10.1988
Blackwell |
Subjects | |
Online Access | Get full text |
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Summary: | 1. Whole-cell recordings of voltage-gated Ca2+ current in single smooth muscle cells from rabbit ear artery were obtained
with 110 mM-Ba2+ as charge carrier. 2. Noradrenaline (NA, 1-20 microM) produced a sustained increase in the dihydropyridine-sensitive
L-type Ca2+ current, ranging up to 3-fold in some cells. The dihydropyridine-resistant T-type Ca2+ current was not affected.
3. The time and voltage dependence of activation and inactivation of the L-type current were not significantly changed during
NA modulation. 4. The NA-induced increase in L-current was enhanced in magnitude and consistency by the inclusion of 200 microM-GTP
in the pipette (internal) solution. 5. The effect of NA on L-current was not abolished by pre-treatment with prazosin, phentolamine
or propranolol, suggesting that it is not mediated by alpha- or beta-adrenoceptors. 6. Phenylephrine (5 microM) was ineffective
as an agonist, while adrenaline was approximately equipotent to NA. In these respects, the pharmacology of L-current modulation
resembles that of 'gamma'-adrenergic receptors (Hirst & Nield, 1980). 7. NA modulation of L-type Ca2+ channels may be particularly
important in promoting sympathetic vasoconstriction in resistance vessels where Ca2+ stores are relatively poorly developed
and where NA-evoked contractions are very sensitive to organic Ca2+ channel antagonists. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.1988.sp017318 |