In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: IV. In vitro bioassay of the vasoinhibitory activity of sera from patients suffering from peripheral ischaemia.
The widespread cutaneous vasodilation which can be induced by low-frequency transcutaneous nerve stimulation (TNS) in humans is, at least in part, due to sympatho-inhibition. Studies on the additional involvement of an active local vasodilator have demonstrated a moderate increase in plasma vasoactive intestinal polypeptide (VIP) but excluded a series of known dilators. In the present study sera from four patients with peripheral ischaemia (three with Raynaud's disease, and one with diabetic polyneuropathy) were assayed for vasoactivity on isolated vascular smooth muscle (rat portal vein) with reactivity towards a wide series of classical neurotransmitters and neuropeptides. In the presence of cholinergic and beta-adrenergic blockade sera collected after TNS-induced vasodilation revealed an inhibitory activity which could not be accounted for by changes in osmolarity, pH or K+. The inhibitory response to the plasma samples developed more rapidly than the response to synthetic VIP. The inhibitory activity of the plasma samples excluded a series of other peptides such as substance P, neurotensin, pancreatic polypeptide, bradykinin and angiotensin II, which all enhanced the contractile activity in the rat portal vein. There was a proportional increase in skin temperature and occurrence of inhibitory activity in cubital plasma samples in response to TNS. The results suggest that a peripheral vasodilator activity besides VIP may be implicated in the sustained dilation induced by TNS in these patients.[1]References
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