Miller V M, Vanhoutte P M
Departments of Surgery, and Physiology and Biophysics, Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905, USA.
Acta Pharmacol Sin. 2000 Oct;21(10):871-6.
To identify the type of prostanoids produced by endothelial cells of trout aorta and to determine whether or not the smooth muscle responds to nitric oxide.
Ventral aortas, with and without endothelium from rainbow trout (S gairdneri), were incubated in a buffered salt solution.
Addition of the calcium ionophore A23187 caused a significant increase in prostaglandin E's and a consistent increase in the stable metabolite of prostacyclin (6-keto-prostaglandin F1 alpha) in the incubation media only when the endothelium was present. This production was inhibited by methylene blue (10 mumol/L). In rings of trout aorta without endothelium suspended for the measurement of isometric force in organ chambers, prostacyclin and prostaglandin E1 but not prostaglandin E2 caused concentration-dependent decreases in tension when the rings were contracted with acetylcholine. The smooth muscle did not relax to nitric oxide but did so to sodium nitroprusside. Relaxations to the latter nitrovasodilator were not inhibited by methylene blue. Descending aorta without endothelium from frogs relaxed in a concentration-dependent manner to nitric oxide.
Predominant endothelium-derived relaxing factors in trout aorta are prostaglandins, the synthesis of which can be inhibited by methylene blue. A phylogenetic appearance of nitric-oxide sensitive mechanism for vasodilatation, perhaps is associated with the transition from water to air respiration.
