Mupanomunda M, Williams J F, Kaiser L
Department of Physiology, Michigan State University, East Lansing 48824-1101, USA.
Am J Vet Res. 1996 Feb;57(2):172-7.
To test the possible role of endothelial cells in mediating fade of norepinephrine-induced constriction and the effect of heartworm infection on these responses.
Rings of pulmonary vein from control and heartworm-infected dogs were constricted with norepinephrine (10(-5.5)M) and followed over 65 minutes. Time profiles were established by measuring active tension every 2 minutes for the first 10 minutes, then every 5 minutes for 15 minutes, then every 10 minutes for 40 minutes. Time profiles were done in pulmonary vein rings with and without endothelial cells, and in the presence and absence of N-nitro-L-arginine methyl ester (L-NAME; nitric oxide synthase inhibitor), mefenamic acid (cyclooxygenase inhibitor), or methylene blue (guanylate cyclase inhibitor).
12 noninfected control and 11 heartworm-infected dogs.
Pulmonary vein constricted with norepinephrine spontaneously loses tension (fades) over time. Fade was not different between control and heartworm-infected dogs. In pulmonary vein from control dogs, methylene blue decreased fade while L-NAME and mefenamic acid did not. In pulmonary vein from heartworm-infected dogs, L-NAME and methylene blue significantly decreased fade, but mefenamic acid did not.
Nitric oxide, but not cyclooxygenase products, mediates fade of norepinephrine-induced constriction in pulmonary vein from heartworm-infected dogs. In control dogs, neither nitric oxide nor cyclooxygenase products appear to be involved in fade. We conclude that in canine pulmonary vein, fade of norepinephrine-induced constriction is mediated, in part, by endothelial cells.
Altered production of endothelium-derived relaxing factors may be important in the pathogenesis of heartworm disease.
