P. Guillaume et al., INCREASED PLASMA ATRIAL-NATRIURETIC-PEPTIDE AFTER ACUTE INJECTION OF ALCOHOL IN RATS, The Journal of pharmacology and experimental therapeutics, 271(3), 1994, pp. 1656-1665
A number of mechanisms may be involved in the protective effect of low
ethanol (ETOH) consumption on the development of the age-dependent hy
pertension in both human and experimental animals. It was the objectiv
e of the present study to test the hypothesis that acute administratio
n of low doses of ETCH would increase the plasma content of atrial nat
riuretic peptide (ANP), a hormone known to decrease blood pressure. Pl
asma 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 r
ather 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 posti
njection. It has been suggested that opioids could play a significant
role in controlling ANP release. In fact, circulating levels of beta-e
ndorphin were also rapidly increased after the ETOH injection, with a
timecourse pattern similar to that of ANP. Furthermore, a highly posit
ive correlation was found between the ETOH-induced changes of plasma A
NP and p-endorphin contents. Significant increases in plasma corticost
erone and adrenocorticotropic hormone, but not aldosterone contents, w
ere 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 sma
ll tachycardia did develop in the FTOH-treated animals. Thus, acute in
vivo administration of ETCH increased plasma ANP content in a dose-de
pendent manner and may play a role in the ''protective'' effect of low
ETOH consumption in the development of the age-dependent hypertension
.