APStracts 3:0070C, 1996.

Intracellular adp-ribose inhibits atp-sensitive k+ channels in rat ventricular myocytes. Kwak, Yong-Geun, Seok-Ki Park, Uh-Hyun Kim, Myung-Kwan Han, Jae-Soon Eun, Kyu-Park Cho, and Soo-Wan Chae. Departments of Pharmacology and Biochemistry, and Institute of Cardiovascular Research, Chonbuk National University Medical School, Chonju 560-182, South Korea; Departments of Pharmacology, Woosuk University College of Pharmacy, Wanju 565-800, South Korea

APStracts 3:0070C, 1996.

Cyclic ADP-ribose (cADPR), an NAD metabolite, has been shown to be a messenger for Ca2+ mobilization from intracellular Ca2+ stores. However, the physiological role of ADP-ribose (ADPR), another metabolite of NAD, is not known. We examined the effects of cADPR and ADPR on the ATP-sensitive K+ channel (KATP) activity in rat ventricular myocytes using the inside-out patch clamp configuration. ADPR, but not cADPR, inhibited the channel activity at micromolar range with a Ki of 38.4 [mu]M. The Hill coefficient was 0.9. ATP inhibited the K+ channel with a Ki of 77.8 [mu]M, and the Hill coefficient was 1.8. Single channel conductance was not affected by ADPR. These findings strongly suggest that ADPR may act as a regulator of KATP channel activity.

Received 2 October 1995; accepted in final form 23 February 1996.
APS Manuscript Number C599-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96