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Differential effects of Angiotensin II on intra‐renal hemodynamics in rats
Author(s) -
Igbe Ighodaro,
Oyekan Adebayo
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.968.1
Subject(s) - endocrinology , medicine , chemistry , angiotensin ii , agonist , hemodynamics , renal blood flow , glibenclamide , receptor , blood pressure , diabetes mellitus
Renal medullary blood flow (MBF) has been shown to differ qualitatively from cortical flow in response to certain vasoactive agents. The effect of AII infusion on intrarenal hemodynamics was investigated in rats testing the hypothesis that AT2 receptor mediates AII‐induced increase in renal MBF. AII (100, 300 and 1000 ng/kg/min) increased mean arterial blood pressure (MAP; 24±7%), decreased cortical blood flow (CBF; 30 ± 2%), but increased MBF (21±8%). Indomethacin (5 mg/kg), a COX inhibitor enhanced AII effects on MAP (154 ± 26%; p<0.05), MBF (141±46 %; p<0.05) and CBF (74±54%; p<0.05). NG nitro‐L‐arginine (L‐NNA), an inhibitor of NO synthase (100 mg/L orally) or 1H‐[1,2,4]oxadiazolo[4,3,‐a]quinoxalin‐1‐one (ODQ), a guanylyl cyclase inhibitor (2 mg/kg) enhanced AII effects on MAP (169±75 or 118±32%, p<0.05), CBF(107±50 or 85±47%, p<0.05) but blunted the effects of AII on MBF(150±21 or 96±15%, p<0.05). However, glibenclamide (20 μg/kg), a KATP+ channel blocker, was without effect. PD123319 (50 μg/kg/min), an AT2 blocker did not change basal or AII‐induced changes in MAP or CBF but blunted AII effects on MBF (60 ±11 %; p<0.05). CGP42112 (10 μg/kg/min), an AT2 agonist, reduced MAP but increased CBF and MBF ‐ effects were antagonised by PD123319. These findings demonstrate that AT2 receptors mediate AII‐induced increase in MBF by mechanisms involving guanylyl cyclase and NO but not prostanoids or KATP+ channels.