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Am J Physiol Renal Physiol 281: F1132-F1140, 2001. First published August 15, 2001; doi:10.1152/ajprenal.0078.2001
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Vol. 281, Issue 6, F1132-F1140, December 2001

Endothelin resets renal blood flow autoregulatory efficiency during acute blockade of NO in the rat

R. Kramp, P. Fourmanoir, and N. Caron

Service de Physiologie et Pharmacologie, Faculté de Médecine et de Pharmacie, Université de Mons-Hainaut, 7000 Mons, Belgium

First published August 15, 2001; 10.1152/ajprenal.00078.2001.---Renal blood flow (RBF) autoregulatory efficiency may be enhanced during NO inhibition in the rat, as recently reported. Under these conditions, endothelin (ET) synthesis and release may be increased. Our purpose was therefore to determine the role of ET in RBF autoregulatory changes induced by NO inhibition. To address this point, ETA/B receptors were blocked in anesthetized rats with bosentan, or selectively with BQ-610 or BQ-788. NO synthesis was inhibited with NG-nitro-L-arginine methyl ester (L-NAME). Mean arterial pressure (MAP) was decreased after bosentan (-10 mmHg; P < 0.01) or increased after L-NAME (25 mmHg; P < 0.001). RBF measured with an electromagnetic flow probe was reduced by L-NAME (-50%) and by BQ-788 (-24%). The pressure limits of the autoregulatory plateau (PA ~100 mmHg) and of no RBF autoregulation (Po ~80 mmHg) were significantly lowered by 15 mmHg after L-NAME but were unchanged after bosentan, BQ-610, or BQ-788. During NO inhibition, autoregulatory resetting was completely hindered by bosentan (PA ~100 mmHg) and by ETB receptor blockade with BQ-788 (PA ~106 mmHg), but not by ETA receptor blockade with BQ-610 (PA ~85 mmHg). These results suggest that the involvement of ET in the RBF autoregulatory resetting occurs during NO inhibition, possibly by preferential activation of the ETB receptor. However, the relative contribution of ET receptor subtypes remains to be further specified.

renal vascular resistance; renal hemodynamics; autoregulation; angiotensin; nitric oxide


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