Key result
NG-nitro-L-arginine significantly attenuated the increase in coronary conductance during functional hyperemia induced by atrial pacing (from 28% to 16%), isoproterenol, and aortic constriction.
Endothelium-derived nitric oxide plays an important role in functional myocardial hyperemia, and may interact with adenosine to produce coronary vasodilation when myocardial oxygen consumption increases.
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Endothelial NO contributes to functional coronary hyperemia in this animal model; leaves open human relevance and therapeutic implications.
To investigate the role of endothelium-derived nitric oxide (EDNO) and adenosine in functional myocardial hyperemia, we examined the effect of NG-nitro-L-arginine (NNLA) and 8-p-sulfophenyl-theophylline (8-ST) on coronary vasodilation in response to increased myocardial oxygen consumption (MVO2) in anesthesized dogs. NNLA significantly attenuated the increase in coronary conductance from 28±6% to 16±2% with atrial pacing, from 69±5 to 36±6% with isoproterenol and from 25±6% to 9±4% with constriction of the aorta. The combined administration of NNLA and 8-ST did not further change coronary conductance. It appears that EDNO may play an important role in functional hyperemia. EDNO and adenosine may interact to produce coronary vasodilation when MVO2 increases.
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Kiyoaki Maekawa (1994) studied Functional myocardial hyperemia (n=20). NG-nitro-L-arginine (NNLA) and 8-p-sulfophenyl-theophylline (8-ST) vs. Saline infusion was evaluated on Increase in coronary conductance with atrial pacing (p=<0.05). NG-nitro-L-arginine significantly attenuated the increase in coronary conductance during functional hyperemia induced by atrial pacing (from 28% to 16%), isoproterenol, and aortic constriction.
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