Key points are not available for this paper at this time.
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.
Benham et al. (1988) studied this question.