Chonnam Med J.
2002 Jun;38(2):135-145.
Influence of Nitric Oxide Donor on the Regulation of ATP-sensitive K+ Channel Activity in Cardiac Myocytes
- Affiliations
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- 1Department of Pharmacology, Chonnam National University Medical School, Gwangju, Korea. kimjh@chonnam.ac.kr
- 2Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
- 3Chonnam National University, Research Institute of Medical Sciences, Gwangju, Korea.
- 4Department of Pharmacology, College of Veterinary Medicine, Gwangju, Korea.
Abstract
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It was investigated that effects of nitric oxide donors on the ATP-sensitive K+ channel (KATP channel) in isolated mouse ventricular cardiac myocytes using patch clamp techniques. In perforated whole-cell patches, sodium nitroprusside (SNP) and spermine NONOate, two nitric oxide (NO) donors, decreased the KATP currents induced by pinacidil or PCO400. In excised inside-out patches, the NO donors did not affect the KATP channel activity and were not effective on the channel activity which had been attenuated in the presence of internal ATP, either. However, in the presence of both ATP and NDP in the bath solution of the inside-out patches, the NO donors decreased KATP channel activity. In cell-attached patches, NO donors potentiated the pinacidil-induced KATP current. 8-bromoguanosine 3',5'-cyclic monophosphate, a cGMP analog, failed to increase KATP current induced by pinacidil. 1H-[1,2,4]oxadiazolo [4,3-a] quinozalin-1-one, a guanylyl cyclase inhibitor did not block the action of the NO donors. From these results it was inferred that nitirc oxide is involved in the regulation of KATP channel activity and evoked a complex pattern of interaction with mouse cardiac KATP channels and that the stimulatory effects of NO on KATP channel activity may cause myocardial relaxation by opening KATP channel resulting in decreased load over the ischemic heart, but the inhibitory effects of NO on the KATP channel activity might seem to be a deleterious effect on heart.