In a rat model of CCl4-induced acute renal failure, the circulating active renin-angiotensin system does not appear to drive pathophysiology, though prorenin levels correlate with renal dysfunction.
Does not implicate active RAS in experimental acute renal failure; hypothesis-generating for prorenin as dysfunction correlate in animal models.
Plasma renin activity (PRA), plasma angiotensin I concentration (ANG I), plasma angiotensinogen concentration (PAC) and the plasma levels of active, total and inactive renin (prorenin) were measured in rats with carbon tetrachloride (CCl4)-induced acute renal failure. Rats were treated with a single oral dose of CCl4 (2.5 mL/kg) and killed 1, 2, 3 and 7 days later. 2. On days 1-3 PRA, ANG I and PAC decreased and increased on day 7. Active renin fell on days 2 and 3, total renin (trypsin treatment) augmented on day 1 and diminished on day 3, prorenin and per cent prorenin increased on days 1 and 2. Angiotensin I concentration paralleled PRA and PAC. The CCl4-induced decrease in PRA was secondary to the fall in active renin and in PAC. Total renin augmented as a consequence of the elevation of prorenin. Renal function, evaluated by serum urea, serum creatinine and creatinine clearance, decreased on days 1 and 2 when PRA was low and plasma prorenin was high. 3. These data do not support the involvement of the circulating active renin-angiotensin system (RAS) in the pathophysiology of acute renal failure induced by CCl4, however, increased prorenin levels were associated with the decrease in renal function.
No takes yet. Share an insight, caveat, or question.
Cruz et al. (1993) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: