The present study was aimed to explore an interaction between endothelium-derived nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in normotensive and hypertensive states. Rats were made two-kidney, one clip (2K1C) hypertensive and supplemented with either $N^G-nitro-L-arginine$ methyl ester (L-NAME, 5 mg/100 ml drinking water) or L-arginine hydrochloride (400 mg/100 ml drinking water). One group supplied with normal tap water served as control. Sham-clipped rats were also divided into the L-NAME, L-arginine, and control groups. The plasma levels and atrial contents of ANP were determined at day 28 following clipping the renal artery. In 2K1C rats, the plasma level of ANP was higher and the atrial content was lower than in the sham-clipped control. L-Arginine increased the atrial content of ANP in association with a decreased plasma ANP, whereas L-NAME significantly affected neither parameter. The increase of blood pressure in 2K1C rats was not affected by L-arginine or L-NAME. In sham-clipped rats, the plasma level of ANP was significantly increased by L-NAME along with an increase in blood pressure. On the contrary, L-arginine did not affect the blood pressure or plasma ANP. The atrial content of ANP was significantly altered neither by L-arginine nor by L-NAME. These results suggest that NO plays a tonic inhibitory role on the ANP release with concomitant increases of the atrial tissue content. In addition, hypertension is suggested to modify the release and tissue storage of ANP.
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