Increased renal atrial natriuretic peptide synthesis in rats with
deoxycorticosterone acetate-salt treatment.
Lee, Yau-Jiunn, Shyi-Jang Shin, Mian-Shin Tan, Tusty-Jiuan Hsieh,
Juei-Hsiung Tsai.
Graduate Institute of Medicine, Kaohsiung Medical College,
Kaohsiung, Taiwan, 80713 Republic of China
APStracts 3:0093F, 1996.
To investigate the role of renal synthesis of atrial natriuretic
peptide (ANP) as a contributor to the water-sodium homeostasis, we
studied the effects of electrolyte-water imbalance on renal ANP mRNA
levels, plasma ANP concentrations and urinary ANP excretion rates by
using reverse transcription-polymerase chain reaction (PCR) and
radioimmunoassay. Male Wistar rats divided into three groups: 1) the
control group, 2) deoxycorticosterone acetate (DOCA)-salt treated
group, and 3) low-salt treated group. The urinary sodium excretion
rate and urine volume in the DOCA-salt rats were significantly
elevated at two days and for the 10-day study. The urinary ANP
excretion rate in DOCA-salt rats was significantly increased at 2
days after treatment and was well correlated to the urinary sodium
excretion rate (r=0.76, p<0.01). Plasma ANP levels in the DOCA
-salt rats were elevated on the day of sacrifice. In contrast, plasma
renin activities were markedly suppressed in DOCA-salt rats and
increased in Low-salt rats. By immunohistochemical study,
immunoreactive ANP materials were mainly localized in the proximal
and distal cortical tubules of the kidney. Using PCR cloning and
sequencing technique, ANP cDNA was cloned from the rat kidney, and
the sequences were identical to that of ANP identified in the atria.
By semi-quantitative PCR technique, the expression of ANP mRNA in the
ventricle and renal cortex tissues was significantly enhanced in the
DOCA-salt rats. Our results confirm that the rat kidney is a site of
ANP synthesis and indicate that renal ANP synthesis is enhanced in a
volume expansion state. We propose that renal synthesized natriuretic
peptide participates in the intra-renal regulation of water
-electrolyte homeostasis and may contribute to renal adaptation during
the mineralocorticoid escape phenomenon.
Received 12 February 1996; accepted in final form 6 May 1996.
APS Manuscript Number F45-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96