Facilitation of renal autoregulation by angiotensin II is mediated through modulation of nitric oxide.

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    • Subject Terms:
      PERFUSION; REGULATION of body fluids; KIDNEYS; ANGIOTENSIN II; NITRIC oxide
    • Abstract:
      Abstract Aims: This study was designed to investigate the influence of angiotensin II (Ang II) and nitric oxide (NO) on autoregulation of renal perfusion. Methods: Autoregulation was investigated in isolated perfused kidneys (IPRK) from Sprague-Dawley rats during stepped increases in perfusion pressure. Results: Ang II (75–200 pM) produced dose-dependent enhancement of autoregulation whereas phenylephrine produced no enhancement and impaired autoregulation of GFR. Enhancement by Ang II was inhibited by the AT[sub 1] antagonist, Losartan, and the superoxide scavenger, Tempol. Under control conditions nitric oxide synthase (NOS) inhibition by 10 μ m N-omega-nitro-ι l-arginine methyl ester (ι l-NAME) facilitated autoregulation in the presence of non-specific cyclooxygenase (COX) inhibition by 10 μ m indomethacin. Both COX and combined NOS/COX inhibition reduced the autoregulatory threshold concentration of Ang II. Facilitation by 100 pm Ang II was inhibited by 100 μ m frusemide. Methacholine (50 nm) antagonised Ang II-facilitated autoregulation in the presence and absence of NOS/COX inhibition. Infusion of the NO donor, 1 μ m sodium nitroprusside, inhibited ι l-NAME enhancement of autoregulation under control conditions and during Ang II infusion. Conclusions: The results suggest than an excess of NO impairs autoregulation under control conditions in the IPRK and that endogenous and exogenous NO, vasodilatory prostaglandins and endothelium-derived hyperpolarizing factor (EDHF) activity antagonise Ang II-facilitated autoregulation. Ang II also produced a counterregulatory vasodilatory response that included prostaglandin and NO release. We suggest that Ang II facilitates autoregulation by a tubuloglomerular feedback–dependent mechanism through AT[sub 1] receptor-mediated depletion of nitric oxide, probably by stimulating generation of superoxide. [ABSTRACT FROM AUTHOR]
    • Abstract:
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