Endothelin-1 and Endothelin-3 increase renal perfusion pressure, with an exaggerated response to ET-1 in spontaneously hypertensive rats that is partially modulated by nitric oxide.
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No immediate clinical implications from rat data; leaves open endothelin modulation of renal perfusion in human hypertension.
We have investigated the effect of endothelin (ET)-1, ET-3 and ET-(16-21) on isolated and perfused rat kidney (IPK). ET-1 and ET-3 produced a similar dose-dependent increase in perfusion pressure of IPK, while ET-(16-21) was completely inactive. The ET-1 effects were greater in spontaneously hypertensive rats (SHR) as compared to normotensive rats (WKYR), whereas the ET-3 effects were greater in the SHR group only at the lowest doses. The pressure response of IPK induced by ET-1 was partially modified by prior application of the nitric oxide synthetase inhibitor L-nitroarginine in both WKYR and SHR.
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Evangelista et al. (1992) studied this question.
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