Abstract
This chapter summarizes several studies that investigate renal interstitial (RIF) dopamine (DA) and urinary DA excretion (U DA V) in anesthetized rats on either normal or high sodium balance and in response to acute administration of a DA prodrug, γ-L-glutamyl-L-dopa (gludopa). Responses of renal sodium excretion and intrarenal blood flow distribution to gludopa have also been examined. The studies confirmed that U DA V increases in response to chronic salt loading. The mechanism underlying the observed reduction in RIF DA with chronic salt loading is not apparent. Histofluorescent and neurochemical findings also suggest the presence of dopaminergic neurons in the kidney, and adrenergic nerves may become dopaminergic under certain circumstances. Vagal afferents have been shown to stimulate renal release of DA and produce a neurogenically mediated natriuresis. The data confirm that the main source of DA in the urine is nonneuronal, and further demonstrate that renal nerve activity does not contribute significantly to either urinary or interstitial fluid DA. The studies presented in the chapter strongly support that intrarenal DA plays a role in the control of natriuresis through a tubule mechanism. The renal sympathetic nerve endings are closely related to the juxtaglomerular apparatus and proximal tubule cells. It has been also demonstrated that intrarenal production of DA and its renal effects are not significantly influenced by renal sympathetic nerve activity.
Published Version
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