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MODULATION OF SYMPATHETIC TRANSMISSION BY NITRIC OXIDE IS MAINTAINED IN RATS WITH PULMONARY HYPERTENSION

Pulmonary hypertension (PH) is a chronic disabling disease that largely affects the pulmonary vasculature. In this study, we have examined the effect of blocking NOS on sympathetic neurotransmission in the pulmonary artery and how this is influenced by PH. Rats treated with MCT developed pulmonary hypertension. Electrical field stimulation (EFS) of the pulmonary artery produced frequency‐dependent contractions. The frequency‐response curve was shifted to the left in artery segments from pulmonary hypertensive rats. The non‐selective NOS inhibitor, L‐NAME (0.1 mM), potentiated EFS‐induced contractions at all frequencies of stimulation in both groups with no difference between the groups. 7‐NI, an inhibitor of neuronal NOS had no effect. Noradrenaline produced concentration‐dependent contractions of pulmonary artery segments from control and MCT‐treated rats. L‐NAME potentiated the contractions in control but not MCT‐treated rats. It was concluded that endothelial NO modulated adrenergic neurotransmission in the rat pulmonary artery and this was not affected by pulmonary hypertension.