Premium
Role of Nitric Oxide Synthase and Cyclooxygenase in Pulmonary Vascular Control in Isolated Perfused Lungs of Ferrets, Rats and Rabbits
Author(s) -
Liu Xia,
Bee Denise,
Barer Gwenda R.
Publication year - 1999
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.1999.01853.x
Subject(s) - dilator , cyclooxygenase , nitric oxide synthase , nitric oxide , enzyme , pulmonary hypertension , blockade , chemistry , pulmonary artery , medicine , lung , endocrinology , pharmacology , biochemistry , receptor
SUMMARY Dilator products of nitric oxide synthase (NOS) and cyclooxygenase (COX) may contribute to the low normal pulmonary artery pressure ( P pa ). In isolated perfused lungs of ferrets, rabbits and rats we investigated this hypothesis by blockade of NOS with L‐NAME (L‐nitro‐arginine methyl ester) and COX with meclofenamate. There were species differences. Inhibition of either enzyme caused little rise in P pa in ferrets and rats but inhibition of both enzymes caused huge increases in P pa . We suggest this might be due to intracellular connections between the excitatory pathways for NOS and COX dilators, such that inhibition of one enzyme leads to activation of the other. Impairment of these endothelial‐based enzymes in pulmonary vascular disease might lead to severe pulmonary hypertension. By contrast, in rabbits, comparable doses of L‐NAME lead to large rises in P pa which were reversed rather than amplified by COX blockade. NO seems to protect against some pressor/oedema forming product of COX in this species.