Captopril lowered blood pressure in normal, nephrectomized, and hypertensive rats, including those with blocked renin-angiotensin systems, suggesting an additional mechanism such as bradykinin potentiation.
Does captopril lower blood pressure through mechanisms other than renin-angiotensin blockade in rat models?
Captopril lowers blood pressure through mechanisms additional to angiotensin blockade, likely including bradykinin potentiation.
The peptide converting enzyme inhibitor captopril was given (1·25 mg/kg intravenously) to normal and nephrectomized rats and rats with renovascular and deoxycorticosterone hypertension. 2. Captopril lowered blood pressure to a small extent in normal and nephrectomized rats. Bradykinin infusion in nephrectomized animals, however, potentiated the vasodepressor action of captopril. 3. Captopril produced a major blood pressure fall in the early stages of Goldblatt two-kidney one-clip hypertension: even when hypertension had been present for more than 4 months, a substantial vasodepressor action was seen. Rats with deoxycorticosterone-induced hypertension also showed a significant blood pressure fall. 4. Captopril was given to salt-loaded and salt-depleted rats in which the renin-angiotensin system had been blocked by infusion of the competitive angiotensin II antagonist saralasin. Captopril still lowered blood pressure in the salt-depleted group. 5. Captopril lowers blood pressure in situations where the renin-angiotensin system is not responsible for blood pressure maintenance. Further, the fall in blood pressure produced in Goldblatt two-kidney one-clip hypertension is greater than would be predicted on the basis of renin-angiotensin blockade. It is likely therefore that captopril lowers blood pressure by an action additional to angiotensin blockade. Bradykinin potentiation is one possible mechanism by which this may take place.
Marks et al. (1980) studied Hypertension. Captopril was evaluated on Blood pressure fall. Captopril lowered blood pressure in normal, nephrectomized, and hypertensive rats, including those with blocked renin-angiotensin systems, suggesting an additional mechanism such as bradykinin potentiation.