Increased vasoconstrictor response to noradrenaline in femoral vascular bed of diabetic dogs. Is thromboxane A2 involved?

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Abstract
Study objective – The aim was to determine the role of cyclo-oxygenase products in the vasoconstrictor response of femoral arterial bed to noradrenaline and to analyse the role of vascular adrenoceptors in the synthesis of cyclo-oxygenase products. Design – The influence of intra-arterially injected cyclo-oxygenase inhibitors indomethacin and acetylsalicylic acid on alterations in conductance of femoral arterial bed induced by noradrenaline was compared in metabolically healthy and alloxan diabetic dogs. PGI2 and TXA2 synthesising ability of isolated femoral arterial rings was measured with and without inhibition of α adrenoceptors by phentolamine. Subjects – 18 metabolically healthy and 18 alloxan (560 μmol·kg−1) diabetic dogs of either sex, weight 16–28 kg, were studied. Measurements and main results – Noradrenaline produced greater (p−1 or by acetylsalicylic acid 140 μmol·kg−1 markedly reduced the response to noradrenaline in alloxan treated animals, but not in controls, thereby eliminating the different responsiveness of the two groups. Femoral arterial rings from diabetic animals synthesised similar amounts of PGI2 as control rings but formed more TXA2 (p−1) markedly reduced the production of TXA2, but not of PGI2, in diabetic vessels. Conclusion – The results show an increased release of TXA2 by isolated diabetic femoral arteries. It is therefore suggested that an α adrenoceptor mediated increase in TXA2 biosynthesis may play a part in the vascular hyperreactivity of the diabetic femoral arterial bed.