Interaction between Gα12 and Gα13 protein subunits and dopamine receptors in renal proximal tubules

Abstract

The cells of the renal proximal tubules (RPTs) have high aromatic L-amino-acid decarboxylase activity. Filtered or circulating L-3,4-dihydroxyphenylalanine can be converted to dopamine after uptake into this extraneuronal compartment, without being subsequently converted to norepinephrine.1 Peripheral dopamine has been characterized as an important modulator of both renal sodium excretion and blood pressure by acting directly on renal epithelial ion transport and by modulating the secretion/release of other hormonal/humoral molecules. These hormonal and humoral molecules include aldosterone, catecholamines, renin and vasopressin, each of which contribute to the regulation of sodium homeostasis and blood pressure. In addition, other hormones may interact with dopamine produced in RPTs to increase (for example, atrial natriuretic peptide) or decrease (for example, angiotensin) its inhibitory effect on tubular sodium reabsorption. The actions of endogenous renal dopamine on water and electrolyte transport are modest under euvolemic conditions, but become magnified during moderate sodium excess. Thus, following a moderate acute or chronic sodium load, up to 50% of sodium excretion is mediated by dopamine produced by the RPTs.2