Abstract
The present study was aimed to characterise the effect of dopamine on rat jejunal electrolyte transport and to evaluate the type of receptors and the intracellular signalling mechanisms involved in the response. Stripped epithelial sheets were mounted in Ussing chambers connected to an automatic voltage current clamp and changes in the short circuit current (μA/cm 2) were measured continuously as an index of electrogenic ion transfer. Dopamine (0.1–100 μM) produced a concentration dependent decrease in I sc with an EC 50 of 1.4±0.1 μM; the effect of dopamine was not changed by propranolol (1 μM), prazosin (1 μM and 10 μM) or (±)-sulpiride (1 μM), but was completely abolished by phentolamine (1 μM). The addition of phentolamine (0.3 μM) or yohimbine (0.3 μM) produced a rightward shift of the dopamine concentration-dependent curve with an increase in EC 50 values up to 30.0±0.2 μM and 11.7±0.1 μM, respectively. The α 2-adrenoceptor-selective agonist, UK14,304 (5-bromo- N-(4,5-dihydro-1 H-imidazol-2-yl)-6-quinoxalinamine), also produced a concentration-dependent decrease in I sc with an EC 50 of 0.04±0.01 μM; the addition of yohimbine (0.3 μM) increased the EC 50 value of UK14,304 to 0.68±0.01 μM. The addition of amiloride (100 μM), a Na + channel blocker, to the fluid bathing the apical side was found not to change the effect of dopamine on I sc. 5-( N-ethyl- N-isopropyl)-amiloride (10 μM), a selective Na +/H + exchanger inhibitor, partially antagonised the effect produced by 100 μM of dopamine. The addition of ouabain (1 mM) to the fluid bathing the basal side, antagonised the effect produced by 50 and 100 μM of dopamine. In contrast, frusemide (1 mM) completely abolished the effect of all concentrations of dopamine. Forskolin (10 μM) and N 6,2′- O-dibutyryl cyclic AMP (1 mM) added to both the apical and serosal sides completely abolished the effect of dopamine on I sc. It is concluded that the dopamine antisecretory effects in the jejunum of adult rats are mediated through α 2-adrenoceptors. This effect is sensitive to increases in intracellular cyclic AMP and is primarily dependent on the basal Na +,K +,2Cl −-co-transport mechanism.
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