Increase in calcium channel current by β‐adrenoceptor agonists in single smooth muscle cells isolated from porcine coronary artery

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Abstract
The action of catecholamines (isoprenaline and noradrenaline) and forskolin on membrane currents was studied in single cells freshly dispersed from the pig coronary artery by use of the whole‐cell clamp method, usually with electrodes containing CsCl. In normal Krebs solution, with and without 30 mm tetraethylammonium (TEA) and 0.5 mm 4‐aminopyridine, isoprenaline (1–5 μm) clearly increased the inward currents elicited by membrane depolarization, without affecting the holding current at −80 mV. The same effect was observed when the external Cl− was replaced with isethionate. The outward current recorded with K+‐containing electrodes was not significantly affected by isoprenaline. In the presence of 67 mm Ba2+ and 30 mm TEA, the maximum inward current recorded with CsCl containing electrodes was 119 ± 7pA (the mean ± s.e.mean, n = 90) in cells where the current was larger than 30 pA. The L‐type Ca2+ channel was considered to be responsible for these currents, based on the threshold voltage, the slow time course of decay, the large depolarization necessary to produce inactivation, and the high susceptibility to the Ca2+ channel antagonist, nicardipine. Isoprenaline and noradrenaline increased the amplitude of inward currents evoked by depolarizing pulses. The maximum inward current was potentiated by 43 ± 7% (n = 12) by isoprenaline and 39 ± 10% by noradrenaline (n = 6) at a concentration of 1 μm. These effects were strongly inhibited by propranolol, but not phentolamine. Forskolin (10 μm) also potentiated the currents to a similar degree. It is suggested that stimulation of β‐adrenoceptors increases the amplitude of inward currents through L‐type Ca2+ channels in the pig coronary artery and that intracellular cyclic adenosine monophosphate is likely to be inolved in this action.