Renal dopamine and sodium homeostasis

Abstract

During the past decade, it has become evident that dopamine plays an important role in the regulation of fluid and electrolyte balance and blood pressure. Dopamine exerts its actions through two families of dopamine receptors, designated D1-like and D2-like, which are identical in the brain and in peripheral tissues. The two D1-like receptors--D1 and D5 receptors--expressed in mammals are linked to stimulation of adenylyl cyclase. The three D2-like receptors--D2, D3, and D4,--are linked to inhibition of adenylyl cyclase. Dopamine affects fluid and electrolyte balance by regulation of renal excretion of electrolytes and water through actions on renal hemodynamics and tubular epithelial transport and by modulation of the secretion and/or action of vasopressin, renin, aldosterone, catecholamines, and endothelin B receptors (ETB) receptors. It also affects fluid and sodium intake by way of "appetite" centers in the brain and alterations of gastrointestinal tract transport. The production of dopamine in neural and non-neural tissues and the presence of receptors in these tissues suggest that dopamine can act in an autocrine or paracrine fashion. This renal autocrine-paracrine function, which becomes most evident during extracellular fluid volume expansion, is lost in essential hypertension and in some animal models of genetic hypertension. This deficit may be caused by abnormalities in renal dopamine production and polymorphisms or abnormal post-translational modification and regulation of dopamine receptor subtypes.

Chronic regulation of the renal Na+/H+exchanger NHE3 by dopamine: translational and posttranslational mechanisms

“…A principal natriuretic effector in vertebrates is the intrarenal dopamine (DA) system (117). DA is synthesized in the mammalian kidney and maintains Na ϩ homeostasis by altering renal Na ϩ transport as an autocrine/ paracrine natriuretic hormone (9,64). The precursor of dopamine, L-dihydroxyphenylalanine (L-DOPA), is taken up into the proximal tubule cell from the glomerular filtrate and plasma, and decarboxylated into DA via the aromatic amino acid decarboxylase in the proximal tubule cell (29,52,86,100,104,110).…”

Inhibition of natriuretic factors increases blood pressure in rats

“…There are remarkable parallels in abnormal D1 receptor signaling in rodent hypertensive models and in human essential hypertension (2,7,19,20). In both, there is a failure of dopamine to activate D1 receptors and cause inhibition of Na/H exchanger and Na-K-ATPase activities in renal proximal tubules (2,7,19,20).…”

Renal Redox Balance and Na+, K+-ATPase Regulation: Role in Physiology and Pathophysiology

“…In the kidney dopamine type 1 receptors can also couple to G q/11 and activate the phospholipase Cdiacylglycerol-protein kinase C pathway. Both a cross-talk between the protein kinase A and protein kinase C signaling pathways or an activation of the phospholipase C-protein kinase C pathway by protein kinase A have been described (Aperia, 2000;Brismar et al, 2000;Gomes & Soares-da-Silva, 2002;Hussain & Lokhandwala, 1998;Jose et al, 2000). Thus, activation of plasma membrane dopamine type 1 receptors stimulates a tissue specific signal cascade that leads to the activation of the protein kinase C δ-isoform.…”