Although
deoxycorticosterone acetate (
DOCA)-
salt hypertension is a volume dependent model of
hypertension, it shows
polyuria and natriuresis. It is expected that dysregulation of
aquaporin water channels (AQPs) and
sodium transporters associated with
natriuretic peptide (NP) system may play an escape role in
sodium retaining state. One week after left unilateral
nephrectomy, rats were subcutaneously implanted with
silastic DOCA (200 mg/kg) strips. Physiologic saline was supplied as a
drinking water to all animals. 4 weeks after operation, the
protein expression of AQPs,
sodium transporters, and
endopeptidase (NEP) was determined in the kidneys by semiquantitative immunoblotting and immunohistochemistry. The
mRNA expression of NP system was determined by real-time polymerase chain reaction. The amount of urinary
ANP excretion was measured by radioimmunoassay. In
DOCA-
salt rats, urine osmolality was decreased while urinary excretion of
sodium was increased. The expression of AQP1-3 as well as that of alpha-1 subunit of Na,K-
ATPase, NHE3, NKCC2 and NCC was decreased in the kidney. The
mRNA expression of
ANP,
brain natriuretic peptide (BNP),
C-type natriuretic peptide (CNP) was increased in the kidney. The expression of NEP was decreased, and urinary
ANP excretion was increased. Downregulation of AQPs and
sodium transporters may contribute to
mineralocorticoid escape in
DOCA-
salt hypertension. Increased expression of
natriuretic peptides associated with downregulation of NEP may play a role in natriuresis.