In experimental heart failure models in dogs, the renin-angiotensin system was activated, whereas in the congestive syndrome produced by DOCA administration, the plasma renin level was suppressed.
A striking increase in the plasma renin level occurred in dogs with low output right heart failure secondary to tricuspid insufficiency and pulmonic stenosis and in three of five animals with high output failure produced by a large arteriovenous fistula. When dogs with a small arteriovenous fistula were given daily injections of DOCA, the renal sodium "escape" phenomenon occurred. In these animals, the level of plasma renin was suppressed during DOCA administration both during the initial period of sodium retention and also later when sodium balance was normal or negative. In contrast, when dogs with a larger arteriovenous fistula but without evidence of cardiac failure were given DOCA, they retained sodium and developed signs of congestive heart failure. However, in these animals with congestion and ascites, in contrast to the dogs that developed spontaneous high output failure, the plasma renin was low. Renin-substrate was unaltered in all of the experimental situations studied except for the decrease observed in dogs with low output right heart failure. In these animals, it seems likely that decreased renin-substrate was secondary to hepatic congestion and liver damage. The renin-angiotensin system does not seem to be related to the "escape" phenomenon, and renin does not appear to be the factor that makes the kidney unusually responsive to mineralocorticoids. Thus, in experimental heart failure the renin-angiotensin system was activated, but in the congestive syndrome produced by DOCA the plasma renin level was suppressed.
Johnston et al. (1968) studied Experimental heart failure. DOCA was evaluated on Plasma renin level. In experimental heart failure models in dogs, the renin-angiotensin system was activated, whereas in the congestive syndrome produced by DOCA administration, the plasma renin level was suppressed.