Endothelium-dependent relaxations in rabbit aorta are depressed in artificial buffered solutions

Contractile and relaxant responses of rabbit aortae in artificial buffered (Tris and N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid) solutions were compared with those in bicarbonate-buffered solution. EC50 values for responses to KCl in aortae equilibrated in Tris and N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid were slightly less than those in bicarbonate; maximum contractions did not differ. There were no significant differences in contractile responses to prostaglandin Fa alpha or histamine in the three buffered solutions. In aortae precontracted with prostaglandin F2 alpha, both acetylcholine and the calcium ionophore, A23187, elicited much less relaxation in artificial buffered solutions than in bicarbonate-buffered solutions. Maximum relaxations to nitroprusside or D600 did not differ among the three solutions. Relaxant responses to isoproterenol were also depressed in artificial buffered solutions. Endothelial damage eliminated relaxant responses to acetylcholine and A23187, as well as the difference in responsiveness to KCl and isoproterenol noted in artificial buffered compared with bicarbonate-buffered solutions. Within the same solution, endothelial damage alone did not alter the responsiveness to KCl or histamine. Total and La -resistant Ca++ binding was similar in all three buffered solutions. Thus, contractile responses are not depressed in Tris- or N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solutions, whereas endothelium-dependent relaxations are attenuated in similar solutions. Overall, the results imply that, in artificial buffered solutions, the production and/or release of an endothelium derived relaxing factor is attenuated or that its action on aortic smooth muscle is, in some manner, functionally antagonized.