|Budget Amount *help
¥2,100,000 (Direct Cost : ¥2,100,000)
Fiscal Year 1996 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1995 : ¥600,000 (Direct Cost : ¥600,000)
Fiscal Year 1994 : ¥1,000,000 (Direct Cost : ¥1,000,000)
The present study was designed to determine whether or not halothane, an inhalation al anesthetic, which could inhibit electrical coupling between endothelium and smooth muscle through gap junction, could inhibit endothelium-dependent hyperpolarization of vascular smooth muscle in caninecoronary arteries. The membrane potential of smooth muscle cells was measured by glass capillary microelectrodes. In the presence of in domethacin and N^G-nitro-L-arginine (NLA), the resting membrane potential wasabout-50 mV,and was not affected by treatment with perindoprilat, an angiotensin converting enzyme in hibitor. In the presence of both in domethacin and NLA,bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat. Halothane did not inhibit membrane hyperpolarization to bradykinin. In higher concentration (10^<-4> M), halothane and heptanol (another inhalational an esthetic) caused depolarization of the membrane, but did not inhibit hyperpolarization to bradykinin. The present findings indicate that endothelium-dependent hyperpolarization in smooth muscle cells does not result from an electrical communication between the endothelium and the underlying smooth muscles, and suggest the existence of endothelium-derived hyperpolarizing factor EDHF.