Endothelin causes contraction of canine and bovine arterial smooth muscle in vitro and in vivo

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Abstract
We have studied the effect of endothelin, an endothelium-derived peptide, on isolated canine and bovine cerebral arteries in vitro and on canine vertebral blood flow (VBF) in vivo. Endothelin produced a dose-dependent contraction of canine and bovine arterial smooth muscle with ED50 values ranging from 4 to 8 nM. The response to endothelin developed slowly and persisted as a sustained contraction. Maximal contraction by endothelin required the presence of extracellular calcium and was independent of the presence of endothelium. The maximal contraction produced by endothelin was approximately 2–3 times greater than that produced by neuropeptide Y or angiotensin II. The injection of endothelin into the vertebral artery decreased vertebral blood flow (VBF) dose-dependently without affecting systemic blood pressure or heart rate. The decrease in VBF produced by endothelin was long-lasting, like that produced by neuropeptide Y, but more potent. The present data, together with our previous study demonstrating that the intracisternal injection of endothelin induces an unusually long-lasting decrease in the basilar artery diameter angiographically, suggests that endothelin may act as a long-acting vasoconstrictor in cerebral vascular disease.