ENDOTHELIUM-DEPENDENT VASCULAR SMOOTH-MUSCLE RELAXATION ACTIVATED BY ELECTRICAL-FIELD STIMULATION

Electrical field stimulation (EFS) produced relaxation of contracted a rteries in the presence of tetrodotoxin. In the present study the cont ributions of vascular smooth muscle repolarization and endothelial rel ease of nitric oxide to the relaxation response were investigated usin g isolated rat tail arteries and bovine aortic endothelial cells (BAEC ). Intact and endothelium-denuded rings or intact, pressurized artery segments were contracted with either phenylephrine or KCl prior to EFS . Electrical field stimulation induced a small relaxation in denuded, phenylephrine contracted rings that was inhibited by the K+ channel bl ockers glibenclamide and BaCl2. In intact, phenylephrine-contracted ri ngs, EFS induced significantly larger relaxations that were inhibited by BaCl2 as well as by L-NAME, an inhibitor of nitric oxide (NO) synth ase, and methylene blue. EFS-induced relaxations were completely inhib ited when BaCl2 and L-NAME or methylene blue were combined. Exposure t o Ca2+ free buffer or diltiazem also inhibited the relaxation while as corbic acid had no effect. Effluent from electrically stimulated BAEC caused denuded, phenylephrine contracted rings to relax. The ability o f the effluent to cause relaxation was almost completely blocked by ex posure of the BAEC to L-NAME or exposure of the recipient vascular smo oth muscle to methylene blue; glibenclamide caused partial blockade. S imultaneous measurements of membrane potential and intraluminal pressu re showed that EFS-induced membrane repolarization preceded changes in steady-state pressure. It is concluded that (1) the smooth muscle cel ls possess an endothelium-independent repolarization mechanism, (2) EF S causes endothelial cells of intact arteries to release NO and possib ly a hyperpolarizing factor, (3) EFS of BAEC causes release of NO, and (4) EFS-induced relaxation depends on vascular smooth muscle cell mem brane repolarization and endothelial cell release of vasoactive substa nces.