Modulation of arterial endothelin-1 receptors following chronic increases in blood flow.
Experiments were designed to determine whether or not increased contractions to endothelin-1 (ET-1) in arteries chronically exposed to increased blood flow were due to a change in the subtype, number, or affinity of ET receptors on the smooth muscle. A fistula was created between one femoral artery and vein in dogs; contralateral blood vessels were operated as shams. After 6 weeks, the femoral arteries were removed. In both fistula- and sham-operated arteries suspended for the measurement of isometric force in organ chambers, the contractile potency was ET-1 > ET-2 > ET-3. Specific binding of [125I]ET-1 as a function of membrane protein was significantly greater in fistula compared to sham-operated arteries (Bmax = 184.8 +/- 35.9 and 117.4 +/- 25.6 fmol/mg, n = 6, respectively). Affinity of binding was the same in each group of arteries. These results suggest that ETA receptors mediate contraction on canine femoral arterial smooth muscle. These receptors may be upregulated when the artery is exposed chronically to increased blood flow.
D000818:Animals; D001783:Blood Flow Velocity; D004285:Dogs; D016232:Endothelins / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D005263:Femoral Artery / Q000378:metabolism* / Q000502:physiology; D008297:Male; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D011869:Radioligand Assay; D017466:Receptors, Endothelin / Q000378:metabolism*; D014661:Vasoconstriction / Q000187:drug effects
D016232:Endothelins; D017466:Receptors, Endothelin