Noradrenaline modulation of calcium channels in single smooth muscle cells from rabbit ear artery.

Abstract

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. Noradrenaline (NA, 1-20 .mu.M) 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. The time and voltage dependence of activation and inactivation of the L-type current were not significantly changed during NA modulation. The NA-induced increase in L-current was enhanced in magnitude and consistency by the inclusion of 200 .mu.M-GTP in the pipette (internal) solution. 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. Phenylephrine (5 .mu.M) 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 and Nield, 1980). 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.