Key result
Endothelin caused a concentration-dependent contraction of canine small renal arteries with a mean EC50 of 3.1 x 10^-10 M, which was partially inhibited by nifedipine and abolished by Ca2+-free solution.
Endothelin is a potent constrictor of canine small renal arteries, acting partially through dihydropyridine-sensitive calcium channels, though electromechanical coupling is not the sole determinant of constriction.
Endothelin potently constricts canine renal arteries partly via calcium channels; leaves open translation to human renovascular disease or therapy.
The contractile response of renal arterial muscle to porcine endothelin (ET-1) was studied by measuring vessel diameters and vascular smooth muscle transmembrane potentials in small arteries (300–600 μm inside diameter) isolated from dog kidneys and cannulated with micropipettes connected to a pressurized reservoir system. Endothelin (10−12 to 10−8 M) was a potent constrictor of these vessels and caused a concentration-dependent contraction at a mean EC50 (median effective concentration) of 3.1 (±1.15) × 10−10 M. Endothelin also produced a modest depolarization of arterial smooth muscle much smaller than had previously been demonstrated to occur in these vessels in response to norepinephrine or transmural pressure elevation. Endothelin-induced contractions were partially inhibited by 10−6 M nifedipine and abolished by Ca2+ -free solution. Although the influx of extracellular Ca2+ ions through dihydropyridine-sensitive pathways contributes to endothelin-induced contractions of these vessels, electromechanical coupling does not appear to be the sole determinant of the magnitude of endothelin-induced constriction in canine small renal arteries.
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Eskinder et al. (1994) studied this question. Endothelin (ET-1) was evaluated on Contractile response (vessel diameter and transmembrane potential) (mean EC50 3.1 x 10^-10 M). Endothelin caused a concentration-dependent contraction of canine small renal arteries with a mean EC50 of 3.1 x 10^-10 M, which was partially inhibited by nifedipine and abolished by Ca2+-free solution.
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