Abstract
Early and chronic angiotensin-converting enzyme (ACE) inhibition in Lyfon hypertensive (LH) rats improves their blunted vasodilator response of renal medullary blood flow (MBF) to angiotensin II (AngII). This study examined the specificity of this effect and the possible involvement of nitric oxide (NO). The renal response to AngII (from 7.5 to 480 ng/kg, IV) and acetylcholine (Ach, from 3 to 192 microg/kg, IV) were examined in 12-week-old anesthetized LH rats treated orally from 3 weeks of age with perindopril (1.5 mg/kg/d), nifedipine (50 mg/kg/d), or a triple therapy with hydralazine, hydrochlorothiazide, and reserpine (75, 15, and 0.75 mg/kg/d, respectively). After 9 weeks of therapy, perindopril lowered systolic blood pressure to 113 +/- 3 mm Hg, nifedipine to 144 +/- 4 mm Hg, and triple therapy to 133 +/- 2 mm Hg compared with 160 +/- 3 mm Hg in untreated LH rats. Despite a significant reduction in blood pressure, only the treatment with perindopril significantly increased the vasodilator response of MBF to AngII. However, the vasodilator response of MBF to Ach was similar among the groups. In conclusion, a renal medullary protection is conferred in LH rats by ACE inhibition, an effect that is not obtained with other antihypertensive treatments and is not explained by Ach-induced NO release.
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