Endothelin-1-induced contraction of bovine retinal small arteries is reversible and abolished by nitrendipine.

Abstract

Endothelin-1 (porcine/human) induced a prompt, reversible, potent, concentration-dependent contraction of bovine isolated retinal small arteries (internal diameter, approximately 200 microns) with a concentration of endothelin-1 required to give half-maximal contraction of 2 x 10(-10) M. The maximal contraction induced by endothelin-1 was equal to 89% of the maximal contractile capacity. The vessel response to endothelin-1 was dependent on extracellular Ca2+. Withdrawal of extracellular Ca2+ or addition of nitrendipine, 10(-6) M, reduced the response of vessels contracted with 10(-9) M endothelin-1 by 80% and 75%, respectively. These results indicate that the endothelin-1-induced contraction of retinal arteries is dependent on an influx of extracellular Ca2+ through membrane potential-operated calcium channels. Endothelin-1, 10(-13)-10(-10) M, did not induce a relaxation of endothelium-intact arteries, indicating that endothelin-1 is incapable of releasing endothelium-derived relaxing factor in the retinal circulation. These results suggest that endothelin may participate in the regulation of retinal artery tone.