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A monolayer culture of adult rat hepatocytes was used to study the effect of various components of the renin-angiotensin-aldosterone system (angiotensin II, aldosterone and angiotensinogen), and intracellular sodium depletion (by ouabaine addition) on the angiotensinogen production rate. Normal hepatocytes synthesized linearly angiotensinogen for 6 h at a mean rate of 110 pg angiotensin I generated/mg intracellular protein each h. The addition of hydrocortisone (0.1 microM) to the culture medium significantly enhanced the angiotensinogen production after 2 h of incubation (P less than 0.05), being about 2-fold higher than normal control values at the 6th h of incubation. In contrast to this increase, the addition of angiotensin II (70 nM) to the medium produced a higher stimulatory effect on angiotensinogen synthesis, being the differences with the control significants after 1 h of incubation (P less than 0.01). At the 6th h of incubation, angiotensin II enhanced the angiotensinogen production over 2 fold in relation to the control group. No change in the angiotensinogen production rate was observed in monolayer culture of hepatocytes in the presence of aldosterone (1 microM), angiotensinogen (0.1 microM) or ouabaine (10 microM). These results provide further evidence that angiotensinogen synthesis is subject to a positive feed-back mechanism by angiotensin II, indicating that this mechanism takes place at physiological levels of plasma AII.

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The effects of endogenous Plasma Renin Substrate (PRS) on the relationship between Plasma Renin Activity (PRA) and the Plasma Renin Concentration (PRC) have been studied in hyperthyroid rats, by l-triiodothyronine (T3) administration and in hypothyroid rats, by propylthiouracil (PTU) treatment, to clarify if PRA changes are an adequate index for evaluating the renin-angiotensin changes during the alterations in the thyroid function.Although in experimental situations studied the induced variation on PRC explains a 62 per cent of the changes in PRA, finding a good lineal correlation between both parameters (r = 0.79, P < 0.001). Not only does PRS play an important role on the kinetic of the enzymatic reaction but also explains jointly with PRC up to a 85 per cent of PRA alterations. PRS changes become more important during thyrotoxicosis where they limit in a higher degree the velocity of reaction due to inverse relationship between PRC and PRS (r = 0.74, P < 0.001).