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摘要
Background: Sodium and water transport across renal proximal tubules is regulated by diverse hormones such as dopamine and urodilatin We have previously reported that Urodilatin stimulates extraneuronal dopamine Uptake in external renal cortex by activation of the type A uptake peptide, receptor,coupled to Cyclic guanylate monophosphate signaling and protein kinase G. Moreover, urodilatin enhances dopamine induced inhibition of Na+, K+-ATPase activity in renal tubules. The aim of the present Study was to evaluate whether urodilatin could also alter renal dopamine Synthesis, release, catabolism and turnover. %26lt;br%26gt;Methods : The effects of urodilatin on dopamine synthesis release, catabolism and turnover Were measured in templet Of renal cortex from Sprague Dawley rats. %26lt;br%26gt;Results: The results indicate that urodilatin increases L-DOPA decarboxylase activity and decreases catechol-o-methyl transferase and monoamine oxidase activity. Moreover, Urodilatin does not affect either dopamine basal secretion or potassium chloride-induced dopamine release in external renal cortex, and reduces amine turnover. %26lt;br%26gt;Conclusions: Both the present results and previous findings show that urodilatin modifies dopamine metabolism in external renal cortex of rats by enhancing dopamine uptake and synthesis and by decreasing catechol-o-methyl transferase and monoamine oxidase activity and dopamine turnover. Those effects taken together May favor dopamine accumulation in renal cells and increase its endogenous content and availability. This would permit D-1 receptor recruitment and stimulation and, in turn, overinhibition of Na+, K+-ATPase activity, which results in decreased sodium reabsorption. Therefore, urodilatin and dopamine enhance netriuresis and diuresis through a common pathway.
- 出版日期2013-12
