Antagonistic effect of d-myo-inositol-1,2,6-trisphosphate (PP56) on neuropeptide Y-induced vasoconstriction in the feline dental pulp

Intra-arterial injection of neuropeptide Y (NPY) (1.3–2.0μg/kg) resulted in decreases of pulpal blood flow by 37.7 ± 5.7% (mean ± SEM). The intra-arterial injection of d-myo-inositol-1,2,6-trisphosphate (PP56) (0.3 mg/kg) alone changed pulpal blood flow by 1.0%. The effect of NPY in the presence of PP56 resulted in significantly smaller decreases in pulpal blood flow ranging from 27.2 ± 5.4 to 16.6 ± 3.5% from control as compared with NPY alone. In effect, PP56 partially blocked the decreases in pulpal blood flow caused by NPY. The electrical stimulation of the sympathetic nerve alone resulted in decreases in pulpal blood flow of 41.7 ± 6.2%. The electrical stimulation of the sympathetic nerve following the intra-arterial administration of PP56 decreased pulpal blood flow by 23.1 ± 6.0% from control, significantly less than the sympathetic nerve stimulation alone. PP56 attenuated the decrease in pulpal blood flow caused by the sympathetic nerve stimulation by 44.4 ± 11.0%. Similarly, the combination of PP56 and phentolamine followed by electrical stimulation of the sympathetic nerve reduced the decrease in pulpal blood flow caused by the sympathetic nerve stimulation alone by 43.0 ± 8.6%. These results provide evidence that the non-peptide PP56 is capable of antagonizing vasoconstriction caused by NPY in the feline dental pulp. In addition, they show functional evidence that NPY as well as noradrenaline are released from the sympathetic nerve endings during its stimulation and cause vasoconstriction.