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Modulation of volume‐sensitive chloride current by noradrenaline in rabbit portal vein myocytes

The effect of noradrenaline on the volume‐sensitive chloride current (ICl(swell)) was studied with conventional whole‐cell recording techniques in freshly dispersed isolated smooth muscle cells of the rabbit portal vein. In the absence of receptor antagonists, noradrenaline produced an increase in the amplitude of ICl(swell) in some cells and a decrease in others. In the presence of the β‐adrenoceptor antagonist propranolol, noradrenaline increased ICl(swell) and in the presence of the α1‐adrenoceptor antagonist prazosin, noradrenaline reduced ICl(swell). The phospholipase C (PLC) inhibitor U73122 reduced the amplitude of ICl(swell) whereas the inactive analogue U73343 had no effect. The phorbol esters phorbol‐12‐myristate‐13‐acetate (PMA) and phorbol‐12,13‐dibutyrate (PDBu) increased the amplitude of ICl(swell) by approximately 60 and 100 %, respectively, in a voltage‐independent fashion. Inhibitors of protein kinase C (PKC) chelerythrine and calphostin‐C decreased the amplitude of ICl(swell) in a concentration‐dependent but voltage‐independent manner. Bath application of 8‐Br‐cAMP decreased ICl(swell) by about 60 % whereas the inhibitor of protein kinase A (PKA) KT5720 increased the amplitude of ICl(swell) by approximately 80–90 %. In the presence of propranolol, chelerythrine prevented the increase of ICl(swell) by noradrenaline; in the presence of prazosin, KT5720 blocked the inhibitory action of noradrenaline. The results show that in rabbit portal vein myocytes noradrenaline enhances ICl(swell) by acting on α1‐adrenoceptors and reduces ICl(swell) by stimulating β‐adrenoceptors. The data suggest that the potentiating and inhibitory effects of noradrenaline are mediated, respectively, by PKC and PKA.