Dopamine is synthesized within the kidney in the proximal tubule from circulating L-dopa, via the enzyme L-amino acid decarboxylase [1-3]. There are also renal nerves that contain dopamine, although the physiologic significance of these nerves is unclear.
The renal actions of dopamine are discussed here. The use of dopamine in patients with shock is presented elsewhere. (See "Use of vasopressors and inotropes".)
Circulating and locally formed dopamine can affect both sodium excretion and renal hemodynamics via activation of the DA1 and DA2 receptors .
Natriuresis — Dopamine is a natriuretic hormone, increasing sodium excretion by diminishing reabsorption, primarily in the proximal tubule [1,2,4,5]. This effect of dopamine appears to involve both of the steps involved in transtubular sodium transport:
- Dopamine, acting via the generation of cyclic AMP, decreases the activity of the Na-H exchanger in the luminal membrane, a transporter that plays an important role in the entry of filtered sodium into the cell .
- Dopamine inhibits the Na-K-ATPase pump in the basolateral membrane [1,2,6]. Sodium that has entered the cell from the lumen is normally transported by this pump out of the cell into the peritubular interstitium (and then the peritubular capillary).