1. ^*Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina, U.S.A.
2. ^†Department of Physiology, Albert Szent-Györgyi Medical University, Szeged, Hungary
3. ^‡Department of Anatomy and Cell Biology, East Carolina University Medical School, Greenville, North Carolina, U.S.A.

Correspondence: Ferenc Bari, Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1083, U.S.A.

Received 21 May 1997; Revised 8 July 1997; Accepted 10 July 1997.

Abstract

Our previous studies indicate that function of ATP-dependent K⁺ channels (K_ATP) in cerebral arterioles is suppressed after ischemia. In the current study, we examined pial arteriolar responses to forskolin, dibutyryl-cAMP, NS-1619, and methionine (met)-enkephalin, activators of calcium-dependent K⁺ channels (K_Ca) before and 1 hour after 10 minutes of total, global ischemia in anesthetized piglets. Arteriolar diameters were measured using a closed cranial window and intravital microscopy. All pharmacologic agents were given topically. Baseline diameters were approximately 100 m, and diameters had returned to normal by 1 hour after ischemia. Forskolin dilated arterioles by 9 3%, 18 4%, and 31 12% at 5 10^-8, 5 10^-7, and 10^-6 mol/L, respectively (P < 0.05, n = 10). In addition, dibutyryl-cAMP dilated arterioles by 8 2% at 10^-4 mol/L and 14 2% at 3 10^-4 mol/L (P < 0.05, n = 6). Also, NS-1619 increased diameter of arterioles by 9 2% at 10^-7 mol/L and 17 9% at 10^-5 mol/L (P < 0.05, n = 5). Finally, met-enkephalin dilated arterioles by 9 2% at 10^-8 mol/L and 16 3% at 10^-6 (P < 0.05, n = 5). At 1 hour after ischemia, arteriolar dilator effects to forskolin, dibutyryl-cAMP and NS-1619, and met-enkephalin were intact. Thus, in contrast to K_ATP, K_Ca in cerebral arterioles are resistant to ischemic stress.