PLASMA-RENIN ACTIVITY AND CHANGES IN TISSUE ANGIOTENSIN-CONVERTING ENZYME

Objectives: Recent evidence suggests that tissue generation of angiote nsins and II depends on the level of the plasma components of the reni n-angiotensin system and on tissue-specific processes. The present stu dy was undertaken to clarify the possible relationship between plasma renin activity (PRA) and tissue angiotensin converting enzyme (ACE) ac tivity in the heart, lung, kidney cortex and kidney medulla of Wistar- Kyoto rats. In the kidney cortex particular attention was focused on r enal brush-border ACE. Methods: Different experimental models known to have opposite effects on PRA were used: changes in salt intake, deoxy corticosterone acetate (DOCA) with or without salt supplements, and th e Goldblatt two-kidney, one clip (2-K,1C) model. Two weeks after the s tart of the experiments the rats were killed, and PRA, and plasma and tissue ACE activity, were measured. Results: At the end of the study t he blood pressure in the treated rats was not significantly different from control. As expected, the PRA were highest in the 2-K,1C and depl eted-salt groups and lowest in the DOCA, DOCA-salt and high-salt group s. ACE responses were different in different types oi tissue, with no relationship between PRA and plasma or tissue ACE activity. For exampl e, DOCA treatment led to increased ACE activity in the heart and the k idney only if the rats were maintained on a high salt intake. DOCA or salt alone failed to have this effect. In the 2-K,1C model the unclipp ed kidneys did not show any significant variation in ACE activity, but the clipped kidneys exhibited increased ACE activity compared with sh am-operated rats. This increase, coupled with increased renal renin se cretion, could play a role in the acceleration of local angiotensin II formation, and could thus initiate and sustain the development of hyp ertension in this model. Conclusion: The present results show that var iations in ACE activity were organ-specific and were not linked either to hypertension or to changes in PRA.