Renal alterations of atrial natriuretic peptide receptors by chronic moderate ethanol treatment

Previous studies have shown that chronic moderate ethanol (EtOH) consumption prevents the age-dependent increase in blood pressure. However, the physiological systems mediating the antihypertensive effects of EtOH are not known. The objective of the present studies was to investigate the effects of chronic (8 mo) moderate EtOH consumption on renal natriuretic receptors of spontaneously hypertensive (SHR) and normotensive (WKY) rats, using competitive binding assay and autoradiographic techniques. In the renal glomeruli, the maximal binding capacity (B-max) of the heterogeneous atrial natriuretic peptide (ANP) receptor population (NPR-A and NPR-C) was significantly lower in EtOH-treated SHR and WKY rats compared with water-treated controls. Quantification of receptor subtypes showed that this decrease was primarily the result of NPR-C downregulation. The apparent dissociation constant (K-d) was also decreased by the EtOH treatment. In the renal papilla, the B-max of the homogeneous receptor population (NPR-A) was significantly elevated by long-term EtOH consumption in both strains compared with water-treated controls. However, the K-d was unaltered by the EtOH administration. Thus EtOH treatment induced specific alterations in renal natriuretic receptors that may play a role in the ''protective'' effect of moderate EtOH consumption on the age-dependent increase in blood pressure.