Endothelial hyperpolarizing factor increases acetylcholine-induced vasodilatation in pulmonary hypertensive broilers arterial rings.

Abstract

Pulmonary arterial hypertension (PAH) develops as result of imbalances between endothelium derived vasoconstrictors and vasodilators. Pulmonary hypertensive broiler chickens (PHBs) are deficient in NO production and endothelin-1 (ET-1) excess. With respect to prostacyclin, it appears that it does not alter vascular pulmonary tone in broilers. However, the role of Endothelium-Derived Hyperpolarizing Factor (EDHF) in PAH in broilers has not been determined. The possible involvement of EDHF in acetylcholine (Ach) induced vasodilatation was studied in pulmonary arterial rings taken from PHB and non-pulmonary hypertensive broilers (NPHBs). Ach induced higher vasodilatation in PHB than in NPHB. This dilatation seems to be directly related to the degree of PAH. Ach derived vasodilatation was inhibited, in PBH but not in NPHB, by blocking EDHF action with K(+) or Apamin plus Charybdotoxin. It is proposed EDHF as an important vasodilator in the pulmonary arteries of PHB, which may play a compensatory role in PAH pathophysiology.