Increased plasma atrial natriuretic peptide after acute injection of alcohol in rats

A number of mechanisms may be involved in the protective effect of low ethanol (ETOH) consumption on the development of the age-dependent hypertension in both human and experimental animals. It was the objective of the present study to test the hypothesis that acute administration of low doses of ETOH would increase the plasma content of atrial natriuretic peptide (ANP), a hormone known to decrease blood pressure. Plasma ANP levels were increased significantly within 15 min after the i.p. injection of 1 or 2 g of ETOH/kg b.wt. The increase in plasma ANP was more pronounced and longer lasting after the i.p. injection of 2 rather than 1 g of ETOH/kg b.wt. This increase in plasma ANP level was associated with a rapid decrease of atrial ANP, but not of ventricular ANP which on the contrary was significantly elevated at 120 min postinjection. It has been suggested that opioids could play a significant role in controlling ANP release. In fact, circulating levels of beta-endorphin were also rapidly increased after the ETOH injection, with a time-course pattern similar to that of ANP. Furthermore, a highly positive correlation was found between the ETOH-induced changes of plasma ANP and beta-endorphin contents. Significant increases in plasma corticosterone and adrenocorticotropic hormone, but not aldosterone contents, were observed after the i.p. injection of 2 g of ETOH/kg b.wt., whereas plasma arginine vasopressin levels were significantly decreased at 15 but not at 120 min postethanol. There was no significant elevation in blood pressure during the 120-min experimental period, although a small tachycardia did develop in the ETOH-treated animals. Thus, acute in vivo administration of ETOH increased plasma ANP content in a dose-dependent manner and may play a role in the "protective" effect of low ETOH consumption in the development of the age-dependent hypertension.