In DOCA salt-hypertensive dogs, ACE inhibitors decreased MAP and increased ERPF via bradykinin, while their natriuretic action involved inhibition of renal ANG II production.
In conscious deoxycorticosterone acetate (DOCA) salt-hypertensive dogs, the angiotensin-converting enzyme (ACE) inhibitors captopril and imidaprilat significantly decreased mean arterial pressure (MAP) and significantly increased urine flow rate, effective renal plasma flow (ERPF), glomerular filtration rate, and urinary sodium excretion. However, the angiotensin type 1 (AT1) receptor antagonist losartan caused a significant increase only in urinary sodium excretion without significant changes in MAP, urine flow rate, ERPF, and glomerular filtration rate. Simultaneous infusion of a bradykinin receptor antagonist inhibited the ACE inhibitor-induced reduction in MAP and increase in ERPF. DOCA salt treatment markedly suppressed plasma angiotensin II (ANG II) concentration (P < 0.001), although it decreased renal ANG II content only slightly (P < 0.05). Comparison of the expression of renal AT1 receptor mRNA in control kidneys with that in DOCA salt-hypertensive kidneys revealed no significant change. These results suggest that, in low-renin hypertension, inhibition of the relatively maintained ANG II production in the kidney participates in the natriuretic action of ACE inhibitors. However, hypotensive and other renal effects are mainly due to the action of bradykinin.
Naitoh et al. (1997) studied DOCA salt-hypertension (low-renin hypertension). ACE inhibitors (captopril and imidaprilat) and AT1 receptor antagonist (losartan) vs. Control was evaluated on Mean arterial pressure (MAP), urine flow rate, effective renal plasma flow (ERPF), glomerular filtration rate, and urinary sodium excretion. In DOCA salt-hypertensive dogs, ACE inhibitors decreased MAP and increased ERPF via bradykinin, while their natriuretic action involved inhibition of renal ANG II production.