Microelectrode study on the ionic mechanisms which contribute to the noradrenaline‐induced depolarization in isolated cells of the rabbit portal vein

Abstract

1 Experiments were carried out to determine the identity of the ionic mechanisms which contribute to the noradrenaline-evoked depolarization recorded with microelectrodes in freshly dispersed rabbit portal vein cells. 2 In normal physiological salt solution with microelectrodes containing 1 M NaCl the reversal potential (Er) of the noradrenaline-induced response was -7.6 + 2.9 mV. When the external NaCl was replaced by equipmolar concentrations of Nal, NaBr and NaNO3, Er was -33 3.5 mV, -29.1 + 5.2 mV and -18.4 1.1 mV, respectively.3 In physiological salt solution E, of noradrenaline-evoked responses recorded with electrodes filled with M NaI or M NaNO3 was + 16.3 3.9mV and + 10.0 7.6 mV, respectively. These results suggest that an increase in anion conductance contributes to the depolarization to noradrenaline. 4 Data from experiments with organic anions indicated that glutamate behaves as a less permeant anion but that benzenesulphonate blocks the anion conductance to unmask another conductance mechanism activated by noradrenaline. 5 When external NaCl was substituted by choline Cl and Tris Cl Er was -21.3 + 3.7 mV and -20.5 + 2.8 mV, respectively. These results suggest that noradrenaline also activates a cation conductance mechanism in freshly dispersed rabbit portal vein cells. It is concluded that the depolarization to noradrenaline recorded with a microelectrode is produced by the simultaneous activation of an anion channel and a separate cation channel.

The developing relationship between receptor‐operated and store‐operated calcium channels in smooth muscle

“…In addition to ATP, noradrenaline, released as a co‐transmitter from sympathetic nerves and acting on α‐adrenoceptors, also produced depolarizations of the rabbit ear artery (Trapani et al ., 1981) by activating a non‐selective cation conductance (Amédée et al ., 1990). The current produced by noradrenaline differed to that produced by ATP in both its time‐ and voltage‐ dependence but was similar to that activated by noradrenaline, again acting on α 1 adrenoceptors, in cells isolated from the rabbit portal vein (Byrne & Large, 1988; Amédée & Large, 1989; Wang & Large, 1991). The channels underlying the current in portal vein were calcium permeable (Byrne & Large, 1988) as required for a ROCC.…”

Interactions between membrane potential and intracellular calcium concentration in vascular smooth muscle

“…(1991 ). There is solid evidence that calcium released from intracellular stores can activate chloride channels in the membrane and thus depolarize the tissue ( Byrne & Large 1988, Amédée & Large 1989, Large 1991, Pacaud et al . 1989 , 1991, 1992).…”

Facilitatory effect of Ca2+ on the noradrenaline‐evoked cation current in rabbit portal vein smooth muscle cells

“…In rabbit portal vein smooth muscle cells noradrenaline activates calcium‐activated chloride and potassium currents ( I Cl(Ca) and I K(Ca) ) and a non‐selective cation current ( I cat ; Byrne & Large, 1988). It has been proposed that the physiological role of I cat is to produce depolarization and provide a direct influx pathway for Ca 2+ and thus lead to contraction of vascular smooth muscle (Amédée & Large, 1989; Wang & Large, 1991).…”