TY - JOUR
T1 - Endothelium-derived nitric oxide does not modulate metabolic coronary vasodilation induced by tachycardia in dogs
AU - Katsuda, Yousuke
AU - Egashira, Kensuke
AU - Akatsuka, Yutaka
AU - Narishige, Takahiro
AU - Shimokawa, Hiroaki
AU - Takeshita, Akira
PY - 1995/9
Y1 - 1995/9
N2 - Endothelium-derived nitric oxide (EDNO) has been implicated in the modulation of coronary arterial tone. The aim of this study was to determine if metabolic coronary vasodilation induced by pacing tachycardia is altered by the inhibition of EDNO synthesis. Before and after the intracoronary infusion of an inhibitor of EDNO synthesis (Nω-nitro-L-arginine-methyl-ester, L-NAME), changes in coronary blood flow (CBF), regional myocar-dial blood flow (MBF), and myocardial oxygen consumption (MVo2) were measured in anesthetized dogs in response to atrial pacing tachycardia. Increasing the heart rate from 109 ± 10 to 160 beats/min by pacing produced significant increases in CBF (p < 0.05), MVo2(p < 0.05), and MBF in each sublayer of the myocardium (p < 0.05). L-NAME did not alter the pacing-induced increases in CBF, MVo2, or regional MBF. In addition, the ratio of the tachycardia-induced increase in CBF to the increase in MVo2was not changed by L-NAME. The coronary vasodilation evoked by acetylcholine was attenuated by L-NAME (p < 0.05). However, the response to sodium nitroprusside was not altered. These results suggest that EDNO does not play a primary role in the mechanism mediating metabolic coronary vasodilation induced by pacing tachycardia in dogs.
AB - Endothelium-derived nitric oxide (EDNO) has been implicated in the modulation of coronary arterial tone. The aim of this study was to determine if metabolic coronary vasodilation induced by pacing tachycardia is altered by the inhibition of EDNO synthesis. Before and after the intracoronary infusion of an inhibitor of EDNO synthesis (Nω-nitro-L-arginine-methyl-ester, L-NAME), changes in coronary blood flow (CBF), regional myocar-dial blood flow (MBF), and myocardial oxygen consumption (MVo2) were measured in anesthetized dogs in response to atrial pacing tachycardia. Increasing the heart rate from 109 ± 10 to 160 beats/min by pacing produced significant increases in CBF (p < 0.05), MVo2(p < 0.05), and MBF in each sublayer of the myocardium (p < 0.05). L-NAME did not alter the pacing-induced increases in CBF, MVo2, or regional MBF. In addition, the ratio of the tachycardia-induced increase in CBF to the increase in MVo2was not changed by L-NAME. The coronary vasodilation evoked by acetylcholine was attenuated by L-NAME (p < 0.05). However, the response to sodium nitroprusside was not altered. These results suggest that EDNO does not play a primary role in the mechanism mediating metabolic coronary vasodilation induced by pacing tachycardia in dogs.
KW - Coronary circulation
KW - Endothelium-derived relaxing factor
KW - Nitric oxide
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U2 - 10.1097/00005344-199509000-00014
DO - 10.1097/00005344-199509000-00014
M3 - Article
C2 - 8583786
AN - SCOPUS:0029086719
SN - 0160-2446
VL - 26
SP - 437
EP - 444
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
IS - 3
ER -