PMID- 10193772
OWN - NLM
STAT- MEDLINE
DCOM- 19990525
LR  - 20181113
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 126
IP  - 4
DP  - 1999 Feb
TI  - Enhanced role for the opening of potassium channels in relaxant responses to 
      acetylcholine after myocardial ischaemia and reperfusion in dog coronary 
      arteries.
PG  - 925-32
AB  - 1. Anaesthetized dogs were subjected to 1 h occlusion of the left circumflex 
      coronary artery followed by 2 h of reperfusion. Relaxant responses were examined 
      in coronary artery rings removed proximal (nonischaemic) or distal (ischaemic) to 
      the site of occlusion. 2. Relaxant responses to acetylcholine (ACh) were similar 
      in nonischaemic and ischaemic artery rings. In addition ACh-induced relaxation of 
      nonischaemic and ischaemic artery rings was equally susceptible to inhibition of 
      nitric oxide (NO) synthase using L-N(G)-nitroarginine (L-NOARG, 10(-4) M), or to 
      inhibition of soluble guanylate cyclase using 
      1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ, 10(-5) M). 3. In nonischaemic 
      arteries, the relaxation to ACh was unaffected by high K+ (67 mM) but in 
      ischaemic arteries, the maximum relaxation to ACh was significantly reduced from 
      113+/-6 to 60+/-2% (ANOVA, P<0.05). Tetraethylammonium (TEA, 10(-3) M), an 
      inhibitor of large conductance calcium activated potassium (BK(Ca)) channels did 
      not inhibit the response to ACh in nonischaemic arteries but in ischaemic 
      arteries TEA significantly shifted the concentration response curve to ACh to the 
      right (pEC(50); nonischaemic, 7.07+/-0.25; ischaemic, 6.54+/-0.21, P<0.01, ANOVA) 
      without decreasing the maximum relaxation. TEA did not affect the responses to 
      sodium nitroprusside in either nonischaemic or ischaemic arteries. 4. In 
      conclusion, ischaemia/reperfusion did not change the sensitivity of 
      endothelium-dependent relaxation to L-NOARG or ODQ indicating that ischaemia did 
      not affect the contribution of NO or cyclic GMP to ACh-induced relaxation. 
      However, in ischaemic arteries the opening of the BK(Ca) channels contributed to 
      relaxation caused by ACh whereas TEA had no effect in nonischaemic arteries. The 
      factor responsible for the opening of this potassium channel was a factor other 
      than NO and may be endothelium derived hyperpolarizing factor (EDHF).
FAU - Chan, E C
AU  - Chan EC
AD  - Department of Pharmacology, University of Melbourne, Parkville, Victoria, 
      Australia.
FAU - Woodman, O L
AU  - Woodman OL
LA  - eng
PT  - Journal Article
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Potassium Channels)
RN  - 169D1260KM (Nitroprusside)
RN  - 2149-70-4 (Nitroarginine)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 4.6.1.2 (Guanylate Cyclase)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/*pharmacology
MH  - Animals
MH  - Coronary Vessels/*drug effects/physiology
MH  - Dogs
MH  - Female
MH  - Guanylate Cyclase/antagonists & inhibitors
MH  - Male
MH  - Myocardial Ischemia/*physiopathology
MH  - *Myocardial Reperfusion
MH  - Nitric Oxide/physiology
MH  - Nitroarginine/pharmacology
MH  - Nitroprusside/pharmacology
MH  - Potassium Channels/*physiology
MH  - Vasodilation/*drug effects
PMC - PMC1571206
EDAT- 1999/04/08 00:00
MHDA- 1999/04/08 00:01
PMCR- 2000/02/01
CRDT- 1999/04/08 00:00
PHST- 1999/04/08 00:00 [pubmed]
PHST- 1999/04/08 00:01 [medline]
PHST- 1999/04/08 00:00 [entrez]
PHST- 2000/02/01 00:00 [pmc-release]
AID - 0702376 [pii]
AID - 10.1038/sj.bjp.0702376 [doi]
PST - ppublish
SO  - Br J Pharmacol. 1999 Feb;126(4):925-32. doi: 10.1038/sj.bjp.0702376.