It is well known that opening of cation channels is one of the major ways of depolarizing and contracting smooth muscle. Activation of adrenoreceptors generally causes hyperpolarization of guinea-pig intestinal smooth muscle (Horinouchi et al. 2003) but if the potassium conductance is blocked often depolarization is produced (Vladimirova & Shuba 1980).

In these experiments on single cells isolated by enzyme treatment from the longitudinal layer of guinea-pig ileum, tight-seal voltage-clamp recordings (in whole-cell configuration) were made using internal (pipette) and bathing solutions containing 124 mM Cs⁺. A 10 mM BAPTA-4.6 mM CaCl₂ mixture was used to clamp [Ca²⁺]_i at 10^-7 M and calcium and magnesium were omitted from the external solution.

Guinea-pigs were humanely killed by cervical dislocation followed by exsanguination. Noradrenaline (10 µM) evoked an inward cation current (nI_cat) of 56 ± 28 pA (mean ± S.E.M., n = 20) at a holding potential of -40 mV which had a U-shaped current-voltage relationship. However, 10 µM carbachol evoked a cationic current of more that 400 pA amplitude (Zholos & Bolton, 1997). The reversal potential for nI_ca was 1 ± 4 mV (n = 8) close to E_Cs (which was 0 mV) and the involvement of Cl^– ions was excluded by replacing 100 mM CsCl with caesium methane sulphonate in the pipette solution. The noradrenaline-evoked conductance curve could be described by a Bolzmann relationship with V_1/2 = -74.8 mV, k = 3.9 mV and G_max = 3.57 nS.

Although carbachol (10 µM) evoked a cation current of more than 400 pA, its current-voltage relationship and reversal potential were very similar to those of nI_cat. Application of 10 µM carbachol prior to 10 µM noradrenaline increased the noradrenaline-evoked cation current by 20-30 %. It appears that both muscarinic and noradrenaline receptors are able to activate the same cation current and that interaction between their signal pathways can occur.