Effect of α-human atrial natriuretic peptide on the synthesis of dopamine in the rat kidney

Open Access
Publisher Website
Google Scholar
Abstract
1 The present study has examined the influence of α-human atrial natriuretic peptide (α-hANP) on the synthesis of dopamine and its deamination into 3,4-dihydroxyphenylacetic acid (DOPAC) in rat kidney slices loaded with exogenous l-dihydroxyphenylalanine (l-DOPA). 2 α-hANP (3.3 and 330 nm) was found to produce a marked reduction (63– 78% reduction) in the time-dependent accumulation of newly-formed dopamine and of its deaminated metabolite DOPAC in kidney slices loaded with 10 μm l-DOPA. α-hANP (330 nm) was also found to decrease the accumulation of newly-formed dopamine (45– 66% reduction) and DOPAC (38– 61% reduction) in experiments in which increasing concentrations (1– 100 μm) of l-DOPA were used. This inhibitory effect was found to be potentiated by zaprinast (M&B 22,948; 10 μm), a guanosine cyclic 3′,5′-monophosphate (cyclic GMP) phosphodiesterase inhibitor. Alone, zaprinast also decreased the accumulation of both dopamine (54–71% reduction) and DOPAC (73– 92% reduction). 3 In kidney homogenates, α-hANP (330 nm) was found to affect neither the formation of dopamine nor its deamination to DOPAC. 4 Both α-hANP (330 nm) and zaprinast (10 μm) were found not to affect the formation of dopamine and DOPAC in kidney slices obtained from rats on a high salt diet during the previous 6 weeks. A similar situation was also found to occur when kidney slices obtained from 24-months old rats were used. 5 The results obtained suggest that the inhibitory effect of α-hANP on the renal synthesis of dopamine is dependent on the activation of a membrane-operated mechanism, coupled to the enzyme guanylate cyclase, controlling the entry of l-DOPA into the cells.