Characterisation of the response of equine digital arteries and veins to substance P.

The research sought to understand how Substance P (SP), a vasodilator found in the nerves of horse limbs, affects blood vessels in those limbs. The results showed that SP causes the blood vessels to dilate in a manner dependent on the amount used and the inner-lining of the vessels. Essential actions in this process involve nitric oxide (NO) pathway in the arteries while both prostacyclin and NO pathways function in the veins.

About the Research method

• This study aimed at investigating the functional responses of blood vessels in horse limbs (equine digital arteries (EDA) and veins (EDV)) to Substance P (SP), which is a potent vasodilator.
• The research was carried out by first inducing constriction in the considered blood vessels and then observing the relaxation response as SP was introduced to the system.
• The investigators used Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME; 300 microm) to inhibit nitric oxide (NO) synthase, which played a crucial role in observing how it affected the relaxation response curve.
• They also applied ibuprofen, to inhibit cyclo-oxygenase for discerning its role in influencing the vessels’ relaxation.

Research Findings

• The introduction of SP caused a two-fold, endothelium (innermost lining of blood vessels), and concentration-dependent dilation of both EDA and EDV. In essence, the response of these vessels to SP depended on the amount of SP introduced and the condition of their inner lining.
• In the arteries, the inhibition of NO synthase using L-NAME reduced both phases of the dilation response significantly by over 70%.
• However, in the veins, the first dilation phase was largely resistant to L-NAME, whereas the second phase was reduced by 60%.
• To inhibit the dilation in the veins by over 80%, both NO synthase and cyclo-oxygenase had to be inhibited using L-NAME and ibuprofen respectively.
• When researchers introduced low concentrations of SP into both veins and arteries, the dialing response was inhibited by a neurokinin-1 (NK1) receptor antagonist.

Conclusion

• The findings concluded that Substance P is a crucial vasodilator in both EDA and EDV, and its effect is dependent on the condition of the endothelium, and the concentration applied.
• The NO pathway plays an essential role in the dilation response in arteries. However, in veins, both prostacyclin and NO pathways are involved.
• The NK1 receptors are shown to mediate the responses of both types of vessels to low concentrations of SP.